Week 3 'Ears' Flashcards

1
Q

Conductive hearing loss
Etiologies

Make acronym: COPDOOOC

A

from (physical/mechanical) problems that limit movement of the sound wave through the external and middle ear; canal, tympanic membrane, auricular bones (Meatus, Incus, Stapes)
ETIOLOGIES:
i. obstructed external ear canal – eg. cerumen impaction, foreign body, exostosis, psoriais
ii. perforated tympanic membrane – eg direct trauma, otitis media, or explosion
iii. dislocated ossicle (malleus, incus, or stapes) - trauma to the ear
iv. Otitis media or serous otitis media
v. Otitis externa - infection of the ear canal that causes it to swell
vi. Otosclerosis or ossicular chain fixation
vii. Congenital: eg external auditory canal atresia
viii. Cholesteatoma: growth of squamous epithelium in middle ear

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2
Q

Sensorineural Hearing loss (SNHL)
Etiologies (11 of them)

Make an acronym: (SHABAM OVI BAM)

A

damage to the hair cells or nerves that sense sound waves in the inner ear
ETIOLOGIES:
i. acoustic trauma - prolonged exposure to loud noises
ii. barotrauma (pressure trauma) or ear squeeze - eg divers, climbers
iii. head trauma - eg fracture of the temporal bone
iv. ototoxic drugs - Bilateral loss, hx of use.
Examples include:
— antibiotics including aminoglycosides (gentamicin, vancomycin), erythromycin, and
​​ tetracycline
— salicylates (aspirin) and NSAIDs (ibuprofen, naproxen)
​ — antineoplastics (cancer drugs)
— cocaine—intranasal or IV
v. Infection – mumps, measles, influenza, herpes, mono, syphilis, meningitis
vi. Aging—presbycusis: progressive bilateral hearing loss (high pitches), normal neuro exam
vii. Acoustic neuroma - tumor in the auditory nerve.
viii. Sudden SNHL (SSNHL): unilateral hearing loss over 72 hr. Associated with microvascular
​event, head trauma
ix. Ménière disease - hearing loss, vertigo and tinnitus. Gradual onset, often progresses to
​​deafness and severe vertigo
x. Vascular diseases eg sickle cell disease, diabetes, polycythemia, and excessive clotting
xi. Multiple sclerosis

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3
Q

Mixed Hearing Loss

A

combination of both conductive and sensorineural loss

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4
Q

Approach to patient for the Ear

  1. PE
  2. Lab
  3. Imaging
  4. Other testing:
  5. Appropriate referral
A
  1. Physical exam
    Vitals
    EENT, Otoscopic, insufflation, hearing tests (whispered voice, tuning forks), neurological, CVS
  2. Laboratory, if indicated
    CBC, chemistry screen (CMP), culture any discharge
  3. Imaging studies, if indicated
    x-ray, CT or MRI to evaluate masses
  4. Other testing: audiology, tympanometry
  5. Appropriate referral
    EENT (otologist), neurologist, audiologist, etc.
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5
Q

Tinnitus

List the 2 main types:

A

perception of sound (eg buzzing, ringing, roaring clicks) in absence of an acoustic stimulus

  1. Subjective tinnitus
  2. Objective tinnitus
  3. Other types/causes
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6
Q

Subjective Tinnitus

Etiology

A

Subjective tinnitus - audible only to pt, due to damage of fine hair cells (MOST COMMON)

   Etiology: ​Acoustic trauma​​​, Presbycusis ​Barotrauma​​​, CNS tumors ​Eustacian tube dysfunction, ​Infections (OM, labryinthitis, meningitis) ​Meniere disease​​​, Ear canal obstruction (wax, foreign body, tumor​​​Drugs (salicylates, loop diuretics, cisplatin, aminoglycosides
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7
Q

Objective tinnitus

A

rare, can be heard by listening directly over the patients ear​
Etiology:
​ A-V malformations​ Turbulent flow in carotid A or jugular V
​ Vascular middle ear tumor (esp if unilateral—R/O by ordering CT)

