ENT AyaSalahEldeen

Prepared by:

Aya Abukhalil Salah Eldeen

Al-Quds university

2010/2011

ENT for medical students Dr. Adel Adwan

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ENT, Dr. Adel Adwan - Al-Quds university Prepared by: Aya Abukhalil Salah Eldeen

The ear

Ear anatomy:

Ear is divided into 3 parts:

1. External ear

2. Middle ear

3. Inner ear

1. External ear: Composed of:

a. Auricle (Pinna) : It is composed of cartilaginous part (upper 3/4) & fibro fatty part

(lobule)

Anatomy :

b. External auditory canal: S shaped tube extending from the auricle to the tympanic

membrane (25 mm). It is pulled backward upward when examining adults and backward downward when examining children. It has two parts:

Cartilaginous part (outer one third): it has thick skin that contains piloseboceramen apparatus: hair follicles, sebaceous glands & ceramen glands (that produce wax). In this part there is more incidence of otitis media. Sometimes infected sebaceous glands is found in it.

Bony part (inner two thirds): it has thin smooth skin adherent to the bone, so any manipulation or minimal trauma (such as cotton swab) may cause injury. It may contain modified sweat glands that secret yellowish to brown wax (seroma glands).

Type of skin in the external auditory canal is keratinized squamous epithelium.

It has 2 areas of stenosis: 1. At the end of the cartilaginous part.

2. 0.5 cm lateral to the tympanic membrane.

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Ink spot test is done to examine the function of the cilia, put ink spot on tympanic membrane, after 5-6 mo will be seen on the external ear.

c. Lateral (outer)surface of the tympanic membrane: It is the outer layer of the tympanic

membrane which is composed of skin of keratinized squamous epithelium.

Tympanic membrane (TM): It is 1 cm in diameter

It is formed of 3 layers: - Outer layer (Lateral layer): skin of keratinized squamous epithelium. - Middle layer (B/w the Lateral & Medial): fibrous layer. - Inner layer (Medial layer): respiratory mucosa (Pseudo-stratified squamous ciliated

mucosa). Theses 3 layers are found in Pars Tensa (4/5 of the TM, it is easily ruptured because it is tight), but the fibrous layer is absent in Pars Flaccid (1/5 of the TM).

TM is obliquely placed, facing downward forward and laterally.

Concave laterally and at the depth of concavity is small depression (the Umbo) produced by the tip of the handle of Malleus.

It is extremely sensitive to pain and is innervated in its outer surface by supplied by Auriclotemporal nerve and auricular branch of Vagus.

We use the pneumatic otoscopy to measure the TM mobility.

On otoscopy: hold it like a pencil, pull the Pinna upward backward in adults and straight backward or backward downward in infants:

1. Color: white gray to pale gray.

2. Pars tensa forming the lower 4/5 of the tympanic membrane.

3. Pars flaccid forming the upper 1/5 of the tympanic membrane.

4. Light reflex Con Flight from austachian tube.

5. Handle of malleous and umbo on its tip which is the most tense area. 6. Lateral process of the malleus (the short process).

7. Anterior and posterior malleolar folds.

8. Mobility of the tympanic membrane is in the range of 1 mm, examined by:

- Pneumatic otoscope - Swallowing during examination : swallowing causes negative middle ear pressure &

movement of the tympanic membarne - Valsalva maneuver during examination - Tympanometry: Objective method

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A: par flaccid, B: short process of malleus, C: pars tensa, D: manubrium of malleus, E: Umbo, F:light reflex. The rest are not important !

2. Middle ear:

Composed of middle ear cleft which contains: a. Tympanic cavity itself including:

ossicles (Malleous, Incus, Stapes),

two muscles(stapedius muscle "innervated by nerve to stapedius, a branch of facial

nerve", tensor tympani muscle "innervated by tensor tympani nerve, a branch of

mandibular division of trigeminal nerve"),

two nerves (horizontal and chorda tympani branches of the facial nerve).

b. Eustachian tube (auditory tube).

c. Mastoid air cells (Air containing cavity in petrous bone of temporal bone).

d. Aditus ad antrum (mastoid antrum) : canal between middle ear and mastoid air cells.

In the middle ear, normally there is No skin, there is only mucosa lined with Pseudo-stratified

columnar ciliated mucosa (respiratory mucosa).

Ossicles:

Malleous Incus Stapes

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Malleous and incus are derived from the first branchial arch, so any patient with mandibular

problem such as mandibular aplasia, you have to suspect middle ear disease or pathology.

Stapes is derived from the second branchial arch.

There are joints between the ossicles:

1. Incudomalleolar joint between Incus &

Malleous.

2. Incudostapedial joint between Incus &

Stapes.

Foot plate is attached to the oval window

Eustachian Tube (Auditory tube):

Connects middle ear and nasopharynx.

It has two parts: Proximal 1/3 is bony & distal 2/3 is cartilaginous.

Lined with respiratory mucosa & has mucous producing cells and ciliated cells.

Usually closed, opens during swallowing.

Opening involves cartilaginous portion.

Muscles that open the Eustachian tube:

1. Tensor veli palatini: has the main action, innervated by the trigeminal nerve.

2. Tensor tympani: innervated by trigeminal nerve.

3. Levator veli palatini: innervated by pharyngeal plexus mostly vagus nerve.

4. Salpingopharyngeus: acts during yawning, innervated by pharyngeal plexus mostly

vagus nerve.

** Eustachian tube in children has longer bony portions, is wider and shorter & straighter than in

adults whose Eustachian tube is J shaped.

