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4-19-10 Disorders of the Ear 1. Describe the pathophysiology of otalgia (ear pain). Otalgia is pain in the ear, or “earache”.

There are two types with different pathophysiologies. 1. primary otalgia: pain is due to lesion in the ear (note that the inner ear has no nerve supply, so it can’t be the source of primary otalgia) a. inflammatory: infection of the external or middle ear i. otitis externa: infection of the external ear 1. bacterial: localized form caused by Staphylococcus, diffuse form is polymicrobial 2. viral: Herpes zoster 3. fungal: aspergillus, mucor, candida 4. necrotizing: pseudomonas in DM patients osteomyelitis of the skull base ii. acute otitis media (AOM): viral infection followed by bacterial infection with accumulation of pus in the middle ear space and mastoid cavity iii. auricular perichondritis: bacterial infection of the cartilage of the auricle b. trauma: i. animal and human bites, burns, frostbite, foreigh body ii. tympanic membrane perforation (i.e. with Q tip) iii. barotraumas: injury to middle and inner ear due to sudden large pressure differences between the environment and middle ear space (rapid descent—flying, diving) c. Neoplastic: i. basal cell carcinoma ii. squamous cell carcinoma iii. melanoma of the external ear 2. secondary (referred) otalgia: source of pain is not from the ear in which it’s perceived a. orofacial region: i. teeth infection ii. oral cavity squamous cell carcinoma or stomatitis (mucous membrane inflammation) iii. nasal/sinus trauma, infection, allergy iv. parotid mumps v. TMJ arthritis or bruxism (tooth clenching or grinding) b. pharynx: i. tonsillitis ii. retropharyngeal abscess c. larynx: i. acute laryngitis ii. GERD iii. Squamous cell carcinoma d. other sources: i. cervical muscle ii. thyroiditis

2. List the three types of hearing loss.

1) Conductive: lesion affects the mechanism that transmits sound energy from external environment to the cochlea. This may include the external ear, tympanic membrane, and the middle ear contents 2) Sensorineural (SNHL): lesion of the cochlea or auditory nerve ● multiple etiologies: noise induced, presbycusis (aging), ototoxicity from drugs (aminoglycosides, salicylates, loop diretics, antineoplastic angents), hereditary, acoustic neuroma (aka vestibular schwannoma compressing CN VIII) ● management: prevention of further hearing loss, hearing aids, and surgery in the form of cochlear implants and auditory brainstem implants 3) mixed: both conductive and sensorineural hearing loss simultaneously 3. Correlate abnormal hearing tests with types of hearing loss. Tuning fork tests: ● Weber: base of tuning fork placed at midline on patient’s head ○ Hearing sound in the affected ear conductive hearing loss ○ Hearing sound in the normal ear sensorineural hearing loss ○ Weber at midline (no lateralization normal hearing ● Rinne: compares bone conduction (tuning fork on mastoid process) with air conduction (tuning fork 2 inches from ear) ○ Air conduction greater than bone conduction: normal OR sensorineural hearing loss ○ Bone conduction greater than air conduction: conductive hearing loss ○ In other words, the Rinne test only screens for conductive hearing loss, not sensorineural hearing loss Audiogram: graphic representation of sensitivity for pure tones as a function of requency Tympanogram: measures the compliance/resistance of the sound conducting apparatus in the middle ear space Brainstem Auditory Evoked Potentials (BAEP): assesses auditory dysfunction at the CN VIII, pons, or midbrain Imaging studies: CT for trauma, infection, or congenital malformation; MRI for evaluation of cerebellopontine angle for acoustic neuromas or sudden sensorineural loss) 4. Manage a patient with sudden hearing loss. Sudden hearing loss is unilateral or bilateral hearing loss developing within seconds, hours, or overnight. It may be maximal at onset or preogress in stages over a period of days, ranging form mild to total deafness. 1. sudden conductive hearing loss: a. due to external auditory canal lesion: cerumen impaction (earwax), foreign body, otitis externa b. due to tympanic membrane lesion: traumatic perforation, myringitis (tympanic membrane inflammation) c. due to middle ear lesion: acute otitis media, longitudinal temporal bone fracture, barotraumas d. symptoms of sudden conductive hearing loss: sensation of “fullness”, otalgia, facial weakness (with acute otitis media), swelling of external ear canal (with otitis externa), discharge (otitis externa purulent, trauma bloody, temporal fracture serous CSF),

