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160 Cards in this Set
- Front
- Back
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Acute Otitis Media
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Preceding upper respiratory infection, feaver otalgia (ear pain), HL, otorrhea (discharge from the ear).
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Chronic MEE (middle ear effusion)
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Possibly asymptomatic, hearing loss, "plugged", "popping". High incidence of persistent MEE after AOM ~ 40 days, higher incidence in <24 mo.
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Tymp progression of OM
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Starts with negative pressure, low frequency conductive loss (b/c more stiffness). Pulls moisture out of mucus mucosa of middle ear. Fluid in middle ear. Flat tymp and flat conductive loss (sometimes dip at 2k). As disease is healing the tympanogram is shallow A type. Still have a small conductive HL.
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Pathology leading to OM
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E tube abnormalities
Mechanical/functional obstruction: Loss of stiffness or muscular control e.g. Downs Syndrome, American Indians. Anatomical obstructions: inflammation, polyps, cholesteatoma, stenosis, compression. Length abnormalities: shorter more likely to reflux into ME. Impaired immunity in children. Allergy, scaring ect. |
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Treatment of OM
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Adults and older children - observation.
Antibiotics e.g. Amoxil, augmetin, zithromax. Antibiotics + steriod: 21% improvement compared to antibiotic alone, prednisone |
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Hearing eval for OM
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Could have SNHL on top of OM.
Degree of CHL. Baseline and pre-op planning. Tympanometry. Assess ET function (sometimes). |
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Medical treatment of OM: Chemoprophylaxis
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Prevention by chemical, controversial.
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Medical treatment of OM: Adenoidectomy + tubes
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28% (at 1 year followup) and 35% (at 2 year f/u) fewer episodes of AOM vs. tube only.
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Medical treatment of OM: Myringotomy and tube insertion
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Decreased # and severity, could be more otorrhea (drainage from ear), persistent perforation, scaring, tube getting stuck, may require prophylaxis if severe.
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Wagner's Granulomatosis
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A life threatening disease with OM as one of the first signs. Sudden onset, resistant to treatment, typical age 40-50 years, caucasion. Disease affects H&N initially. Autoimmune multiway stem disease cause unknown, may be immune response to something environmental. If untreated patient can die in 5 months.
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Importance of ET function
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Middle ear to naospharynx. Lumen shaped (isthmus where they come together). Mucous providing and hair cells. Two purposes: ventilation (pressure regulation), and keep the mastoid aerated. Protection: nasopharyngeal sounds and secretions. Clearance of ME secretions (passive): mucociliary (muscles), musculary.
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Differences between adult's and children's Etubes
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Adults have longer cartilaginous portions, children have longer bony portion. Adults at 45 degree angle, children horizontal with slight angle. Isthmus is bigger in children than adults. Nasopharyngeal orifice is bigger in adults.
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Opening Etube
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Opens during swallowing, yawning, sneezing, crying ect.
Can only open cartilaginous portion. Tensor veli palatine mainly responsible for active tubal opening (patulous=open). No constrictor function. |
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Etube function test rational
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Is the TM intact? Are they prone to OM? When TM is perforated can predict surgical outcome. Monitor disease
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Inflation/deflation Etube test (pressure-swallow test)
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Designed for intact TM.
Baseline TM. Positive pressure (200) applied and held (inflation) or negative pressure applied and held (deflation). Swallows with the applied pressure. Post-test tymp. Should see about a 25 daPa change in pressue from swallowing. |
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Toynbee Etube test
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Baseline tymp
Release pressure Swallow with nose pinched with no pressure applied Post test Should see a negative shift in peak pressure |
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Valsalva Etube test
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Baseline tymp
Blow with nose pinched and mouth closed Pose test Should see a positive shift in peak pressure |
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Sniff test Etube test
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Valsalva
Baseline tymp Close off one nostril and sniff Post test Should see a negative shift in peak pressure |
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Etube test for perforated TM
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Inflation-deflation procedure
Positive pressure applied (200-400 daPa). Swallows successively, observe pattern. Abnormal pattern 1: positive pressure alone causes ET to open, swallows will approach 0, negative pressure applied: swallows will not open ET. Abnormal pattern 2: no effect of swallows. |
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Etiology of TM perfs
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Infection is most common, bacterial or viral.