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8
Q

Other causes of tinnitus

A
  1. Other types/causes: hyperlipidemia, allergies, diabetes, hypertension, hypotension, syphilis, CV disease, TMJ disorders, cervical injuries, stress, dietary deficiencies, intake of stimulants (nicotine, caffeine).
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9
Q

Work-up for tinnitus
History:
PE:

A

History: get good description of “sound” (episodic/constant, pitch, quality)
Ask re: noise exposure, head trauma, hearing problems, dizziness, loss of balance, recent dental problems/work, bruxism, stress, medications, smoking, caffeine, HTN, anxiety, insomnia

       PE:   Otoscopic exam, cranial N VIII function and hearing (whispered, tuning fork tests)
         Check for: carotid artery bruits, HTN, oral exam, neck/jaw hypertonicity, TMJ dysfunction ​Additional work-up: audiology, angiography
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10
Q

Vertigo

A

a type of dizziness
​sensation of altered spatial orientation “illusory movement”
most often caused by dysfunction of the vestibular, visual, or proprioceptive (posterior column)
​​systems
more common in aging, increased incidence of falling in those > 65 years.

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11
Q

List the two types of vertigo:

A

Types:

i. subjective if patient has the impression they are “moving in space” (self-motion)
ii. objective if objects “moving around” the patient (motion of the environment)

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12
Q

True Vertigo
SSX:

How do you tell if true vertigo is peripheral or central vertigo?

A

True Vertigo - sensation of movement (most common cz)
Caused by asymmetry in the vestibular system (CN8, inner ear, cerebellum)
​ SSX: either surroundings are moving or patient is moving within surroundings
​ Postural instability, nausea and vomiting, sweating
​ Vertigo is worse when moving head
​ Nystagmus is commonly seen on eye exam (involuntary movements of the eye)
Further classified as
i. Peripheral vertigo: labyrinth or CN VIII
​​​​ ii. Central vertigo: cerebullum, vestibular cortex in temporal lobe​

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13
Q

Peripheral vs. Central Vertigo (true vertigo)

A

Table in NOTES!

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14
Q

Non-vertigo-syncope, fainting

List the 3 types:

A

Non-vertigo - syncope, fainting
Types:
​ i. lightheadedness
​​“graying out” of vision, pallor, roaring sound in the ears
​​ suggests hypoperfusion of the brain from:
​ ​​hypotension​ drugs, ​​decreased cardiac output, ​hypoglycemia,
​​​shock ​​dehydration, severe anemia, ​​​cardiac arrythmias

       ii disequilibrium ​​occurs while standing or walking (gait impairing), unsteadiness without dizziness   ​​Source of problem may be: ​​​Cerebellar dysfxn         cervical spondylosis​​​
                       frontal lobe tumor       stroke​​   motor neuron diseases ​​​
          iii. miscellaneous ​​    chronic hyperventilation syndrome
               new eyewear   ​​    phobias: eg agoraphobia, acrophobia ​​    extra-ocular muscular palsy results in diplopia
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15
Q

Work up for vertigo:

  1. Hx
  2. PE
A

History:
–Onset: sudden or gradual?
i. Sudden onset and recall of episodes are often due to inner-ear disease,
ii. Gradual and ill-defined vertigo most common in CNS, cardiac, and systemic diseases
–Duration:
i Episodic true vertigo that lasts for seconds, associated with head or body position changes
​​eg. benign paroxysmal positional vertigo (BPPV)
ii. Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease
iii. Vertigo that lasts for hours or days probably caused by Ménière disease or vestibular
​​neuronitis

    Physical Exam for Vertigo
      i. General examination - vital signs, supine and standing BP, orthostatic BP, CVS
      ii. Otological exam: examine ears for cerumen, discharge, foreign body ​  ​​​ TM - perforation may result in sudden vertigo​ ​           iii Extraocular movements “H in space” check for nystagmus (eye jerking movements)
                    horizontal plane - most common form ​​        vertical plane - always abN, brain stem function disorder ​                    pendular - often congenital or after prolonged period of blindness ​           iv. Hearing tests    Whispered voice test​​ ​                                         Weber/ Rinne to assess conductive or sensorineural loss
          v. Sensory exam to assess proprioception ​          vi. Vestibular imbalance: ​                  Past-pointing with eyes closed​                
                  Romberg test: tend to fall toward the vestibular lesion
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16
Q