** Function of Eustachian Tube:

Protection from nasopharyngeal secretions

Clearance of middle ear secretions

Ventilation (pressure regulation) of middle ear

Physiology of hearing: The middle ear transforms air waves to fluid waves.

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3. Inner ear

Composed of:

a. Bony labyrinth, consists of:

1. Cochlea (spiral shaped, making 2 3/4 turns around its axis).

2. Vestibule

3. Semicircular canals: Anterior (or superior), Lateral (or Horizontal) & Posterior

semicircular canals.

b. Membranous labyrinth (which is found inside the bony labyrinth), consists of:

1. Organ of corti (in the cochlea) : The sensory organ of hearing.

2. Utricle and saccule ( in the vestibule): They are sensitive to linear acceleration

3. Semicircular ducts (in the semicircular canals): They are responsible for angular

acceleration.

Physiology of hearing: The inner ear transforms fluid waves to electrical waves.

The vestibular system

It lies in the otic capsule in the petrous

portion of the temporal bone.

It consists of 5 distinct end organs:

- 3 semicircular canals that are sensitive

to angular accelerations (head

rotations)

- 2 otolith organs "utricle & saccule" that

are sensitive to linear (or straight-line)

accelerations.

The vestibular fluids:

Perilymph: In the bony labyrinth. It is similar to the extracellular fluid (low potassium, high

sodium).

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Endolymph: In the membranous labyrinth. It is similar to the intracellular fluid (high potassium,

low sodium). It is continuous with the endolymph of the cochlea. It is secreted by epithelial cells

continuously and drains from the inner ear into the venous sinus in the dura mater of the brain.

The otolith organs: Utricle & Saccule

** The sensory organs of the utricle

and saccule are the maculae.

Each macula consists of hair cells

and supporting cells.

The ciliary bundles of the hair cells

project into the overlying gelatinous

matrix known as the otolith

membrane.

Otoliths are mineral and protein

particles embedded in the otolith membrane (Calcium Carbonate crystals).

Macula:

It consists of supporting cells and hair cells.

It detect and respond to the position of the

head with respect to linear acceleration and

pull of gravity

Each macula contains thousands of hair cells

that synapse with sensory endings of

vestibular nerve

Each hair cell has 60-80 small cilia called

stereocilia plus one large cilium called

kinocilium

The kinocilium is always located in one side,

and the stereocilia gradually become shorter.

Minute filaments connect the Tip of each sterocilium to the Next longer cilia and finally to

kinocilium .

When stereocilia bend to the direction of

kinocilium, it results in opening of K+ channels

at the tip of the stereocilia, allowing K+ ions to

enter and depolarize the hair cell. In respone

to depolarization voltage-gated Ca+2 channels

are activated allowing for Ca+2 influx and the

subsequent liberation of transmitters to

produce an action potential.

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Conversely, bending of stereocilia in the opposite

direction (backward to the kinocilium ) reduces the

tension on attachments and this closes the ion

channels causing receptor hyperpolarization and

inhibition of the cell.

When the head is upright, the hairs project upward

into the gelatinous material.

When the head bends forward, backward, or to one

side, the hair cells are stimulated as the gelatinous

material of the maculae sag in response to gravity

causing the hair to bend.

Stimulated hair cells signal nerve fibers resulting in

impulses traveling to the CNS on the vestibular

branch of the vestibulocochlear nerve and informing

the brain of the heads new position.

Brain responds by sending motor impulses to skeletal

muscles to contract/relax to maintain balance.

In the utricle, maccula lies in the horizontal plane of

the inferior surface of utricle so it determines the

orientation of the head in upright position, senses

motion in the horizontal plane(eg, forward-backward

movement, left-right movement, combination).

In the saccule, macula lies in the vertical plane and senses

motions in the sagittal plane (eg, up-down movement).

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The semicircular canals

Lateral or horizontal, Anterior or

superior and Posterior.

The semicircular canals are

connected to the utricle at their

bases.

Oriented at right angles to one

another.

At the end of each canal is an

enlarged chamber, the ampulla.

The ampulla contains a sensory

receptor called crista ampullaris.

** The sensory organ of the

semicircular duct is crista

ampullaris.

The crista consists of a

gelatinous mass, the cupula.

Embedded in the cupula are the

cilia of hair cells.

The basal membranes of the hair cells synapse on the sensory neurons of the vestibular nerve.

Crista ampullaris:

Detect and respond to angular

acceleration & deceleration of the head.

Rapid turns of the head or body stimulate

the hair cells of the crista ampullaris.

Appropriate rotation of the head in one

direction bends cilia in the opposite,

depolarizing the cells.

Nerve fibers send impulses to the brain cerebellum

Analysis of information allows the brain to predict the

consequences of the rapid body movements and signal

appropriate skeletal muscle to maintain balance.

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Each semicircular canal works in

concert with a partner located on

the other side of the head, which

has its hair cells aligned oppositely

There are three such pairs: the two

pairs of horizontal canals, and the

superior canal on each side working

with the posterior canal on the

other side

Head rotation deforms the cupula in

opposing directions for the two

partners, resulting in opposite

changes in their firing rates.

For example, the orientation of the

horizontal canals makes them

selectively sensitive to rotation in

the horizontal plane. More

specifically, the hair cells in the canal

towards which the head is turning

are depolarized, while those on the

other side are hyperpolarized. For

example, when the head turns to

the left, the cupula is pushed toward

the kinocilium in the left horizontal

canal, and the firing rate of the relevant axons in the left vestibular nerve increases. In

contrast, the cupula in the right horizontal canal is pushed away from the kinocilium, with a

concomitant decrease in the firing rate of the related neurons. If the head movement is to

the right, the result is just the opposite.