Trauma: penetrating trauma (self induced), blunt (tbone fractures, longitudinal/transverse, slap injury). Thermal: welders and steelworkers, lightning. Barotrauma: cadaver studies 14-33 lbs/in2 or 195-199 dB SPL Iatrogenic (induced inadvertently by a physician or surgeon or by medical treatment or diagnosis procedures): retained ventilation tubes, tubes in >36 months lead to 40% incidence in perforation vs. <36 months 19% |
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TM healing
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80% heal spontaneously. Thermal injuries 40% heal spontaneously. Other negative factors: age >30, large kidney bean shaped central perfs, posterosuperior perfs, infection
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Tympanoplasty purpose
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Restore function and stabilize trouble-free ear
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TM Anatomy
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3 layers - 130 microns
Outer epithelial - keratinizing squamous Middle fibrous - superficial radial, deep circular Inner - mucosa |
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Tympanoplasty
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Reconstruction of the TM, addresses middle ear pathologies such as cholesteatoma, adhesions, ossicular chain problems. Usually involves elevating the TM from its sulcus.
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Tympanoplasty Type I
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Myringoplasty: reconstruction of a perforation of the TM. Assumes normal ME mucosa and ossicles. Graft to TM/malleus. TM not elevated from its sulcus.
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Tympanoplasty Type II
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May be some malleus remnant. Graft to incus.
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Tympanoplasty Type III
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No malleus or incus. Graft to stapes suprastructure.
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Tympanoplasty Type IV
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No stapes suprastructure. Graft to footplate. Could use a prosthesis to replace the ossicles. Use TORP (total ossicular replacement prosthesis) with cartilage stiffener.
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Tympanoplasty Type V
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Fenestration. Graft to a fenestration in horizontal semicircular canal.
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Indications for Surgery
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Eliminate recurrent disease: CHL from perforation or ossicular dysfunction, chronic or recurrent otitis media, progressive HL due to chronic ME pathology.
Perforation or HL persistent >3 months due to trauma, infection or surgery. Inability to bathe or participate in water sports safely. |
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Goals of Surgery
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Establish an intact TM. Eradicate middle ear disease and create an air-containing middle ear space. Restore hearing by building a secure connection between the ear drum and the cochlea.
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Tympanoplasty Techniques
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Overlay (lateral grafting): execllent exposure, high graft take rate, acceptable to all cases. Requires precision, longer healing time (months vs. weeks), possibility of blunting, lateralization or epithelial pearls.
Underlay (medial grafting): less blunting or lateralization, high graft take, simpler technique. Limited visualization, larger anterior perf less suitable, difficult with small EAC. |
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Types of PE tubes
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Short term 8-18 months: grommets, semipermeable; stay 2-4 months, gas exchange but not water.
Long term >15 months: T-tubes |
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Does place of perforation effect size of ABG?
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No
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Does volume of ear canal effect HL?
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Yes. The person who has more normal ear canal volume (nice aerated mastoid air cells) has more normal hearing even with a larger perforation.
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Does size of perforation effect HL?
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The size of the perf has some effect when the ear canal volume is accounted for. The ear canal volume is still the most important factor.
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Transducer for PE tubes
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Insert thresholds were significantly worse than TDH thresholds. 15 dB worse at 250 and 10 dB worse at 500 Hz. No significant difference in normal ears.
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Which transducer is recommended by Voss & Herrmann (2005)
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Recommended the use of standard supra-aurals due to the fact that they provide a more stable calibration over a wide range of ear-canal volumes and impedances.
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What to do if you are having trouble getting a seal
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Re-fit. If that isn't working dial in a little negative pressure. It tightens up the TM. DiGiovanni & Ries foudn that you can get better ARTs for patients with peak Ytm >_ 2.1 mmho if you dial in -50 daPa.
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What did Walkup & Coomes (2008) find about transducers?
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Insert earphones yielded poorer thresholds that did headphones in the low frequencies. Larger conductive components when using inserts.
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Ososclerosis gender
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Female to male 2:1
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Otosclerosis race
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More common in Caucasians, rare in African-Americans
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Otosclerosis Age
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15-45 most common age of presentation. Rare in children and after 55.
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Otosclerosis Pathophysiology
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Simultaneous resorption and formation of new bone. Limited to the temporal bone and ossicles. Inciting event unknown. Could be hereditary, autoimmune, hormonal, vascular, infectious, endocrine, metabolic ect.
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Two phases of otosclerosis
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1. Active (otospongeosis): osteolytic resorption of bone with sheets of vascular connective tissue replacing the bone. Schwartze's sign.
