A study set on Case History/ Report Writing, ENT Diagnostic Studies, Radiologic Studies, Cerumen Impaction, Aural Atresia, External Ear Conditions and Infections, Eustachian Tube Dysfunction (ETD), Myringosclerosis and Tympanosclerosis, Acute Otitis Media, Chronic Otitis Media / Cholesteatoma, Barotrauma /TM Perforation, Paraganglioma (Glomus Tumors), Otosclerosis, Basal Skull Fracture, and Ossicular Chain Discontinuity
What are the Medicare minimum requirements for chart documentation?
Why the patient is there for a visit
Signs and symptoms
Previous history
Chief complaints
Description of what was done (audiogram alone isn’t sufficient)
Clinical assessment of the outcome and what it means
Recommendations (state “no recommendations” if applicable)
What are the specific uses of imaging in otologic diseases?
Unilateral or asymmetrical SNHL
SNHL in children
Cochlear implant evaluation
Pulsatile tinnitus
Evaluation of pediatric conductive HL
Evaluation of chronic ear disease
Temporal bone trauma
What are the contraindications for cerumen removal?
Anticoagulants
Immunocompromised state
Diabetes Mellitus
Prior radiation to head and neck
Ear canal stenosis
Exostosis
Non-intact tympanic membrane (PE tubes)
HIV/AIDS
Ear malformations
Cognitive impairment or developmental delay
What is the CT/CAT scan good at imaging?
Bones and dense materials
What is the MRI good at imaging?
Soft tissues
How do CT/CAT scans work?
Uses several x-ray tubes in an array to take many x-rays from different angles. Beam is rotated in several steps to get a differential tissue absorption patterns through a single section of a patient’s body.
How do MRIs work?
High strength magnets on hydrogen bonds (in water) excite the protons and as it relaxes, it emits a radiofrequency signal
What is cerumen made up of?
Sebum (fat) and spocrine (sweat)
What are the two types of cerumen?
Dry and wet
What methods are used remove cerumen?
Mechanical
Suction
Water irrigation
Definition of acute otitis media
Infection/inflammation of middle ear with effusion behind intact TM, purulent due to bacterial colonization
Epidemiology of acute otitis media
Otalgia
Fever
Rubbing face/tugging on ear
Irritability
Vomiting
Diarrhea
Otorrhea
Hearing loss >30dBHL (CHL w/ABG)
Poor attention Span
URI
Sleeplessness
Audiologic results in acute otitis media
Otoscopy - TM is erythematous, opaque and bulging
Tympanometry - raises sensitivity and specificity to 90% when combined with otoscopy - usually follows jerger pathway through development to resolved A - C - B - C - A
Mild-Mod LowHz CHL - uni or bi
SRT = PTA
Word Rec = 96-100 (excellent)
OAE - absent
ABR elevated
Medical treatment of acute otitis media
Antibiotics
Analgesics
Decongestants
Antihistamines
Steroids
PE Tubes - Myringotomy, 3 or more episodes in 6 months (RAOM)
Prevention- Vaccinations
Audiological management in acute otitis media
“Watchful Waiting” 3 months from date of effusion onset or diagnosis - 70-90% of episodes resolve by 3 months and changes to a non type-B tymp. ⅓ relapse
Parental Counseling
Communication Strategies
Swim/Water protection w/PE tubes
Referral needs of acute otitis media
ENT for PE tubes
SLP if speech is affected
Definition of chronic otitis media
Associated with a permanent defect in the TM
Erosion of the ossicles
Irreversible mucosal changes in middle ear cleft
Presence of granulation tissue
Cholesteatoma
Epidemiology in chronic otitis media
Damaged TM
Atelectasis or Cholesteatoma
Audiologic results in chronic otitis media
Otoscopy - damage to TM, ossicles, scarring
Tympanometry - Type B; Type C if due to attic retraction of TM, suggestive of Cholesteatoma
Mild to mod flat CHL, AU
SRT = PTA
Word Rec 80-100
ARTs absent
OAEs absent
ABR elevated
Medical treatment with chronic otitis media
Antibiotics
Analgesics
Decongestants
Antihistamines
Steroids
PE Tubes - Myringotomy, 3 or more episodes in 6 months (RAOM)
Prevention- Vaccinations
Referral needs of chronic otitis media
ENT for PE tubes
SLP if speech is affected
Definition of Cholesteatoma
Tumor-like growth/cyst in epithelium of middle ear, attic, mastoid, or petrous apex
Infection or inflammation can stimulate tissue growth
“Unsafe ear”
Can erode temporal bone, ossicles, inner ear
Acquired & Congenital Types
Epidemiology of cholesteatoma
Otalgia
Drainage
Occasional vertigo
Gradual loss of hearing
Facial weakness/ paralysis
Audiologic results in cholesteatomas