RED FLAG CONCOMITANTS for vertigo:

A

head or neck pain
ataxia
loss of consciousness
focal neurological deficit​

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17
Q

Non-vertigo tests:

A

Non-vertigo tests:​
i. lightheadheadness
orthostatic hypotension- increase in pulse by 30 bpm, systolic BP drop of 15-20 mm Hg
​ carotid sinus massage
valsalva maneuver
ii. disequilibrium: drifts toward side of lesion
​ cerebellar (coordination) and proprioception testing
​​observe walking and turning; forward & backward walking
iii. miscellaneous
hyperventilation: sitting, breathe quickly and deeply (2 minutes while observing for nystagmus)

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18
Q

Otalgia

A

Ear pain

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19
Q

List some causes of Otalgia:

A

EARACHE/ ear pain (otalgia)
Eg Causes:
external ear –impacted cerumen or foreign body, local trauma, otitis externa
middle ear – eustacian tube obstruction, OM, neoplasm
referred pain from TMJ, wisdom teeth
local infections: tonsillitis, enlarged adenoids, peritonsillar abscess
atlas/axis subluxation
tumor in pharynx, tonsils, tongue, larynx; thyroiditis
neuralgia: trigeminal, sphenopalatine, glossopharyngeal, geniculate
colds, allergies, cold wind blowing in ear

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20
Q

Red Flag concomitants with otalgia:

A

Red flag concomitants: Diabetes or immunocompromised pt, redness/pain over mastoid,
​Severe swelling of canal meatus, chronic pain with head/neck symptoms

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21
Q

Otorrhea

A

Ear discharge

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22
Q

Causes of ear discharge:

A

EAR DISCHARGE (otorrhea)
Eg Causes:
Acute d/c ​​​​​​Chronic d/c
​Acute OM with TM perforation​​​, Cancer of ear canal
​Post-tympanostomy tube​​​, ​Cholesteatoma
​CSF leak from head trauma, ​​​Chronic purulent OM
​OE—infection or allergy​​​, ​Foreign body (usu kids)

23
Q

Red flag concomitants with ear discharge:

A

Red flag concomitants: head trauma, cranial nerve dysfunction, fever, erythema of the ear, diabetes
​​or immune compromised

24
Q

External Ear obstruction can be caused by:

Sxs:

A

cerumen may block & cause:
Sxs: itching, pain, conductive hearing loss

 foreign body, esp. with children- beads, erasers, insects, just about anything!
25
Q

Acute Otitis Externa AOE
Etiology:
SSXs:
PE:

A
Acute Otitis Externa  AOE
Etiology
   1) Infection- e.g. strep, staph, E. coli, pseudomonas, aspergillus
   2) "swimmers ear"
   3) forceful cleaning of the ear
   4) trauma

Signs & Sxs: itching, pain, discharge possible, loss of hearing (canal becomes swollen or filled with purulent debris)

PE:​ “pull on pinna or push on tragus could cause tenderness”pinna & tragus painful when pressed or tugged (different from OM)
​external canal appears red, swollen
TM (may not be visualized) is normal pearly gray
​Pseudomonas infx produces purulent green/ yellow otorrhea
​Aspergillus looks like a fine white mat topped by black spores
​fever, swollen lymph nodes possible

26
Q

Chronic Otitis Externa
Etiology:
SSXs:
PE:

A

Chronic Otitis Externa: Pretty much the same as acute but not as intense, and lasting longer

Etiology:​i) psoriasis, seborrheic dermatitis, eczema
​ ii) allergy or fungus
Signs & Sxs: pruritis, redness, discharge
PE:​pinna & tragus less likely painful
​external canal appears irritated, perhaps dry, flaking tissue
​TM not usually affected
May get secondarily infected, increasing pain and swelling

27
Q

Perichondritis

A

auricular perichondritis involves infection of the pinna due to infection of traumatic or surgical wound or the spread of inflammation into depth.