2. Mature (sclerotic phase): formation of dense sclerotic bone in areas of previous resorption, signifies the late phase of otosclerosis. The resulting disorganized bone, with narrow vasculature and few recognizable haversian systems. |
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Schwartze's Sign
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Increased vasculariyy of an active focus of otosclerosis (otospongiotic phase) imparts a pinkish hue, otosclerosis bone is softer and bleeds more easily when traumatized. Cause by reflection of light from an active, vascular focus of otosclerosis on the promontory. This rare sign is more likely seem in young adult and indicate a poor prognosis.
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Clinical otosclerosis
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Pathology involving the fixing the footplate of stapes. Clinically represented by CHL.
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Histological otosclerosis
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Pathology involving areas of the otic capsule away from the footplate of the stapes, which remains freely mobile. Usually only discovered after death.
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Cochlear otosclerosis
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Pathology involves a large part of the labyrinthine endosteum. Metabolites diffuse to inner ear injuring the hair cells. Clinically represented by SNHL component which adds to the existing HL (resulting in Mixed or rarely pure SNHL
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Otosclerosis
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Genetically-mediated primary metabolic bone disease that affects only the human otic capsule and ossicles (typically just the stapes)
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Otosclerosis inheritance
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Autosomal dominant with incomplete penetrate (40%) and variable expressivity.
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Most common foci of otosclerosis
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Just anterior to oval window niche at the fissula ante fenestrum 80-90%. Wedges the footplate posteriorly.
Can have otosclerosis in round window niche (30-50% of cases). Can involve RW itself, causes more HL. If complete RW involvement, >60 dB ABG possible. Anterior wall of IAC |
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Osteogenesis imperfecta
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Systemic disease similar to otosclerosis, bone disorder with a triad of signs/symptoms: blue sclera (whites of eyes), fragile bone disorder (fractures), stapes fixation/disarticulation.
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Symptoms of Otosclerosis
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Hearing loss (slowly progressive), tinnitus (75%), vestibular symptoms (uncommon, 25%), paracusis willisii (the patient hears better in a noise environment, not specific to otosclerosis. This occurs because people speak louder in noisy surroundings.).
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Signs of otosclerosis: otosclerosis
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Otoscopy: normal or schwartze's sign.
Pneumatic otoscopy: normal or reduced mobility of TM. |
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Signs of otosclerosis: pure tone audiometry
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CHL or mixed
Charhart's notch: notch in bone conduction at 2kHz, look for a reduced ABG. (Khatchetoorians 2010, showed notch can occur at other frequencies, .5, 1 & 2 kHz. |
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Progression of otosclerosis
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BC stays the same but AC gets progressively worse. Low freq hearing loss because it is stiffness dominated
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Modes of bone conduction
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Distortional mode: vibrates bony capsule, walls of cochlea, sets up fluid vibrations.
Inertial mode: from the ossicles. ~2kHz common. Osseotympamic mode: vibrating the bony portion of the EAC. |
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Multi frequency tympanometry for otosclerosis
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Can be useful to confirm increased stiffness. Higher resonant frequency.
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Normal middle ear resonance
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800-1200 Hz
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Resonant frequency with disarticulation
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<200 Hz
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ARTs for otosclerosis
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Reflexes absent in more advanced stages. Reflexes are biphasic (on-off effect) in early stages. This is due to a sudden increase in compliance when the stupendous pills hard enough to suddenly release the stapes from the rough edges around the oval window, but you should also see the effect of deceased compliance from muscle contraction as with any other reflex.
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Differential diagnosis for otosclerosis
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Congenital stapes fixation, malleus head fixation, superior canal dihissance, Paget's disease, osteogenesis imperfecta, ossicular discontinuity, MEE.
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Management of Otosclerosis
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Amplification, medical therapy, surgery (fenestration, stapes mobilization, stampedectomy, stapedotomy). There is not cure/reversal. Can only treat what is currently there.
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Who is credited for the first modern stampedectomy where oval window was covered with a graft and not left open
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Shea 1956
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Good candidate for Otosclerosis surgery
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Good health
Age not very important 512 Hz rinne tuning fork test is BC>AC, first freq where you see a conductive loss due to otosclerosis. Pt motivated Good BC (neural status) No Hx of perforation, OM or trauma Gradual onset of loss and not congenital (congenital fixation is much more likely to have CSF leak) Absent acoustic reflexes Normal or As tymp No congenital syndromes, since often the VII and arteries can be in different places No evidence of Meniere's: if active hydrops, when footplate removed, a ballooning of the saccule can occur significantly increasing risk of damage/puncture when drilling Negative fistula test |
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How good is otosclerosis surgery
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94-95% change of improved hearing to less than or equal to 10 dB ABG. 4% show no improvement. 1% dizziness and dead ear.