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Ear Examination:

Inspect the auricles for:

Shape

Redness

Swelling

Ulceration

Tumors

Fistula

Retroauricular skin.

Preauricular fistua

Postauricular fistua : First branchial clet fistula type I which opens in the middle ear

& First branchial clet fistula type II which opens in the external auditory canal.

Palpate the auricles for:

Tenderness

Pre or Post auricular swelling or tenderness.

Inspect the external canal: Pull the auricle upward backward in adult or backward

downward in infants and young children to see the external canal, which is S shaped, by this

movement you find out whether there is tenderness or not. Tenderness means otitis extena .

Using the Otoscope, inspect the tympanic membrane (Remember the normal land marks!!), &

examine for the mobility of the tympanic membrane.

o Red congested Acute otitis media (OM). OM causes also a reduction in the mobility

of the tympanic membrane.

o Atrophic retrscted with prominent handle of malleus in long standing negative pressure

Secretory or adhesive OM.

o Thick with calcification white in color Myringosclerosis (due to recurrent OM or

multiple ear surgeries ).

o Perforated: Central / Marginal.

Ear discharge:

o Brown mass Wax (& can be gold or even black, all are normal).

o Moist keratin debri otitis externa

o Moist dirty mass Fungus : Candida albicans, Aspergillus flavus, Aspergillus niger (most

common one)

o Mucoid or mucoperulent discharge Chronic or acute otitis media.

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o Scanty offensive perulent discharges Cholesteatoma

o Clear fluid CSF .. How to confirm that it is CSF ?

1. Halo sign : Non specific

2. Glucose level : Non specific

3. Beta-2 transferrin : Found only in CSF so it is the most accurate & specific one.

o Bleeding trauma, tumor.

o Serosangious discharge Polyp, viral otitis media, and traumatic rupture of tympanic

membrane.

Special tests:

Tuning fork tests:

Weber's test

Rinne's test

1. Weber's test: place the vibrating tuning fork (512Hz) in the midline on the forehead or

upper central incisors. The patient may hear:

- Equal in both ears = normal.

- Better in the diseased ear = conductive hearing loss.

- Better in the normal ear = sensory neural hearing loss.

2. Rinne's test: place the vibrating tuning fork (512 Hz) initially on the mastoid process

until sound is no longer heard, the fork is then immediately placed opposite to the

external canal.

- Rinne positive: the air conduction is better than bone conduction= normal hearing

or sensorineural hearing loss.

AC > BC = Normal or Sensorineural hearing loss

- Rinne negative: the bone conduction is better than air conduction = conductive

hearing loss.

BC > AC = Conducive hearing loss

Polyp: Pediculated portion of edematous mucosa,

so any inflammation in the middle ear can cause

polyp.

Three types of polyps:

1. Inflammatory polyps.

2. Fibrous polyps.

3. Mixed: fibrous-inflammatory polyps.

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Audiometry:

Pure Tone Audiometry (PTA):

Subjective method of testing hearing. It is performed

by presenting a pure tone to the ear through an

earphone and measuring the lowest intensity in

decibels (dB) at which this tone is perceived 50% of

the time. This measurement is called threshold. The

testing procedure is repeated at specific frequencies from 250 to 8000 hertz for each ear, and the

thresholds are recorded on a graph called an audiogram. Bone conduction testing is done by placing

an oscillator on the mastoid process and measuring threshold at the same frequencies. The

audiogram is a graph depicting hearing thresholds in decibels and frequency in hertz.

The unit of sound measurement is decibel (dB).

Degrees of hearing loss:

0-15 dB Normal hearing

16-25 dB Slightly hearing loss

26-40 dB Mild hearing loss

41-55 dB Moderate hearing loss

56-70 dB Moderate-severe hearing loss

71-90 dB Severe hearing loss

> 90 dB Profound hearing loss

Conductive hearing loss:

- Bone Conduction (]) :

within normal (0-15 dB)

- Air conduction (X):

Abnormal

- Air-Bone gap > 10 dB

Sensorineural hearing loss:

- Bone conduction (]):

Abnormal


Abnormal

- Air-Bone gap < 10 dB

> 90 db (profound hearing loss) is an

indication for cochlear implantation.

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Mixed hearing loss:

- Bone conduction (]):

Abnormal


Abnormal

- Air-Bone gap > 10 dB

Tympanometry:

Objective method of testing middle ear pressure, TM

mobility, ossicular chain function, Eustachian tube

function & stapedial reflex.

The test is performed by inserting the tympanometer

probe in the external auditory canal. The instrument

changes the pressure in the ear, generates a pure tone, and measures the TM mobility in response

to the sound at different pressures. Tympanogram is the graphic picture that results as the pressure

is varied against the TM.

Normal middle ear pressure: 0 100 mm H2O.

Normal TM mobility 0 mm.

Type A tympanogram:

represents normal middle ear function.

Type A curves have normal mobility and

pressures and typify normal hearing and

sensorineural hearing loss with normally

functioning middle ear systems.

Type B tympanogram:

represents restricted tympanic membrane

mobility (reduced compliance). This curve is

very typical of a stiff middle ear system as is

seen in acute OM, secretory OM, chronic

OM with perforation, adhesive OM,

atelectatic ear, hemotympanium.

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Type C tympanogram:

represents significant negative pressure in

the middle ear cavity. Type C curves have

normal mobility but it needs higher

pressure.

Type As tympanogram:

represents normal middle ear pressure but

reduced mobility suggesting limited mobility

of the tympanic membrane and middle ear

structure, commonly seen in fixation of the

ossicular chain.