trauma, insect bites may lead dec blood supply to ear cartilage: avascular necrosis/deformity

28
Q

Tumors/lesions of ear

A

Tumors/lesions:
​sebaceous cysts, osteomas (bony growths) may occlude ear canal
​gouty deposits (tophi on outer ear)
basal cell (BCC) and squamous cell carcinomas (SCC)- hx of sun exposure on external ear

29
Q
Acute Otitis Media  AOM
Claim to fame:
Etiology:
Risk factors:
SSXs:
PE:
A

Etiology: ​
Claim to fame: 2nd most common dz of childhood (URI # 1)
Causes: Organism, anatomic position of eustacian tube and immunologic factors
​ Common: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis ​
Less common: Group A streptococcus (older kids), Staph aureus, Gram neg bacilli (newborns,
​​immunocompromised), viruses, Mycoplasma pneumoniae
Can also be sterile effusions (no organism found)

Risk factors
daycare exposure. (also source for URI)
bottle-feeding
smoker(s) in the household

Signs & Sxs: throbbing pain (or maybe NO pain), fever, dec hearing, n/v, moodiness, irritability
​ child may tug on ear; sleep may be disrupted due to pain
PE:​bulging, red (or cloudy) TM, possible fluid line (yellow-gray if pus)
​decreased mobility on pneumatic otoscopy (insufflation)

30
Q

Approach to patient:

History taking for ear pain

A

i. pain: LMNOPQRST
ii. any hearing loss?
iii. any vertigo (dizziness)?
iv. any tinnitus (ringing)?
v. any hx of recent infection?
vi. any discharge? If so, how much (quantitative), what color? (qualitative)

31
Q

Middle Ear issues: (4 main ones)

A
  1. AOM may persist during Tx
  2. OME fluid behind TM
  3. COME
  4. CSOM
32
Q

Chronic Otitis Media (general term that includes:)

A
  1. Otitis Media with Effusion (OME) (sometimes listed as Serous OM)
  2. Chronic Suppurative Otitis Media: (CSOM)
33
Q
Otitis Media with Effusion (OME)
What is it?
Risk factors:
SSxs:
PE:
A

Otitis Media with Effusion (OME) (sometimes listed as Serous OM):
Effusion (fluid) in the middle ear–incomplete resolution of acute OM or due to inflammation
Risk factors
Prior tympanostomy tube placement
Allergy (often food – dairy, oranges, apples; environmental)
Summer or Fall months

Signs & Sxs:
Hearing impairment – child’s behavior may be described as inattentive (ADD misdiagnosis?)
Mild otalgia - intermittent ear pain tends to worsen at night
​ear fullness or popping
May also have overlapping sx of common cold: nasal d/c, sore throat

PE: Amber or gray TM, INTACT but typically retracted or in the neutral position
Impaired mobility of the TM during insufflation​
Bubbles or air/fluid level may be seen
Chronic cervical LA
Course: can persist: (COME) fluid behind intact TM; Risk of infection, recurrent AOM and/or perforation

34
Q
Chronic Suppurative Otitis Media (CSOM)
Etiology:
SSxs:
PE:
Course:
DDX:
A

Chronic Suppurative Otitis Media: (CSOM)
chronic inflammation of middle ear that persists at least 6 wks with TM perforation and otorrhea
Etiology​
i) acute OM resulting in perforation - central perforation leading to conductive hearing loss
ii) trauma to ear, head

Signs & Sxs: hearing loss, chronic purulent d/c, painless
PE:​​
Perforation of the tympanic membrane
May see: retraction pocket in the posterosuperior quadrant, choleseatoma, granuloma

Course: sometimes a chronic bacterial infection develops.
May flare up after an URI or after water enters the middle ear while bathing or swimming. Usually, flare-ups result in a painless discharge of malodorous pus from the ear..
Persistent chronic infection can destroy parts of the ossicles leading to conductive hearing loss. In a child, this can lead to delayed intellectual development

DDX: Otitis externa, cholesteatoma (congenital or acquired), myringits, chronic mastoiditis, impacted cerumen, tympanosclerosis, Wegener granulomatosis