When you have to do a revision: 80% chance of improvement. 8% risk of SNHL.5p |
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Why would otosclerosis surgery fail?
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Incus necrosis: wire crimp not tight enough
Prosthesis loosens or pops out Prostheists too long: causes dizziness if the person sneezes or burps ect. Wasn't otosclerosis to begin with. |
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Risks of otosclerosis surgery
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Infection leading to SNHL
OM infection healing with Granulomatosis tissue filling middle ear, can get dizziness, pain , SNHL. Taste disturbance Tinnitus Vertigo, usually short term VII nerve paralysis |
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Medical treatment options
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Floride can slow down otosclerosis
Usually with little CHL and they want to stop the destruction. 50% of people stabilized at 2 years out. Can have fetal problems, gastric side effects. Might prevent further SNHL. Reduces tinnitus, reverses Schwartze's sign. Biphosphonates if Floride not tolerated. |
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Amplification for otosclerosis
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Harris says satisfaction rate is less than surgery.
Poor surgical candidates, only-hearing ear, pts who don't want surgery. Postop: patients with mixed HL or failed surgery. BAHA is a good option. |
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Overall prevalence of histologic otosclerosis
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10%
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Overalls prevalence of clinically significant otosclerosis
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1%
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How common is otosclerosis in Caucasian males and females?
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7.3% and 10.3%
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Otosclerosis side
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Bilateral in 70% of cases
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Otosclerosis family Hx
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Positive in more than 50%
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Paget's disease
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Systemic disease similar to otosclerosis. Pagetic osteoclasts larger and more effective bone resorbers than normal osteoclasts. Osteoblasts react to this active resorption and create new bone. localized to 1-2 areas of the body, or widespread. Hearing can be effected when skull is involved. HF SNHL & LF ABG possible. Consequences: malleus, incus, stapes fixation, compression of VIIIN, **loss of bone mineral density of cochlear capsule**, crowding in epitympanum - partial ossicular fixation, elevated bone-specific alkaline phosphatase (BSAP) levels, skeletal bone involvement. Affect on hearing established well before signs appear in facial skeleton. Affects 3% of people over 40 (exact number not know b/c many people who have it don't know). World-wide but more prevalent in some areas (Europe and Australia). Greater in men than women, usually over age 40.
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Cases where you can have a conductive loss and present reflexes
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Ossicular discontinuity medial to the stapedius, early otosclerosis, SCD
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Dehisce in Latin
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To split along a natural line
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Fistula
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An unnatural opening from the inner that allows perilymph to leak out into the middle ear/mastoid air cells, round and oval window common
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SCD
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Rare and debilitating. First described by Lloyd Minor of Johns Hopkins University, 8 pts with sound/pressure induced vertigo. He found an abnormal opening in the superior canal.
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Tullio phenomenon
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When loud sounds induce vertigo
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Hennebert's sign
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When pressure induces vertigo. Intracranial: coughing, sneezing, straining. Tympanometry: causing pressure from the outside. Dizziness with tymps does not always mean SCD, could be Minnear's or other conditions.
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Dehiscence
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Similar to fistula but not as severe. Bone is missing, usually over superior SCC, uncovering membrane. A dehiscence allows for pressure wave to be "directed" through the vestibular system. Makes ear more sensitive to pressure and intense noise.
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VOR
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Vestibular Ocular Reflex
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Nystagmus
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Rapid, involuntary, rhythmic eye movement which occurs normally during and after head rotation and sometimes with dizziness.
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Typical sign of SCD
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Vertigo 90-100%
Oscillopsis ~97% pt experiences oscillating, bouncing, swinging vision when moving. When stable they are fine. Can be very debilitating. Increased inter cranial pressure causes vertigo ~82% Most complain of chronic disequilibrium. Hyperacusis 39% Gaze-evoked nystagmus also common Nystagmus in the plane of the superior canal evoked by sound 89%, vertical with a tortionl component slow phase away from affected canal. |
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Unique findings for SCD
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Sensitive to bone conduction (ABG), supra threshold BC thresholds. Unexplained ABG.