Otoscopy abnormal
Tympanometry - Type B
CHL - mixed or SNHL indicates extends into otic capsule
VEMP absent on diseased side
MRI - abnormal soft tissue in ME
CT - bony erosion of temporal bone
Valsalva - induced dizziness
Medical treatment of cholesteatoma
Goal: remove disease, restore hearing
Re-Look Procedure: 3-5 years open back up to look again
Audiological management for cholesteatoma
Referral to ENT
Aural atresia definition
Embryonic malformation and hypoplasia or aplasia of the EAM
Usually associated with deformity or absence of pinna and ME abnormalities
EAM fails to form when canalization of epithelial plug does not occur (26-28 weeks gestation)
Classifications of atresia by Schuknect (1989)
Type A (meatal): involves the lateral cartilaginous portion of the canal, which is extremely narrowed and prevents skin and cerumen from exiting the canal
Type B (partal): narrowing of cartilaginous and bony portions of the canal. Typically allows visualization of TM, but malformations of the ossicles are common
Type C (total): complete atresia of the cartilaginous and bony portions of the canal, but mastoid and middle ear are aerated. TM is typically absent and ossicles are fused
Type D (hypopneumatic): similar to type C but mastoid is poorly pneumatized and the facial nerve has an aberrant course within the temporal bone
Anotioa
no development of auricle
Types of microtia
Type I/Mild: minimal or no auricular deformity with slightly stenotic or normal EAM
Type II/Moderate: most common; EAM partially or completely atretic (frequently operated)
Type III/Severe:
Markedly deformed/absent auricle, complete osseous atresia, hypoplastic or absent tympanic cavity
Benign dermatological conditions
Seborrheic Keratosis
Seborrheic Dermatitis
Chondrodematitis
Nodularis Helicus
Chronicus
Psoriasis
Premagnilant dermatological conditions
Actinic Keratosis
Malignant dermatological conditions
Basal Cell Carcinoma
Squamous Cell Carcinoma
Melanoma
What is the epidemiology of aural atresia?
Occurs in 1 out of 10,000 to 20,000 of live births, affects males more than females, unilateral is 3x more common, right ear is slightly more frequent than the left
What syndromes does atresia frequently accompany?
Pierre Robin, CHARGE, BATER, Treacher Collins
How is atresia classified?
Type A (meatal): involves the lateral cartilaginous portion of the canal, which is extremely narrowed and prevents skin and cerumen from exiting the canal
Type B (partal): narrowing of cartilaginous and bony portions of the canal. Typically allows visualization of TM, but malformations of the ossicles are common
Type C (total): complete atresia of the cartilaginous and bony portions of the canal, but mastoid and middle ear are aerated. TM is typically absent and ossicles are fused
Type D (hypopneumatic): similar to type C but mastoid is poorly pneumatized and the facial nerve has an aberrant course within the temporal bone
What are the symptoms for occluded ETD?
Pain and pressure in the ear as TM becomes retracted, difficulty “popping” ears, tinnitus, disequilibrium
What are the symptoms of patulous ETD?
Autophony
What are the epidemiological characteristics of obstructed ETD in children?
ETD in 70-90% of children by the age of 2 years
More common under age 5
More common in males
More common Native Americans
More common in lower socioeconomic sector
Why are children more prone to obstructed ETD?
ET is shorter in children and reaches adult size by age 7. ET slopes from 10 degrees on the horizontal plane whereas adults slope at a 45 degree angle
What is the etiology of obstructed ETD?
Horizontal slope of ET, inflammation of nasal cavity (Tobacco, gastroesophageal reflux, nasal polyps, allergic rhinitis, chronic sinusitis, URI), congenital deformities (cleft palate), or a mass in the nasopharynx
What is the etiology of patulous ETD?
Weight loss, pregnancy, or neurologic insult that causes muscle atrophy (stroke, MS)
What role does tympanometry play in ETD?
You can use tympanometry to see how the ET is working. For baseline, artificially create positive or negative pressure, ask patient to swallow several times, if results in retracted membrane then ET is functional (obstructed = negative pressure or reduced compliance), (patulous = oscillations coincide with breathing).
What other types of audiological tests are performed for patients with obstructed ETD?