Type Ad tympanogram:

represents normal middle ear pressure but

hypermobility. This pattern is indicative of a

flaccid tympanic membrane due to

disarticulation of the ossicular chain or

partial atrophy of the eardrum.

A.B.R ( Auditory Brainstem Response )

Conventional x-ray mastoids

C.T brain and skull base with or without contrast

M.R.I : e.g: MRI Cholesteatoma protocol to confirm cholesteatoma although it can be seen

through the otoscope.

Functional assessment of the Eustachian Tube.

- Valsalva's test.

-Tympanometry for both - intact membrane or dry perforation.

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Diseases of the external ear

Diseases of the auricle

1. Otohematoma or aurohematoma:

- It is caused by trauma or frost bite.

- It collects between the perichondrium and the cartilage.

- It is dangerous because cartilage receives its blood supply by perfusion from

perichondrium so it results in malnutrition to the cartilage, necrosis and ear deformity

(cornflower ear).

- It is an emergency, needs incision and drainage then pressure to prevent the formation

of hematoma again.

- It occurs more commonly in psychotic patients.

2. Perichondritis:

- It is inflammation of the perichondrium.

- It can be local perichondritis or systemic perichondritis.

o Systemic perichondritis, such as autoimmune

perichondritis (so do RF & ANCA), which may involve

laryngeal cartilage, nasal cartilage or auricule.

- The most common cause is combined, gram negative

bacteria

- An emergency, because of the risk of necrosis and cornflower ear.

- It is an indication for admission and give antibiotics for gram negative & gram positive

bacteria.

3. Furuncle:

- It is abscess in the hair follicles or sebaceous glands.

- The most common cause is Staphylococcus aureus.

- Patients may present with swelling in the retroauricular

area or concha.

- It is treated by incision & drainage and antibiotics.

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Acute otitis externa

There are 8 types:

1. Acute diffuse otitis externa (swimmer disease):

- There is a history of water invasion or trauma.

- Mostly caused by gram neg. bacteria: Pseudomonas, Proteus, E. coli but can be caused

by Staphylococcus aureus.

- Patients present with severe pain, difficulty in opening the mouth, severe tenderness on

examination, severely stenosed external auditory canal due to edema.

- There is keratin containing discharge (whitish moist debri).

- Treatment: Clearance, put a wick, give topical antibiotics (such as quinolones)&

corticosteroids for edema. If not responding to topical treatment, give systemic

antibiotic covering gram negative.

2. Fungal otitis externa (otomycosis):

- Aspergillus species are the commonest cause, mainly Aspergillus flavus &

Aspergillus niger. But it can be caused by Candida.

- Patients present with hearing loss, earache, tinnitus, severe pain and tenderness.

- There is dirty moisty foul smelling material, white in Candida, yellow in Aspergillus flavus

& black in Aspergillus niger. Sometimes we may see the hyphae of the fungus in the

external auditory canal.

- Treatment: Clearance, dryness, protection from water exposure & topical antifungal

such as nystatine or ketoconazole (This is for the mentioned noninvasive infections).

- If invasive fungus, such as in the immunocompromised patients, give systemic

antifungal, amphotricine B.

3. Herpetic otitis externa (herpes oticus):

- It is caused by herpes virus.

- Presents as a part of ramsay hunt syndrome, which is a triad of:

Vesicles on the tympanic membrane or in the external auditory canal.

Sensori neural hearin loss.

Otalgia.

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& may be associated with facial palsy, vertigo, or nystagmus.

- Treatment: Acyclovir 800 mg X 5 times at least for 7 days. If facial palsy is present,

treatment with high dose dexamethasone as early as possible.

4. Seborrhoic otitis externa:

- It is infection in the sebaceous glands.

- Patients present with pain and ear fullness.

- Treatment: Clearance, topical antibiotics & corticosteroids

5. Eczematous otitis externa:

- Treatment: Topical corticosteroids and antibiotics

6. Granular myringitis:

- It usually occurs after trauma to the lateral layer of the tympanic membrane or after the

insertion of ventilation tubes that results in the formation of a granuloma.

- Treatment: Cauterization of the granuloma with silver nitrate or topical corticosteroids

and antibiotics.

7. Myringitis bellousa hemorrhagica:

- There is usually a history of URTI, measles or chickenpox.

- Patients present with severe pain, bulla of blood on the tympanic membrane.

- It is thought to be caused by viral infection or Mycoplasma.

- Treatment: Macrolides (erythromycin) for 7-14 days.

8. Necrotizing otitis externa (Malignant otits externa):

- It is a severe form of acute diffuse otitis externa.

- It affects immunocompromised patients, mostly diabetic patients or patients with

nephritic syndrome taking steroids, patients taking chemotherapy & AIDS.

- It is usually caused by Gram negative bacteria: Pseudomonas, E. coli or Proteus.

- It may lead to osteomyelitis of bone or intracranial complications.

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- Test of choice to detect the presence of osteomyelitis is bone isotope scan.

- Treatment: Antibiotics for gram negative bacteria, such as ceftazidime, meropenim or

quinolones (such as ciprofloxacin) at least for 21 days, but may continue to 8 months.

Any diabetic patient with otitis externa should be admitted to the hospital (DM is an

indication for admission).

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Diseases of the middle ear

Otitis media

Definition: Inflammation of the middle ear cleft (( not middle ear cavity)).

Classification:

1. Acute: less than 3 weeks (or one month roughly)

a. Nonsuppurative There is No pus

b. Suppurative There is pus & indicates tympanic membrane perforation.