Describe very unusual auditory sensations/autophony. Hearing joints moving, eye movement, heart beat, heals striking during walking, tuning fork placed at distal extremity. Always test BC! |
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Physical findings for SCD
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Spontaneous nystagmus, use frenzel goggles to see subtle nystagmus.
Tympanometry, pneumatic otoscopy and valsalva may produce the nystagmus. Weber to the affected side usually with a 256 or 516 Hz tuning fork. Often BC>AC on Rinne test. |
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Acoustic reflexes can help differentiate between
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Otosclerosis and SCd
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Pathogenesis of SCD
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Not totally clear.
Common theory: developmental abnormality. The bone develops in three separate layers, first an innermost endosteal layer then mid and outer layers ~3 yo. Usually identified at age 40. |
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VEMP test
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Vestibular Evoked Myogenic Potential.
Don't expect a response under 70 dB. Abnormal is low threshold (<70 dB) and very large response at a high level (90 dB HL). Often reported in SPL (~30 dB higher then HL). |
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Treatment of SCD
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Observation
Hearing aids Vestibular suppressants Tympanostomy tube Surgery: very involved and complicated -transmastoid -middle fossa -resurfacing -plugging |
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SCD Surgery
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Risk of HL
Indications: Dizziness related to ear with SCD Very debilitated by disorder |
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Middle fossa craniotomy for SCD
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Brain gently retracted
Watching for GPN Looking for arcuate eminence Examining entire tegmen Plugging or resurfacing Risks: Death, stroke, cranial palsied, and cerebrospinal fluid leaks. Go home in 1-7 days. 95% positive outcome. |
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Transmastoid repair
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Approach behind ear, through mastoid, to superior canal.
Make new holes in canals to reach SCD. Greater risk of HL with this procedure. 5% positive outcome |
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Resurfacing vs plugging
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See notes!
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Canal occlusion/ablation
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See notes!
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Oval/round window reinforcements
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See notes!
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Types of Meniere's: possible Meniere's
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Episodic vertigo of the Meniere's type without hearing loss, or SNHL, fluctuating or fixed, with disequilibrium but without definitive episodes. Other causes excluded.
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Type of Meniere's: probable Meniere's
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One definitive episode of vertigo. Audiometry calls documented HL on at least on occasion. Tinnitus or aural fullness in the treated ear. Other causes excluded.
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Types of Meniere's: definite Meniere's
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Two or more definiteve spontaneous episodes of vertigo 20 min or longer. Audiometrically documented HL on at least one occasion. Tinnitus or aural fullness in tht treated ear. Other cases excluded.
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Types of Meniere's: certain Meniere's
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Histological confirmation
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Staging of HL in definite/certain Meniere's
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Based on 4 tone dB average.
1 <_25 dB 2 26-40 3 41-70 4 >70 |
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Meniere's Stats
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In the US 50% have positive family Hx.
Prevalence is 150 in 100,000 population. Incidence ~ 38,000 per year 75% unilateral Women>Men Age 40-50 diagnosis 23% bilateral Takes about 7.6 years to convert from unilateral to bilateral. |
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Production of endolymph theory: longitudinal
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Produced in membranous labyrinth, flow to endolymphatic sac, then to dural venous sinuses.
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Production of endolymph theory: diffuse
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Produced and absorbers along the membranous labyrinth.
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Production of endolymph theory: periodic flow
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Endolymph flows only with change in volume and pressure.
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Hydrops
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Too much endolymph exist within the membranous labyrinth. Leads to distortion of the membranous labyrinth.
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Diagnosis of Meniere's
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The pattern of symptoms: fluctuating HL, vertigo, tinnitus, fullness.
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Atypical type of Meniere's
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Cochlear: fluctuating HL and aural fullness but no vertigo (80% progress to classic)
Vestibular: episodic vertigo with no change in hearing (20% progress to classic) Tumarkin spells: drop attacks (otolithic crisis), Lermoyez- hearing improves with attack. |
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Physical exam for Meniere's
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The Romberg test generally show significant instability, worsening with eyes closed.
Weber tuning fork test lateralized to non-effected side. Rinne AC>BC Complete neurological eval is necessary. Need to r/o stroke, migraine or brainstorm compression. |
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Arnold-Chiari malformations
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Cerebellum squished down into opening where spinal cord goes.
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How is EVA defined on a CT scan?