Valsalva test- Start at -300daPa. Patient holds their nose and blows. If normal ET function, pressure will shift positively toward the normal pressure region
Toynbee test-note peak pressure and increase to +400daPa. Patient closes mouth, holds nose closed, and swallows while a new tympanogram is taken. If ET is function normally, the pressure should shift negatively
Define Tympanosclerosis
A condition where white calcified plaques of connective tissue occur around the TM and/or the head of the malleolus
Epidemiology of tympanosclerosis
Myringosclerosis is more common than tympanosclerosis
Incidence: varies between 7-33% among patients with chronic OM
Slight predominance towards females
Unilateral or bilateral (Bilateral 40-60% of cases with chronic OM)
Approximately 32% of ears that have PE tubes have tympanosclerosis a. Males affected more than females b. Larger plaques associated with multiple intubations
Myringosclerosis can occur at any age
Incidence is highest in children (Increased incidence of otitis media and PE tubes)
Thought that Intratympanic Tympanosclerosis incidence is higher in adults
Incidence of 49% over the age of 30
What does otoscopy look like for myringosclerosis?
whitish plaques on TM
What does otoscopy look like for tympanosclerosis?
If intratympanic then normal otoscopy, unless there is a perf where you can see the oval window
What are the theories for how the plaques form in myringo/tympanosclerosis?
End product of the healing process (post inflammatory): Collagen in fibrous tissue gets hyalinized due to inflammation of chronic OM leading to calcium deposits
Increased fibroblast activity results in deposition of collagen and calcium phosphate plaques form
Insertion of PE tubes: if aspiration is performed than there is an increased risk of tympanosclerosis
How does myringo/tympanosclerosis progress over time?
Sclerotic changes seem to be stabilized by 3 years, but do not seem to resolve with time
What are the audiological findings in patients with tympanosclerosis?
Conductive HL affecting the low frequencies more, and may have a mixed HL from stapes fixation, sometimes a false Carhart notch
Tymps: type A with slightly reduced compliance (depends on extent)
ARTs: Absent ipsilateral and contralateral reflexes in affected ear if tympanosclerosis causes conductive loss
OAEs: Absent with conductive loss
SRT/WRS: Excellent
ABR: Consistent with degree and type of hearing loss (if conductive)
What are the audiological findings in patients with myringosclerosis?
Minimal or no hearing loss, but may have a mixed HL due to stapes fixation (22%)
What other ME disorder does tympanosclerosis need to be differentiated from?
Otosclerosis
Define acute OM
An infection or inflammation of the middle ear with effusion (fluid) behind an intact TM
What is meant by "pururlent' versus "serous" versus "mucoid" otitis media with effusion (fluid)
Serous- thin, watery
Purulent- pus, secretory
Mucoid- viscous, thick (glue ear)
What are the symptoms of acute OM?
Otalgia, fever, irritability, vomiting, diarrhea, otorrhea (red or reddish yellow), hearing loss >30 dB HL, poor attention span, URI, sleeplessness, tugging on ear/rubbing on face
What complications can arise from untreated acute OM?
Meningitis, labyrinthitis, petrositis, brain abscess, facial paralysis, coalescent mastoiditis
What is the Incidence and Prevalence of acute OM in children?
By 1 year, 23% of children experience more than one episode and 60% by 3
Much less common in children over 6
Approximately 2.2 million episodes of OM with effusion are diagnosed annually in the US
Core common in males, but recent studies suggest it to be equally distributed
Higher incidence in Native Americans, Alaskan / Intuit, Canadian Natives, and Australian aboriginal children
What are risk factors for acute OM?
Premature birth
Genetic predisposition
Craniofacial anomalies / Cleft-Palate
Smoke exposure
Supine bottle feeding
Low socioeconomic status (SES)
Group day care & ICU
Seasonal fluctuations: fall/winter > spring/summer
Congenital and acquired immune deficiency
Eustachian tube dysfunction (ETD)
What are the audiological findings in patients with acute OM?
Mild to moderate low frequency or flat conductive HL, unilateral or bilateral. Tympanometry would result in a type B (with more effusion), or a type C (retracted TM) dependent on stage. The earlier the stage, the better the hearing, the later the stage, the more impact.
How is acute differentiated from "chronic" OM?
Acute OM is the inflammation of the middle ear (with or without effusion), while chronic OM is persistent inflammation and disease of the middle ear with compromise of the TM
What other disorders may occur concurrently with chronic OM?
Cholesteatoma and atelectasis. Atelectasis is the complete or partial adhesions between the pars tensa and the medial wall of the middle ear or the long process of the incus or the stapes. A cholesteatoma is a tumor like growth in the epithelium of the middle ear.
What are the symptoms of chronic OM?