hemotympanum (presence of blood in the tympanic cavity, usually from basilar skull fracture) e. management depends on cause: i. audiogram; otomicroscopic exam ii. removal of cerumen or foreign body iii. debridement of external auditory canal iv. antibiotics v. analgesics vi. myringotomy (incision in the tympanic membrane to relieve pressure in the tympanic cavity from acute otitis media) vii. surgical repair of the TM (from perforation) and ossicular chain


sudden sensorineural hearing loss: unlike sudden conductive hearing loss, this is a measureable loss of hearing function, pitch or speech perception that occurs over a matter of minutes to days a. causes: idiopathic (mumps, measles, herpes simplex, HIV, vascular compromise, intracochlear membrane rupture), autoimmune disease, noise trauma (130-160 decibels), transverse temporal bone fracture, barotraumas, electric shock, cerebellopontinte angle tumors) b. evaluation: history, physical, CBC, ESR, lipid panel, blood glucose, thyroid function test, MRI with contrast of temporal bone c. management: i. spontaneous recovery rate is 63%! Prognosis depends on age, degree of hearing loss, and onset of recovery. ii. Start meds immediately: corticosteroids and acyclovir iii. Surgical exploration of the middle ear for oval and round window perilymph fistula

5. Treat a patient with chronic hearing loss. Chronic hearing loss is extremely common. It ranges from an almost indetectable degree of disability to a profound alteration. Chronic hearing loss typically occurs bilaterally and develops over a period of months or years. Complete deafness is rate and there is no spontaneous improvement. ● Common causes: ○ Lesions of the external auditory canal: Atresia (abnormal closure) Exostosis (formation of new bone) Malignant tumor ○ Lesions of the middle ear: Otitis media ● Def: inflammatory condition of the middle ear without reference to pathogenesis ○ Otitis media with effusion (OME): serous or mucoid accumulation in the middle ear ○ Acute otitis media (AOM): rapid onset inflammatory process with thickening, erythema, and bulging of TM and accumulation of pus in the middle ear ○ Chronic otitis media (COM): perforation of TM, serous or purulent discharge, occasional cholesteatoma formation (growth fo skin) ● Etiology ○ Eustacian tube dysufunction: middle ear inflammatory disease ○ S. pneumo, H. influenziae, Moraxella catarrhalis, and mixed (aerobic+anaerobic) bacteria ● Management ○ Audiogram; otomicroscopic exam ○ Antibotics ○ Analgesics ○ Myringotomy ○ Myringotomy and placement with pressure qualizing tube ○ tympanoplasty Otosclerosis** (abnormal growth of new bone in the middle ear)

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Def: primary disease of the otic capsule characterized by abnormal resorption and deposition of bone in the labyrinthine and middle ear Autosomal dominance; more commonly seen in Caucasians than in African Americans or American Indians Etiology ○ Disorganized bone rich in osteocytes ○ Enlarged marrow spaces with abundant blood vessels ○ Spongy bone deficient in mature collagen Signs and symptoms ○ Conductive hearing loss ○ Tinnitus ○ Occasional unsteadiness ○ Normal appearing TM, rare red bluck in the lower part of the TM Management ○ Audiogram ○ Stapedectomy ○ Stapedectomy and placement of a prsthesis ○ Sodium fluoride ○ Hearing aids