35
Q

Complications with AOM

A

Complications:
Otitis media with effusion most common.
If bilateral, hearing loss with resultant speech delay may occur in infants.
Mastoiditis used to be a common complication, but now rare.
Perforation (rupture) of the TM is frequent, but usually not serious (unless peripheral)
​​IF TM perforates: discharge and sudden loss of pain
​​If perforation is peripheral, check regularly for cholesteatoma
May persist during Abx treatment, or relapse within 1 mo

36
Q

Diagnostic Criteria for OM (may not have copied and pasted well)

A

Diagnostic Criteria for OM

Type
Diagnostic Criteria
Acute Otitis Media
(AOM)
Acute onset AND
Middle ear effusion (bulging TM), limited or absent mobility
air-fluid level behind membrane AND
SSx of middle ear inflammation (red TM, otalgia)
Persistent AOM
Persistent features of middle ear infection during antibiotic
treatment OR
Relapse within one month of treatment completion
Otitis Media with Effusion
(OME)
Fluid behind intact TM in the absence of features of acute infx
Chronic OM with Effusion
(COME)
Persistent fluid behind intact TM in the absence of acute infx
Chronic Suppurative OM
(CSOM)
Persistent inflammation of the middle ear or mastoid cavity
Recurrent or persistent otorrhea through a perforated TM

37
Q
Myringitis
Primary causes:
Acute bullous Myringitis:
Acute hemorrhagic myringitis:
Secondary causes:
PE:
A

Painful Inflammation and/or infection of the TM. Primary or Secondary, Acute or Chronic forms
​Primary causes: can accompany Mycoplasma pneumonia URI
​​​TM trauma (foreign body, cleaning, explosion)
​​​Acute bullous Myringitis: vesicles on TM from infx (S pneumoniae, herpes)
​​​Acute hemorrhagic myringitis: bact or viral infx
​​​Secondary causes: Acute otitis media, acute otitis externa
​​​ Chronic otitis media, chronic otitis externa​
Signs & Symptoms:
Serosanguinous otorrhea, otalgia, hearing impairment
​​ if acute: sudden onset of ear pain that lasts 24 to 48 hours, fever
PE:​Vesicles develop on the TM in bullous form

38
Q

Cholesteatoma

A

Cholesteatoma:
Growth of keratinizing squamous epithelium in middle ear and/pars tensa
Etiology: congenital, primary acquired, and secondary acquired. (prev perforation, retraction pocket)
Signs and symptoms:
Painless otorrhea, either unremitting or recurrent.
Conductive hearing loss initially, then can grow into inner ear causing mixed hearing loss
Dizziness possible but uncommon

  PE: canal filled with muco-pus and granulation tissue
        TM perforation is present in >90% of cases.
  May require surgical removal
39
Q
Acute Mastoiditis:
What is it?
Etiology:
SSXs:
PE:
Complications:
A

Acute Mastoiditis:
Suppurative infection in the mastoid air cells (decreasing in prevalence)
Etiology:
Complication of severe AOM
​ Streptococcus pneumoniae (most common), Streptococcus pyogenes, Staphylococcus spp, Haemophilus influenzae
Pseudomonas aeruginosa

   Signs & Sxs: redness, swelling, tenderness behind ear, fever, hearing loss, profuse creamy ear d/c ​           throbbing pain​​
 PE:    Bulging erythematous TM
             Tenderness (redness, swelling) over the mastoid area
         Postauricular fluctuance
              Protrusion of the auricle, downward displacement of auricle
40
Q

Acute Mastoiditis
Complications:
Refer:

A

Complications: subperiosteal abscess, CN 7 palsy, hearing loss, osteomyelitis, meningitis, venous sinus thrombosis
Refer: MRI or CT. Treatment with drainage and antibiotics

41
Q

Ostosclerosis

A

Otosclerosis:
Genetic (autosomal dominant) metabolic bone disease affecting otic capsule and ossicles
-overgrowth of footplate in stapes/dysfunction
F>M 2:1; much more common in whites, most commonly appears 15-35 yrs.