Ear pain, drainage, occasionally vertigo, and gradual loss of hearing.
What are the audiological findings in patients with chronic OM?
Otoscopy: Abnormal
Pure tones: Mild to moderate flat conductive HL AU
Tymps: Type B, but can be Type C if due to retraction of TM and cholesteatoma
ARTs: absent, contralaterally and ipsilaterally (if bilateral conductive loss)
OAEs: Absent with conductive loss
SRT/WRS: Excellent
ABR: Elevated threshold, Wave I, III and V will each be delayed by the same amount (absolute latencies delayed); normal interpeak latencies
What complications can arise from untreated chronic OM?
TM perf
Erosion of the ossicles
Presence of granulation tissue in the middle ear
Cholesteatoma
Define atelectasis
Atelectasis is the complete or partial adhesions between the pars tensa and the medial wall of the middle ear or the long process of the incus or the stapes.
Define cholesteatoma
A cholesteatoma is a tumor like growth in the epithelium of the middle ear.
Where do cholesteatoma's occur?
Tend to develop in the anterior mesotympanum or the protympanum, Most common location of a is the posterior epitympanic space (AKA Prussak’s space)
What is the etiology of cholesteatoma?
Congenital- believed to be remnant of embryonic epithelial cell nests trapped in the middle ear during development
Chronic OM with a cholesteatoma is a result of ETD
What is the epidemiology of cholesteatomas?
General a. 6-12 per 100,000 b. 10% are bilateral
Acquired a. Incidence: 6:1000 b. Occurs secondary to eustacian tube dysfunction c. Persistent negative ear pressure d. Most common type e. Where is the most common location for acquired primary cholesteatoma?
Congenital a. Incidence: 1:10,000 b. Pearly white mass grows behind intact TM c. Negative history of OM d. more prevalent in males (3:1) e. mean age of origin is 4.5 years of age f. embryonic cell deposit g. Usually, asymptomatic
What are the complications for untreated/unmanaged cholesteatoma?
Nerve deafness
Vertigo
Infection around or inside the brain
Facial weakness or paralysis
Differentiate acquired versus congenital cholesteatoma.
Acquired- collection of squamous epithelial cells that collect either adjacent to or through a compromised TM to affect the middle ear a. Primary acquired- squamous collection within a retracted TM pocket b. Secondary acquired- squamous cell migration through a TM perf into the middle ear
Congenital- presence of squamous cells within the middle ear with no history of TM perf, OM, or ETD
Define “relook procedure”
A “relook” procedure is a procedure where the doctor goes back to the middle ear space 6-12 months post op to examine the ossicles
What are the primary causes of tympanic membrane perforations?
Overpressure, thermal or caustic injuries, blunt or penetrating injuries, barotrauma
How does the size of the perforation relate to degree of hearing loss?
Small TM perf are none or minimal HL, while large TM pers are up to 50 dB of conductive HL
What would you expect to see in terms of tympanogram and acoustic reflex testing with a TM perf?
Increased middle ear volume and increased intensity ARTs, if not unavailable due to perf size
How are TM perforations medically treated?
TCA cautery- Saturated solution of tricholoracetic acid onto rim of perforation.
Myringoplasty “Paper Patch”
Tympanoplasty: faccia or perichondrium tissue graft
Define barotrauma
Injury to the TM that results from increased air or water pressure (failure to equalize pressure)
What is the underlying physical basis of barotraumatic injury?
Boyle’s law: pressure of a given mass is inversely proportional to its volume if temperature remains constant ant the amount of gas remains unchanged in a current system
What does otoscopy look like for barotrauma?
TM perf, blood in the middle ear or ear canal
Define paraganglioma
Benign, slow growing and highly vascularized neoplasms (abnormal and excessive growth of tissue) that comes from the paraganglion cells
What is the epidemiology of paragangliomas?
Hereditary transmission as autosomal dominant traits- Penetrance increases with age (localized to Chromosome 11)
Estimated annual incidence of 1 case per 1.3 million
Female to male ratio is 3-6:1
Occur primarily in patients 50-70 years old
Tends to occur unilaterally (left > right)
What are the two types of paragangliomas?
Glomus tympanicum and glomus jugularis
Define glomus tympanicum
Glomus tumor originating in the tympanic cavity on the promontory (back wall by the ET). Originates from the Jacobson’s or Arnold’s nerve
Define glomus jugularis
Glomus tumor originating in the dome of the jugular bulb and involving the jugular foramen
What are the symptoms of glomus tympanicum?