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A diameter greater than or equal to 1.5 cm measured halfway between the operculum and the common crus.
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EVA
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Progressive fluctuating SNHL. Congenital. Symptoms developed and can be provoked by head injury. May have large ABGs (enhanced BC). May also have Pendred Syndrome.
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AIED
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Autoimmune inner ear disease. Syndrome that may include: sudden or progressive HL, both ears, tinnitus, dizziness, aural fullness.
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Characteristics of AIED
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Bilateral SNHl (79%) usually asymmetric.
Rapid unilateral progression then bilateral. Impaired WRS. 50% vestibular problems. 25-50% tinnitus and/or aural fullness Ménière's disease and AIED seem to be closely intertwined. More women than men have AIED. Systemic autoimmune disease 29%. Usually responds to steroids (immunosuppression). |
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Tests for AIED
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Positive 68kd using Western Blot test.
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Sudden acoustic trauma
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Single exposure: blast
Suddent, permanent Mild to profound HL Mechanical injury Symptoms: sudden painful loss, followed by tinnitus Signs: otological trauma More known about Pathophysiology of this type of hear loss than chronic NIHL. |
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Chronic NIHL Characteristics
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SNHL
Usually bilateral, symmetrical 3000-6000 Hz notch, progressing to sloping HF HL greater than predicted based on age Other symptoms: tinnitus, temporary or permanent (can have some recovery) |
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Why a 3-6 kHZ notch
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Shape of the cochlea: sound wave slams into the first wall.
Pinna resonates at that frequency. Acoustic reflex more effective at some frequencies than others. |
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Two types of damage
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Mechanical: from high levels (~125 SPL)
Metabolic: from moderate levels- over stimulation, over activity of cochlea may lead to altered homeostasis. Cell membranes damage... Ionic regulation disrupted |
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Synergistic effect
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Combined effect is larger than the two added together.
Ototoxic drugs Chemical pollutants Mercury, led, xylene, trimethyltin, tobacco, vibration? |
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Protection against noise
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Antioxidants eg. NAC
Ca2+ antagonists NMDA receptor blockers Growth factors Noise conditioning or training? |
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Tinnitus overview
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Unilateral or bilateral
In the ears or in/around the head May be the first or only symptom of a disease process or auditory/physiological annoyance |
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How many people in the US are affected and seriously affected by tinnitus
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50 million
2 million seriously affected |
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How many people in the US are affected enough by tinnitus to seek medical attention
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12 million
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Most common age for tinnitus
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40-70 years old
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Is tinnitus more common in males or females
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Males
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Tinnitus definition
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Perception of sound in the absence of external stimuli.
Tinnere means ringing in Latin |
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The typical tinnitus patient
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Type A
Life is put on hold/altered Depression/anxiety Spinning out of control May be suicidal due to tinnitus HL common Hyperacusis/fear or dislike of sounds This is a vulnerable time for the patient |
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Classifications of tinnitus
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Objective: sound produced by the ear or paraauditory structures which may be heard by an examiner. Could be audible SOAE. Pulsatile often but not always objective. Matches pulse or a rushing sound. Possible vascular etiology. Increased or turbulent blood flow through para-auditory structures.
Subjective: sound is only perceived by the patient (most common). Muscular and neural causes. |
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Causes of objective pulsatile tinnitus
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Arteriovenous malformations (congenital)
Vascular tumors Venous hum (hearing blood flow) Atherosclerosis Persistent stapedial artery Vascular loops |
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Vascular tumors
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Glomus tympanicum: middle ear tumor, CHL, pulsatile tinnitus (decrease with ipsilateral carotid compression?). Reddish mass behind TM which may "blanch" with positive pressure.
Glomus jugulare: jugular fossa tumor, pulsatile tinnitus, CHL if into middle ear, possible cranial neuropathies. |
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Venous hum causes
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Variety of causes: all vascular.
Benign intracranial hypertension (BIH) Dehiscence jugular bulb Transverse sinus partial obstruction Increased cardiac output (pregnancy, thyrotoxicosis, anemia). |
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Ototoxicity definition
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Functional impairment/damage to the cochlea or vestibular apparatus form exposure to a chemical source.