    SSX:  Progressive bilateral (conductive) hearing loss and tinnitus (occasionally, vertigo)
42
Q

Tympanosclerosis
SSX:
PE:

A

Tympanosclerosis:
Sclerosis of TM: from chronic OM, post T-tube
stiffening of the tympanic membrane and impaired conductive hearing
SSX: early asymptomatic, but hearing loss progresses
PE: Whitish plaques on TM (areas of hyalinization with deposition of calcium and
​​phosphate crystals)

43
Q

INNer ear issues can be divided into two main categories:

A
  1. Peripheral vestibular disorders

2. Central vestibular disorders

44
Q

Peripheral Vestibular Disorders:

A

most common causes of vertigo

  1. Viral labyrinthitis
  2. Bacterial labyrinthitis
  3. Vestibular neuritis
  4. Benign Paroxysmal Positional Vertigo (BPPV)
  5. Acoustic Neuroma
  6. Meniere Disease
45
Q

Viral Labyrinthitis

A
  1. Viral labyrinthitis
    URI precedes the onset of symptoms in up to 50% of cases
    ​sudden unilateral hearing loss and severe vertigo, frequently assoc nausea and vomiting
    patient is often bedridden while the symptoms gradually subside.
    vertigo eventually resolves after several days to wks; however, unsteadiness and positional vertigo
    ​​may persist for several mos
    Adults aged 30-60 years, rarely observed in children.PE: spontaneous nystagmus towards the normal side with diminished or absent caloric responses in the affected ear.
    hearing loss: mild to moderate, often higher frequencies (>2000 Hz)a. Unique form of viral labyrinthitis is Herpes Zoster Oticus, (Ramsay-Hunt syndrome).
    Caused by reactivation of a latent varicella-zoster virus infection, yrs after the primary infection.
    SSX: initial deep, burning, auricular pain followed a few days later by the eruption of a vesicular rash in the external auditory canal and concha. Vertigo, hearing loss, and facial weakness may follow
    Symptoms typically improve over a few weeks; however, patients often suffer permanent hearing loss and persistent reduction of caloric responses.
46
Q

Bacterial labyrinthitis

A

Bacterial labyrinthitis
Caused by either direct bacterial invasion (suppurative labyrinthitis) or through the passage of bacterial toxins into the inner ear (serous labyrinthitis).
a. meningitis typically affects both ears. Bacteria spread from the cerebrospinal fluid to the membranous labyrinth by way of the internal auditory canal or cochlear aqueduct.
b. infections of the middle ear or mastoid most commonly spread to the labyrinth through a dehiscent horizontal semicircular canal. Usually, the dehiscence is the result of erosion by a cholesteatoma.
SSX: profound hearing loss, severe vertigo, ataxia, and nausea and vomiting
now rare in the post-antibiotic era

47
Q

Vestibular Neuritis

A

benign and temporary disorder of the vestibular nerve, vertigo NOT assoc with hearing loss
more common in the fourth and fifth decades of life . M=F
URI often precedes. More common in the spring and early summer, commonly viral
​ SSx: sudden acute vertigo without hearing loss in an otherwise healthy patient.
PE: horizontal nystagmus may be present, some gait instability, NO hearing loss

48
Q

Benign Paroxysmal Positional Vertigo (BPPV)

A

Benign Paroxysmal Positional Vertigo (BPPV)
sudden vertigo elicited by provocative positions, triggering nystagmus. The character and direction of the nystagmus are specific to the part of the inner ear affected and the pathophysiology.

a. Subclassifications:
i. Location: semicircular canal (SCC) (ie, horizontal, posterior, or superior)
ii. Pathophysiology: canalithiasis and cupulolithiasis
​ –canalithiasis (literally, “canal rocks”) particles residing in the canal portion of the SCCs. These densities are free floating and mobile, causing vertigo by exerting a force.
–cupulolithiasis (literally, “cupula rocks”) refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating.
BPPV is due to posterior semicircular canal canalithiasis ~ 90% of the time.