Pulsatile tinnitus (76%)
Hearing loss – conductive (52%), sensorineural (5%), or mixed (17%)
Aural pressure/fullness (18%)
External canal bleeding (7%)
Headache (4%)
What are the symptoms of glomus jugularis?
Pulsatile tinnitus
Hearing loss
Otalgia
Aural fullness
Hoarseness or dysphagia (CN IX (Glossopharyngeal), X (Vagus), XI (Accessory)
Vertigo
Facial weakness
Headache
What are the classifications of glomus tympanicum?
Type I- Small mass limited to the promontory
Type II- Tumor completely filling ME cavity
Type III- Tumor filling ME and extending into mastoid
Type IV- Tumor filling ME, extending into the mastoid, through the TM into and fill the EAC; + ICA involvement
What are the classifications of glomus jugularis?
Type I- Small tumors involving the jugular bulb, ME, and mastoid
Type II- Tumor extending under the IAC; might have intracranial extension
Type III- Tumor extending into the petrous apex; might have intracranial extension
Type IV- Tumor extending beyond petrous apex into clivus or infratemporal fossa; might have intracranial extension
What are the audiological findings of paragangliomas?
Pure Tone Results: a. Conductive hearing loss: when tumors of the ME are present b. Sensorineural hearing loss: Extension into the otic capsule, temporal bone, or internal auditory canal
SRT/WRS: Results will be fairly consistent with PTA, WRS varies on a case by case basis
Tymps: Type A, As, or B
ART: Pulsatile tracing using ART test settings and will be absent when stimulating the affected ear
Decay: Will not test in the affected ear if absent reflexes, may use this sensitive setting to record vascular pulsations
OAE’s: Will be absent when stimulating the affected ear
ABR: Poor morphology and poor reproducibility
Define otosclerosis
Metabolic bone remodeling disease of the temporal bone that primarily affects the otic capsule and ossicles
What is the epidemiology of otosclerosis?
Age: in the 20’s or 30’s
Gender a. Women > Men b. 2:1, women: men c. Women “lower” (poorer) bone conduction thresholds. d. Women more sensorineural in nature e. Accelerated by pregnancy
Race/ethnicity a. Clinical otosclerosis greater in Caucasians (10%) vs. 1% in overall population b. Clinical otosclerosis is rare for Blacks & Native Americans. c. Histological otosclerosis is 3.4% Caucasians, 1% for Blacks, 5% for Asians, yet Caucasians develop the clinical otosclerosis more commonly
What are the symptoms of otosclerosis?
Hearing loss- slowly progressive, conductive may progress to mixed, unilateral
Occlusion complaints- difficulty hearing while chewing or their own voice sounds loud
Paracusis willisii- understand speech better than noise
Tinnitus
Vertigo- unlikely
Define Paracusis Willisii
When you understand speech better in noise. People usually speak louder when in the presence of background noise and the low frequency background noise is filtered out through the pathology
Where in the middle ear does otosclerosis most commonly occur?
Most common site is an area just anterior to the stapes footplate (fissula ante fenestrum)
What other bone diseases may be confused with otosclerosis?
Paget’s disease: Excessive breakdown and formation of bone tissue; bones weaken, fracture, arthritis. Only localized in a few bones
Osteogenesis imperfecta- “brittle bone disease”: Defective connective tissue due to deficiency of type I collagen. Identified by blue sclera
What is a "Flamingo's Flush"?
Also called Schwartze sign, where there is increased vascularity of the promontory seen through the TM. The TM looks really, really red
What are the audiological findings with otosclerosis?
Otoscopy: schwartze sign
Pure Tone Results: low frequency conductive HL, Carhart’s notch where B worsen at 2 kHz
SRT/WRS: excellent, unless comorbid SNHL
Tymps: A or As, may have reduced width
ART: Absent ipsilateral and contralateral reflexes in the affected ear. May have “on off effect” where there is a negative deflection at both the onset and offset of the stimulus
Decay:
OAE’s: Absent
ABR: consistent with degree and type of HL a. Elevated threshold b. Delayed absolute latencies c. Normal interpeak d. Poor waveform morphology
What is a Carhart's notch and what frequencies does it occur at?
Notch at around 2 kHz that is not a true BV threshold and is attributed to normal mechanical effects on middle ear system due to the stapes fixation. It can occur at 5 dB at 500, 10 dB at 1000, 15 dB at 2000, and 5 dB at 4000
What is the difference between a stapedectomy and stapedotomy?
A stapedotomy includes the use of a laser to make a precise hole (fenestration) in the stapes footplate. While a stapedectomy typically removes the entire stapes footplate and has it replaced with a micro prosthesis.