Med Aspects Test 1

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

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* 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?

1. ETD in 70-90% of children by the age of 2 years
2. More common under age 5
3. More common in males
4. More common Native Americans
5. 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?

1. Valsalva test- Start at -300daPa. Patient holds their nose and blows. If normal ET function, pressure will shift positively toward the normal pressure region
2. 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

1. Myringosclerosis is more common than tympanosclerosis
2. Incidence: varies between 7-33% among patients with chronic OM
3. Slight predominance towards females
4. Unilateral or bilateral (Bilateral 40-60% of cases with chronic OM)
5. Approximately 32% of ears that have PE tubes have tympanosclerosis
a. Males affected more than females
b. Larger plaques associated with multiple intubations
6. Myringosclerosis can occur at any age
7. Incidence is highest in children (Increased incidence of otitis media and PE tubes)
8. Thought that Intratympanic Tympanosclerosis incidence is higher in adults
9. 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?

1. End product of the healing process (post inflammatory): Collagen in fibrous tissue gets hyalinized due to inflammation of chronic OM leading to calcium deposits
2. Increased fibroblast activity results in deposition of collagen and calcium phosphate plaques form
3. 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?

1. Conductive HL affecting the low frequencies more, and may have a mixed HL from stapes fixation, sometimes a false Carhart notch
2. Tymps: type A with slightly reduced compliance (depends on extent)
3. ARTs: Absent ipsilateral and contralateral reflexes in affected ear if tympanosclerosis causes conductive loss
4. OAEs: Absent with conductive loss
5. SRT/WRS: Excellent
6. 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)

1. Serous- thin, watery
2. Purulent- pus, secretory
3. 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?

1. By 1 year, 23% of children experience more than one episode and 60% by 3
2. Much less common in children over 6
3. Approximately 2.2 million episodes of OM with effusion are diagnosed annually in the US
4. Core common in males, but recent studies suggest it to be equally distributed
5. Higher incidence in Native Americans, Alaskan / Intuit, Canadian Natives, and Australian aboriginal children

What are risk factors for acute OM?

1. Premature birth
2. Genetic predisposition
3. Craniofacial anomalies / Cleft-Palate
4. Smoke exposure
5. Supine bottle feeding
6. Low socioeconomic status (SES)
7. Group day care & ICU
8. Seasonal fluctuations: fall/winter > spring/summer
9. Congenital and acquired immune deficiency
10. 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?

1. Otoscopy: Abnormal
2. Pure tones: Mild to moderate flat conductive HL AU
3. Tymps: Type B, but can be Type C if due to retraction of TM and cholesteatoma
4. ARTs: absent, contralaterally and ipsilaterally (if bilateral conductive loss)
5. OAEs: Absent with conductive loss
6. SRT/WRS: Excellent
7. 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?

1. TM perf
2. Erosion of the ossicles
3. Presence of granulation tissue in the middle ear
4. 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?

1. Congenital- believed to be remnant of embryonic epithelial cell nests trapped in the middle ear during development
2. Chronic OM with a cholesteatoma is a result of ETD

What is the epidemiology of cholesteatomas?

1. General
a. 6-12 per 100,000
b. 10% are bilateral
2. 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?
3. 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?

1. Nerve deafness
2. Vertigo
3. Infection around or inside the brain
4. Facial weakness or paralysis

Differentiate acquired versus congenital cholesteatoma.

1. 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
2. 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?

1. TCA cautery- Saturated solution of tricholoracetic acid onto rim of perforation.
2. Myringoplasty “Paper Patch”
3. 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?

1. Hereditary transmission as autosomal dominant traits- Penetrance increases with age (localized to Chromosome 11)
2. Estimated annual incidence of 1 case per 1.3 million
3. Female to male ratio is 3-6:1
4. Occur primarily in patients 50-70 years old
5. 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?

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1. Pulsatile tinnitus (76%)
2. Hearing loss – conductive (52%), sensorineural (5%), or mixed (17%) 
3. Aural pressure/fullness (18%)
4. External canal bleeding (7%)
5. Headache (4%)

What are the symptoms of glomus jugularis?

1. Pulsatile tinnitus
2. Hearing loss
3. Otalgia
4. Aural fullness
5. Hoarseness or dysphagia (CN IX (Glossopharyngeal), X (Vagus), XI (Accessory)
6. Vertigo
7. Facial weakness
8. 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?

1. 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
2. SRT/WRS: Results will be fairly consistent with PTA, WRS varies on a case by case basis
3. Tymps: Type A, As, or B
4. ART: Pulsatile tracing using ART test settings and will be absent when stimulating the affected ear
5. Decay: Will not test in the affected ear if absent reflexes, may use this sensitive setting to record vascular pulsations
6. OAE’s: Will be absent when stimulating the affected ear
7. 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?

1. Age: in the 20’s or 30’s
2. 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
3. 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?

1. Hearing loss- slowly progressive, conductive may progress to mixed, unilateral
2. Occlusion complaints- difficulty hearing while chewing or their own voice sounds loud
3. Paracusis willisii- understand speech better than noise
4. Tinnitus
5. 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?

1. Paget’s disease: Excessive breakdown and formation of bone tissue; bones weaken, fracture, arthritis. Only localized in a few bones
2. 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?

1. Otoscopy: schwartze sign
2. Pure Tone Results: low frequency conductive HL, Carhart’s notch where B worsen at 2 kHz
3. SRT/WRS: excellent, unless comorbid SNHL
4. Tymps: A or As, may have reduced width
5. 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
6. Decay:
7. OAE’s: Absent
8. 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.