2. Subacute: 3 weeks-3months (or up to 90 days)

a. Nonsuppurative

b. Suppurative

3. Chronic: More than 3 months (or more than 90 days)

a. Nonsuppurative :(AKA: Secretory OM / Serous OM/ Exudative OM/ OM with effusion

(OME) / Blue ear)

** In adults, unilateral secretory OM is nasopharengeal carcinoma until proven

otherwise.

b. Suppurative:

- Type 1 (Safe type): Tubotympanic type, there is central perforation & is not

associated with cholesteatoma.

- Type 2 (Unsafe type): atticoantral type, there is marginal or peripheral perforation

& is associated with cholesteatoma.

Epidemiology:

Account for almost 1/3 of the office visit to pediatricians

Peak incidence 6-24 month of life

More common in boys and in low socioeconomic persons

Incidence increased in children with: HIV , cleft palate, trisomy 21

Risks factors:

1. Young age

2. Bottle feeding

3. Pacifier

4. Day care attendance

5. Caretaker smoking

6. Craniofacial anomalies

7. Genetics tendency

8. Allergic disease

9. Immunodeficiency

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Pathophysiology

Acute otitis media usually arises as a complication of a preceding viral upper respiratory infection (URI). The secretions and inflammation cause a relative obstruction of the eustachian tubes ( eustachian tube dysfunction). Normally, the middle ear mucosa absorbs air in the middle ear. If this air is not replaced because of obstruction of the eustachian tube, a negative pressure is generated, which pulls interstitial fluid into the tube and creates a serous effusion. This effusion of the middle ear provides a fertile media for microbial growth. If growth is rapid, a middle ear infection develops.

Microbiology

80% bacterial:

1. S.pneumonia 50%

2. H.influenzae 25%

3. M.catarrhalis 12%

4. Group A strep 2-4%

20% viral:

RSV, Rhinovirus, Parainfluenza, Influenza viruses.

Diagnosis

Acute OM:

Hx: preceding URTI, fever, otalgia, hearing loss, otorrhea. Can be with nausea, vomiting, diarrhea.

In neaonate: irritability, tugging at ear, poor feeding, vomiting and diarrhea.

Exam: pneumotic otoscopy, is the gold standard. Shows loss of all normal marks on tympanic membrane, change colour, bulging of membrane, normal or hypomobile. Decreased mobility is the most important sign.

Chronic OM with effusion: otoscopy showes:

1. Bulging tympanic membrane.

2. Retraction of tympanic membrane (prominent handle of malleus).

3. Tympanic membrane mobility loss.

4. Air fluid level behind the tympanic membrane.

5. Air bubbles behind the tympanic membrane.

6. Bluish ear drum.

D.D. of bluish tympanic membrane:

1. Long standing secretary otitis media (SOM).

2. Hemotympanum: it is a skull base fracture until proven otherwise. Halos sign might be positive due to CSF otorrhea detected by B2 transferrin test.

3. Para ganglion tumors: like para carotid tumor (chemodectoma or glomus jugulare tumor "glomus tympanicum").

4. Dehiscence: high jugular bulb.

5. Late stages of otosclerosis that gives red reflex (Shwartzs sign).

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Acute OM Chronic OM with effusion

Treatment

Acute OM

1st line therapy is amoxicillin (high doze 80-90 mg/kg/ day in 2 divided doses)

2nd line therapy amoxicillin/clavulanic acid, 2nd or 3rd genaration cephalosporin(oral), IM

ceftrixone

Acetaminophen and ibuprofen for fever

Recurrent AOM

Chemoprophylaxis

o Sulfisoxazole, amoxicillin, ampicillin, PNC

Myringotomy and tube insertion

Adenoidectomy

OME (OM with effusion)

MEE > 3 moths or associated hearing loss, vertigo, frequency, ME pathology, discomfort

Antibiotics

Antibiotics + steroid

o 21% improvement compared to ATB alone

o prednisone 1 mg/kg day x 7 days

Myringotomy & tympanostomy +/- adenoidectomy

Complications:

Intratemporal: hearing loss (CHL, SNHL or mixed), TM perforation, cholesteatoma, mastoiditis, labryrinthitis, adhesive OM, facial paralysis.

Intracranial: meningitis, extradural abscess, subdural empyema, brain abscess, lateral sinus thrombosis. The most common complication is mastoiditis. The most common cause of hearing loss is otitis media.

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TM perforation

Pathogenesis

1. Recurrent acute OM: brings to chronic changes in middle ear and tympanic mucosa, leading to

perforation.

2. Traumatic perforation.

Chronic OM

(subtotal perforation) Total perforation Traumatic perforation

Symptoms:

1. Hearing loss (conductive). Perforated lose 20% of its hearing capacity.

2. Recurrent otorhea.

3. Occasionally pain.

Treatment:

1. Ear protection from water.

2. Nasal decongestant to prevent Eustachian tube dysfunction.

3. Antibiotic for 7 days is controversial.

4. Wait for 3 months to close spontaneously (90% of heals spontaneously).

5. If not closed after 3 months, do tympanoplasty.

Prognosis:

Central perforation has better prognosis than peripheral perforation.

Perforation of pars flaccid has worse prognosis than pars tensa, although not affecting hearing

initially.

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Cholesteatoma:

Definition:

Chronic O.M. with accumulation of keratin and

debris in middle ear and mastoid.

Pathogenesis:

Collection of keratin where it is normally not

found (epidermis in a wrong place).