Unavoidable side effect of life-threatening disease treatment. Purposeful selective lesions to reduce symptoms (eg. Meniere's disease- gentamicin to kill vestibular system). Tinnitus "universal" sign of over accumulation. Many sources: heave metals, herbs, pharmaceuticals. |
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Classification of ototoxic drugs
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Permanent: aminoglycocydes, chemotherapy (cisplatin, carboplatinum)
Temporary: macrolides (erythro, clarity rio, azithromycin), loop diuretics, quinine, solvents, salicylates (aspirin). |
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Monitoring of cochlear toxicity
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ASHA guidelines for threshold shift: >_ 10dB in thresholds of two or more contiguous frequencies. >_ 20dB in thresholds of one or more frequencies. Loss of response at 3 frequencies.
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Risk factors for ototoxicity
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Diuretics, renal failure, prolonged treatment, old age, preexisting SNHL, mixing meds.
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Grading systems for ototoxicity
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Grades how bad the change is from one test to the next.
Chang grade (for kids). Brock grade. |
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What did Fausti find about the sensitive region for ototoxicity?
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Individualized region of 5 consecutive frequencies on slope of hearing loss.
84% sensitive for AMG. 94% sensitivity for cisplatinum. |
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Molecules that acts as antibiotics
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Strepto-, kana-, neo-, tobra-, siso-, netil- ect.
Route of administration: systemically (IV, intramuscular ect), topically (inhaled, eyedrops, superficially), enternal (by mouth, feeding tube, rectally). Don't know how meds make their way into the ear. Secreted into the perilymph by spiral ligament or endolymph by Syria vascularis? Diff we through round window membrane? Meds eliminated by kidneys. |
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Mitochondrial mutations
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May genetically predispose to ototoxicity.
AG1555. More common in Asians. |
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Vestibular toxicity
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Vestibular hair cells are vulnerable.
Pathologically: type I hair cells more sensitive. Cristea then utricle and saccule affected. Clinically: ataxic gait, lose balance when turning, bobbing oscillopsia, usually bilateral. Assessment is difficult (can't compare the two sides because impairment it bilateral). Dynamic posturography can detect. Head shake test. |
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Prevention of ototoxicity
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Pharmacological: knowledge of susceptibility, adjusting meds, blood tests.
Clinical: consider less ototoxicity drugs (netilmicin), identify high risk patients (weekly audios, ENG prior, history and daily physical exam, adjust or switch drugs). |
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Chemotherapeutic drugs
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Cisplatin
Carboplatin Nitrogen Mustard- original chemo drug. Usually more cochlear than vestibular toxic. |
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Macrolides
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Erythromycin, Azithromycin, Clarithromycin.
Hearing with or without tinnitus within 2 days. All frequencies, recovery after stopping. Rarely permanent. Incidence unknown. |
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Loop Diuretics
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Three types of diuretics: thiazides, loop, and potassium-sparing.
Organic compounds acting on epithelial cells in loop of Henle. |
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Quinine
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Made from the cinchona tree bark.
Leg cramps and malaria. High pitched tinnitus, first HF SNHL, reversible symmetric mild flat SNHL, occasional vertigo, headache, nausea. Mechanism: decreased perfusion, direct damage to OHCs, biochemical alterations. |
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Salicylate and NSAIDS
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Most common OTC drugs in US.
Change in blood flows. Decreases enzymes. Outer hair cells swell up. Reduction of amplification the OHCs provide. Tinnitus, reversible hearing loss, reduced tuning, OAE reduced. |
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Heavy metals and carbon monoxide
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Cases of poisoning in children.
Selective hair cell loss shown in animal models. |
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Usual ototoxicity hearing loss configuration
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Aminoglycocydes- high frequency.
Other drugs- flat loss. |
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Congenital outer ear malformations occur in 1 in every _____ births
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12,500
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Microtia
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Malformed pinna, partially developed
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Atresia
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Absent opening. Often occurs with microta
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Stenosis
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Abnormally small opening, any narrowing of ear canal
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Microtia stages
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I: small but recognizable pinna
II: remnants of helix or cartilage with a closed off or stenotic external ear canal producing a conductive hearing loss. III: (50%) no external ear, soft tissue only, small vestige structure with no EAC. IV: no external parts |
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Congenital Aural Atresia
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Incidence: 1 in 10,000-20,000
Unilateral 3-5X more common than bilateral Males>Females Right>Left Inheritance - sporadic. Autosomal recessive or dominant. |
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Goals for surgical repair of ear
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Restore functional hearing.
Construct patent and infection-free EAC. |
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Cauliflower ear
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Caused by blunt injury
Bruising between cartilage and connective tissue Blood collects and causes deformity No serious consequences to hearing |