Tumor 6. Differentiate pulsatile from non-pulsatile tinnitus. Pulsatile Tinnitus: ● Etiology: ○ High rise jugular bulb ○ Glomus tumors ○ Benign intracranial hypertension ○ Aberrant carotid artery ○ Carotid-cavernous fistula ● Etiology: less common than non-pulsatile tinnitus but the etiologies are more life threatening ● Management: treat underlying etiology Non-pulsatile tinnitus: ● Etiology: noise trauma, presbycusis (age-related hearing loss), Meniere’s Disease (excessive inner ear fluid), ototoxicity (drugs) ● Epidemiology: ten million sufferers (more common than pulsatile); most common between 40 and 70 years of age; 70% have hearing loss, mostly sensorineural ● Management: ○ Masking: hearing aids for hearing impaired, tinnitus instrument for those with L hearing ○ Habituation: reconditioning of connections within subcortical centers (binaural broadband noise generators) ○ Medical: antidepressants 7. Elicit information from a dizzy patient to differentiate peripheral from central vertigo. Dizziness is any perceived impairment of spatial orientation. It includes: ● Lightheadedness: sensation of fainting due to diminished blood supply to the brain ● Unsteadiness: tendency to fall due to compromised proprioception ● Vertigo: sensation of spinning due to lesion in peripheral (labyrinth) or central (brainstem)

vestibular system, the latter of which would cause unsteadiness or a swaying motion. 8. List the three most common causes of peripheral vertigo. Three most common causes of vertigo: ● benign paroxysmal positional vertigo (BPPV): severe rotatory vertigo associated with a change in head position. It is sudden onset and lasts for several seconds. The bouts of vertigo are clustered in time and separated by months of remission. There is NO HEARING LOSS. ○ This is the most common type of vertigo; incidence increases with age ● Pathophyisology: ○ Otoconia dislodge from otolith organs ○ Floating otoconia accumulate on the cupula of semicircular canals (canallithiasis) ○ Changes in movements of the head with respect to gravity cause movement of the particles and stimulation of the semicircular canals ● Signs and symptoms: ○ Absence of hearing loss and tinnitus ○ Classical eye movement (nystagmus) brought about by DixHallpike positional maneuver ● Management: ○ electronystagmography ○ vestibular autorotation test (VAT) ○ diazepam during acute phase ○ repositioning (Epley) maneuver (effective in 90% of cases) Meniere’s Disease: disorder of the inner ear associated with spontaneous episodic attacks of vertigo. The only one that HAS TINNITUS AND HEARING LOSS> ● Familial occurrence with patients with allergy and autoimmune disorders at increased risk; 50% cases occur bilaterally ● Pathophysiology: ○ Overaccumulation of endolymph (endolymphatic hydrops) ○ Distortion of membranous labyrinth ○ Rupture of membranous labyrinth ● Signs and symptoms: ○ Fluctuating sensorineural hearing loss (unlike BPPV, which has no hearing loss) ○ Tinnitus ○ Sensation of aural fullness; attacks of vertigo preceded by aura ○ Attacks last for minutes to hours ● Management: ○ Electronystagmography ○ Vestibular autorotation test (VAT) ○ Surgery Endolymphatic sac decompression Vestibular neurectomy Instilling of gentamicin in the middle ear space Labyrinthectomy for nonhearing ear ○ Prophylaxis (effective in 60-80% patients!) Reduction in endolymph accumulation Salt restriction

Diuretics Allergy tests and desensitization vestibular neuritis: dramatic sudden onset of vertigo with nausea, vomiting and photophobia. There is NO HEARING LOSS. ● Pathophysiology: ○ Vestibular nerve degeneration (peripheral receptors spared) ○ Cochlear nerve and organ of Corti spared ○ Infection with neurotropic virus (like herpes) ● Signs and symptoms: ○ Vertigo lasts for days ○ Gradual definite improvement ○ Balance-related complaint (of rapid head motion) may persist for months ○ Absence of tinnitus and hearing loss ● Management: ○ Supportive and symptomatic ○ Quiet semi-dark rooms ○ Hostipalization for IV hydration ○ Antiemetics ○ Diazepam ○ Early ambulation encouraged