{ In the middle ear, normally there is No skin, there is only mucosa lined with Pseudo-stratified

squamous ciliated mucosa (respiratory mucosa)}.

Cholesteatoma is dangerous, due to enzymatic activity in the

cholesteatoma which causes destruction to the bone leading to facial

palsy, & may eventually reach the brain causing brain abscess.

Therefore, it needs aggressive treatment !

There are two types:

1. Congenital: Remnant of the neural tube (ectoderm) in the middle ear due to neural tube

defect.

2. Acquired: 3 theories:

a. Primary: Retraction pocket theory: In any middle ear pathology, there is Eustachian tube

dysfunction, resulting in a negative middle ear pressure causing the tympanic membrane

to be pulled medially mostly at the pars flaccid (retraction).

b. Secondary: Migration theory: where there is marginal perforation in the tympanic

membrane allowing the skin to enter to the middle ear (migrate).

c. Metaplasia of the respiratory mucosa to keratinized squamous epithelium.

** a & b are more common than c.

Complications:

Slowly destructs ossicles, invades middle ear and mastoid structures, invades CNS, inner ear, facial

canal.

Treatment:

Mastoidectomy

25


Otosclerosis

Normal stapes Otosclerosis

Definition:

Sclerosis of the joints between the ossicles.

Pathogenesis:

Osteolysis followed by new osteogenesis. Most frequent between stapes footplate and

oval window.

Male: Female 1:2

Undergoes progression during pregnancy, suggesting hormonal factor as etiology.

50% - hereditary, 50% - sporadic.

Rare in osteogenesis imperfecta (bleu sclera).

Can be caused by histocytosis X:

a. Eosinophilic granuloma.

b. Hand-Schuller-Christian disease.

c. Letterer-Siwe disease.

Symptoms:

Progressive mixed hearing loss.

Treatment:

Stapedectomy.

26


Middle ear surgery

Myringotomy & Grommets (ventilation tubes):

The most common middle ear surgery.

Myringotomy:

It is a surgical procedure in which a small incision is made in the eardrum (the tympanic

membrane

Indications of myringotomy:

1. Secretory OM.

2. Acute mastoiditis.

3. To diagnose otitis media in patients younger than 8 months of age.

4. In the immunocompromised child.

Indications of ventilation tubes:

1. Secretory OM.

2. Recurrent OM, 3 times/6 months or 4 times/12 months.

3. Acute mastoiditis.

4. Retracted tympanic membrane.

5. Craniofacial anomalies that predispose to middle ear dysfunction (e.g. cleft Palate,

which cause malfunction of the tensor veli palatine muscle).

6. Eustachian tube dysfunction.

7. Injection of gentamycin to treat vertigo such as in Mnire's disease, as

gentamycine is vestibulotoxic.

8. Injection of steroids to treat sudden sensorineuronal hearing loss in patients with

DM or HTN (can't use systemic steroids).

27


Tympanoplasty +\- ossiculoplasty :

Tympanoplasty

Grafts used: fascia (temporalis fascia; the mostly used), cartilage, perichondrium, periosteum.

*** Skin is NOT used as graft here because it causes cholesteatoma.

Goals of surgery:

1. Establish an intact TM.

2. Eradicate middle ear disease and create an air-containing middle ear space.

3. Restore hearing by building a secure connection between the ear drum and the

cochlea.

Types of tympanoplasty:

1. Type I tympanoplasty is called myringoplasty, and only involves the restoration of the

perforated eardrum by grafting.

2. Type II tympanoplasty is used for tympanic membrane perforations with erosion of the

malleus. It involves grafting onto the incus or the remains of the malleus.

3. Type III tympanoplasty is indicated for destruction of two ossicles, with the stapes still

intact and mobile. It involves placing a graft onto the stapes, and providing protection for

the assembly.

4. Type IV tympanoplasty is used for ossicular destruction, which includes all or part of the

stapes arch. It involves placing a graft onto or around a mobile stapes footplate.

5. Type V tympanoplasty is used when the footplate of the stapes is fixed.

28


Types of incisions:

1. Retroauricular incision.

2. Endoaural incision.

3. Transmeatal incision: in the external auditory canal, 6 mm from the tympanic

membrane. Incision is made from 12 o'clock to 6 o'clock.

Refreshment of edges of TM

Elevation of tympanomeatal flap

Insertion of the graft below the flap

Repositioning the tympanomeatal flap

29


Tympanoplasty with ossiculoplasty

Incus interposition:

Cartilage is taken

from the auricle and

shaped like the incus,

then it is placed

between the malleus

and stapes.

PORP: Partial

Ossicular

Replacement

Prosthesis. Prosthesis

is placed between

the head of stapes

and TM.

TORP: Total Ossicular

Replacement

Prosthesis

Prosthesis is placed

between the stapes

footplate and TM.

31


Mastoidectomy

Simple mastoidectomy/ Cortical mastoidectomy/ Schwartz mastoidectomy: involves

removal of the mastoid air cells only, done for acute mastoiditis.

Radical mastoidectomy: involves removal of the mastoid air cells, the TM, the ossicles

and chorda tympani.

Modified radical mastoidectomy: involves removal of the mastoid air cells with

reconstruction of the TM (Tympanoplasty) and preservation of the ossicles.

Combined approach tympano-mastoidectomy:

Stapedectomy

Involves removal of the anterior and posterior crura of the stapes, replacing it with a

prosthesis between the incus and footplate and creating fenestrations in the footplate.

30


Diseases of the inner ear:

Vertigo

Epidemiology

- Dizziness and vertigo are among the most common symptoms causing patients to visit a

physician (as common as back pain and headaches).