Etiology: risk factors–inactivity, alcohol, caffeine, major surgery, and CNS disease.
Idiopathic​​​head/ear trauma otitis media
vestibular neuritis ​​Ménière disease otosclerosis
SSNHL acoustic neuroma vertebral basilar insufficiency

Signs & Sxs:
Sudden onset: vertigo while trying to suddenly sit up, lying down, rolling over in bed, looking up.
​ Symptoms start very violently and usually dissipate within 20 or 30 seconds
even the slightest head movement causes N&V.
Between episodes, patients usually have few or no symptoms.
In many, the symptoms periodically resolve and then recur.

49
Q

BPPV

PE: _______ is the standard clinical test for BPPV.

A

PE Generally unremarkable.
Dix-Hallpike maneuver is the standard clinical test for BPPV.
Positive test: classic rotatory nystagmus with delay and limited duration is considered pathognomonic.
Procedure: rapidly move the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side. Vertigo and nystagmus seen in posterior canal dysfunction

50
Q

Acoustic Neuroma

A

Acoustic Neuroma (Vestibular Schwannoma)
benign, slow growing tumor derived from Schwann cells of CN VIII
SSX: unilateral, progressive SN hearing loss
Vertigo, tinnitus, disequilibrium can be concomitant
Headaches are present in 50-60% of patients
Facial numbness occurs in about 25% of patients
!!Consider any unilateral sensorineural hearing loss an acoustic neuroma until proven otherwise.!!
A large tumor can compress the brainstem and affect other cranial nerves, inc intercranial pressure

51
Q
Ménière disease
Age:
Etiology:
SSXs: triad:
Diagnostic Criteria: 3 of em
DDx:
A

Ménière disease (lesion called “endolymphatic hydrops”)
increase in volume and pressure of the endolymph in the endolypmhatic spaces of inner ear.
Age: typically occurs in early- to mid-adulthood; M=F
Etiology: exact cause is unknown. Up to 50% of patients have a positive FHx
Signs & Sxs: Triad: 1. waxing and waning SN hearing loss, 2. tinnitus, 3. vertigo
a. Prodrome: fullness or blocked sensation in one ear (like listening to shell)
​ b. Tinnitus followed by a decrease in hearing (esp low pitches)
​ nausea, vomiting, diarrhea, pallor, and sweating common with an acute attack
c. Vertigo is experienced concurrently with or follows shortly after the hearing symptoms;
​​​typically lasts min to hrs but may last several days.
d. Headache and gait unsteadiness may persist for several days
Course: following an acute episode, hearing may return to normal. Recurrence is common but unpredictable; hearing usually is decreased over time
​ Rarely, patients may experience such severe vertigo that they will collapse to the ground, known as Tumarkin crises.
PE: complete neurological examination is necessary to R/O other conditions, esp. cranial nerve examination
​ vestibular maneuvers (ie Dix Hallpike) may be helpful in diagnosing this syndrome.

Diagnostic Criteria (Amer Acad of Otolaryngology + Head + Neck Surgery)
i. isolated attacks of whirling, vertigo usu with n/v for at least 20 min, up to several hrs
ii. tinnitus - multipitched, multisounds, roaring, whistling: severe, unilateral, constant or fluctuating
iii. sensory hearing loss (progressive) [10-15% are bilateral]

DDx: migraine headache, hypothyroidism, labyrinthitis, multiple sclerosis, OM, ischemic stroke subarachnoid hemorrhage​, TIA, vestibular neuritis, acoustic neuroma, salicylate toxicity

52
Q

Nystagmus

A

condition of involuntary eye movement, acquired in infancy or later in life, that may result in reduced or limited vision

53
Q

Central Vestibular Disorders

A
  1. Toxic vestibulopathy (Hs of toxic agent ingestion)

2. Others: migrinous vertigo, brainstem ischemia, multiple sclerosis, cerebellar infarct

54
Q

Toxic Vestibulopathy

A

Toxic vestibulopathy (history of toxic agent ingestion)
Agentsaminoglycoside antibiotics - creates bilateral vestibular damage, may have blurred vision while moving the head (eg streptomycin, gentamicin most vestibulotoxic; neomycin, kanamycin, tobramycin most auditory toxicity)​
​ aspirin can produce dose-related reversible tinnitus, hearing loss, dizziness
​ alcohol produces reversible positional nystagmus