- The overall incidence of dizziness, vertigo, and imbalance is 5-10%.

- It reaches 40% in patients older than 40 years.

History

- Ask the patient to describe their symptoms by using words other than "dizzy."

- Dizziness includes light-headedness, unsteadiness, motion intolerance, imbalance, floating, or a

tilting sensation.

- A critical distinction is differentiating vertigo, which is a subtype of dizziness, from other types of

dizziness.

- Vertigo is defined as an illusion of movement caused by asymmetric input of the vestibular

system

- true vertigo is often due to inner-ear disease, whereas other symptoms of dizziness may be due

to CNS, cardiovascular, or systemic diseases.

Onset:

- Sudden onset of vertiginous episodes are often due to inner-ear disease, especially if hearing

loss, ear pressure, or tinnitus is also present.

- Gradual and ill-defined symptoms are common in CNS, cardiac, and systemic diseases.

Time course:

- Episodic true vertigo that lasts for seconds and is associated with head or body position

changes is probably due to benign paroxysmal positional vertigo (BPPV).

- Vertigo that lasts for hours or days is probably caused by Mnire disease (if associated with

hydropic ear symptoms) or vestibular neuronitis (if hydropic ear symptoms are absent).

- Vertigo of sudden onset that lasts for minutes can be due to brain or vascular disease,

especially if cerebrovascular risk factors are present.

CNS symptoms:

- Brainstem characteristics, including diplopia, autonomic symptoms, nausea, dysarthria,

dysphagia, or focal weakness.

- Patients with cerebellar disease are frequently unable to ambulate during acute episodes of

vertigo. Patients with peripheral vertigo can usually ambulate during episodes and are

consciously aware of their environment.

- A history of headaches, especially migraine headaches, can be associated with migraine-

related dizziness.

32


- Previous viral illness, cold sores, or sensory changes in the cervical C2-C3 or trigeminal

distributions usually indicate vestibular neuronitis or recurrent episodes of Mnire disease.

- head trauma

- ear diseases, trauma, or surgery

- History of prescription medicines, over-the-counter medications, herbal medicines, and

recreational drugs (including smoking and alcohol) can help to identify pharmacologically

induced syndromes

- DM, HTN, or any cardiovascular or cerebrovascular disease.

Physical examination

- Supine and standing blood-pressure measurement.

- Evaluation of the cardiovascular and neurologic systems.

- Examine the ears for visible infection or inflammation of the external or middle ear. Test

hearing and discrimination by using a tuning fork and by whispering and asking the patient

to repeat heard words.

- Examine the neck for range of motion and flexibility.

- Focused neurologic examination of the cranial nerves, motor and sensory modalities and

gait.

Vestibular examination

1. The vestibulo-ocular reflex

(VOR)

It is a reflex eye movement that

stabilizes images on the retina

during head movement by producing

an eye movement in the direction

opposite to head movement, thus

preserving the image on the center

of the visual field. For example,

when the head moves to the right,

the eyes move to the left, and vice

versa. Since slight head movements

are present all the time, the VOR is

very important for stabilizing vision:

patients whose VOR is impaired find

it difficult to read, because they cannot stabilize the eyes during small head tremors. The VOR reflex

does not depend on visual input and works even in total darkness or when the eyes are closed.

A normal oculocephalic reflex and intact visual acuity with active head movements (dynamic visual

acuity) reflect good VOR. Absence of the oculocephalic reflex or a decrease in visual acuity with head

movements reflect decreased vestibular function.

33


2. Vestibulospinal reflex (VSR)

It can be examined with Romberg and gait tests.

These tests provide information about the patient's postural stability when his or her visual and

proprioceptive inputs are removed.

Posture and gait:

Ask the patient to repeatedly run the heel from the opposite knee down the shin to the big toe, and

look for incoordination.

Watch the patient walking, performing tandem gait. The normal gait is characterized by an erect

posture, moderately sized steps, and the medial malleoli of the tibia tracing a straight line.

The Romberg examination is conducted by asking the patient to stand with the heels together, first

with eyes open, then with eyes closed. Then, ask the patient to stand on a high-compliance surface

and note any excessive postural sway, posteroanterior or to one side.

3. Fixation suppression test:

It is important for checking the vestibulocerebellum.

Failure of fixation suppression can be tested by asking the patient to stretch his arms and look at his

thumb while being passively rotated (manual rotation of examination chair). A visible

nystagmus (right or left) indicates failure of fixation suppression that is always central in origin.

4. Nystagmus is observed under Frenzel glasses after rapid head shaking

reflects asymmetric vestibular input.

Characterization of nystagmus

- Nystagmus, whether spontaneous, gaze-induced, or positional, must be completely

characterized to be correctly interpreted.

- Examine eye movements for spontaneous nystagmus, gaze-evoked nystagmus, and ocular

motor abnormalities.

- Differentiating peripheral and central nystagmus is a key step.

- Central nystagmus is a purely horizontal or vertical gaze and not suppressed by visual fixation.

- Peripheral nystagmus is usually rotatory and most evident with removing visual fixation (eg, by

using Frenzel goggles or infrared video nystagmography). It also obeys the Alexander law; that

is, the intensity of nystagmus increases with gaze in the direction of the fast phase.

- Nystagmus is divided into 3 grades:

Grade I: Jerky nystagmus is evident only in the direction of the fast phase, i.e. on

conjugate deviation to one side.

Grade II: When in addition, it is evident in the primary position.

Grade III: When it is evident in all positions of the eyes.

34


5. Positioning examination

The positioning examination (Dix-

Hallpike test) is an important

component of the vestibular

examination to identify BPPV

commonly caused by otolith debris

(canalith) floating in the semicircular

canals (canalithiasis) or adhering to

the cupula (cupulolithiasis).

The Dix-Hallpike maneuver is

performed by guiding the patient

rapidly from a sitting position with

the head turned 45 to one side to a

supine position.

BPPV is due to posterior semicircular

canal canalithiasis approximately

90% of the time.

Typical nystagmus related t posterior

semicircular canal benign positioning and its symptoms are delayed by several seconds (latency).

They peak in 20-30 seconds and then decay (paroxysmal), with complete resolution of symptoms

while the patient maintains the same head position (habituation). Symptoms and reversed

nystagmus may occur when the patient is brought back to a sitting position. Therefore, benign

positioning nystagmus is latent, paroxysmal, geotropic, reversible, and fatigable.

Nystagmus of the less common horizontal semicircular canal canalithiasis form of BPPV is purely

horizontal, geotropic (beating toward the down ear), and asymmetric. The direction reverses with

the change in head position from one side to the other in the supine position. The intensity of

nystagmus is strongest when the head is rotated to the involved side.

6. Caloric test examination

Cold or warm water or air is

irrigated into the external auditory

canal, usually using a syringe.

The temperature difference between the body and the injected water creates a convective current

in the endolymph of the nearby horizontal semicircular canal. Hot and cold water produce currents

in opposite directions and therefore a horizontal nystagmus in opposite directions.

In patients with an intact brainstem:

If the water is warm (44C or above) endolymph in the ipsilateral horizontal canal rises, causing an

increased rate of firing in the vestibular afferent nerve. This situation mimics a head turn to the

ipsilateral side. Both eyes will turn toward the contralateral ear, with horizontal nystagmus to the

ipsilateral ear.

35


If the water is cold, relative to body temperature (30C or below), the endolymph falls within the

semicircular canal, decreasing the rate of vestibular afferent firing. The eyes then turn toward

the ipsilateral ear, with horizontal nystagmus (quick horizontal eye movements) to

the contralateral ear.

To remember this:

COWS

Absent reactive eye movement suggests vestibular weakness of the horizontal semicircular canal of

the side being stimulated.

Investigations:

Electronystagmography(ENG)

diagnostic test to record involuntary movements of the eye caused by nystagmus. It can also be used

to diagnose the cause of vertigo, dizziness or balance dysfunction by testing the vestibular system.

ENG provides an objective assessment of the oculomotor and vestibular systems

The test is performed by attaching electrodes around the nose and measuring the movements of the

eye in relation to the ground electrode

The standard ENG test battery consists of 3 parts:

oculomotor evaluation

positioning/positional testing

caloric stimulation of the vestibular system

can be used to record nystagmus during oculomotor tests such as saccades, pursuit and gaze testing,

optokinetics and also calorics (bithermal or monothermal).

Abnormal oculomotor test results may indicate either systemic or central pathology as opposed

to peripheral (vestibular) pathology.

The caloric irrigation is the only vestibular test which allow the clinician to test the vestibular organs

individually, however, it only tests one of the three semi circular canals - the horizontal canal.

While ENG is the most widely used clinical laboratory test to assess vestibular function, normal ENG

test results do not necessarily mean that a patient has typical vestibular function.

ENG abnormalities can be useful in the diagnosis and localization of site of lesion; however, many

abnormalities are nonlocalizing; therefore, the clinical history and otologic examination of the

patient are vital in formulating a diagnosis and treatment plan for a patient presenting with dizziness

or vertigo.

36


Differential diagnosis of dizziness

Cardiovascular causes:

- Arrhythmias (fast or slow rate).

- Orthostatic hypotension.

- Hypovolemia or anemia.

- Myocardial ischemia.

- Structural cardiac or valvular disease.

- Hypoxia.

- Vasovagal episode (also neurologic).

Neurologic-Otologic causes:

Peripheral vestibular causes:

- Vestibular neuritis.

- Benign Paroxysmal Positional Vertigo (BPPV).

- Mnire's disease.

Central vestibular causes:

- CVA

- Vertebrobasilar ischemia.

- Cerebellopontine angle mass.

- Multiple sclerosis.

- Basilar artery migraine.

Other

Drug effects:

- Aminoglycosides.

- Anticonvulsants.

- Antihypertensives.

- Hypoglycemic.

- Antipsychotics.

- Sedative/hypnotics.

- Alcohol.

Psychiatric (hyperventilation, anxiety)

Thyroid disorders

37


Peripheral vertigo

1. Vestibular neuritis

- The most common cause of acute vertigo, with an incidence of 170 cases per 100,000

people.

- result from a reactivation of herpes simplex virus that affects the patient's vestibular

ganglion and vestibular nerves.

- A prodromal upper respiratory tract illness may or may not be present

- Vertigo is without auditory or other CNS symptoms and lasts for several days. Patients are

usually ill and cannot perform home or work activities.

- A brief course of antiemetic and vestibular suppressants is usually needed in the acute

phase, but should be withdrawn as soon as possible to facilitate the process of central

vestibular compensation (3-5days)

- Corticosteroids may improve long-term outcomes

- Early vestibular rehabilitation is important

- Antiviral medications have not proven helpful, possibly because a large spectrum of viruses

can cause vestibular neuronitis.

- One third of patients have chronic vestibular symptoms and develop BPPV.

2. Benign paroxysmal positioning vertigo (BPPV)

- Second most common cause of vertigo

- The typical symptom is brief episodic vertigo upon changing head or body position, Patients

may have a residual sensation of disequilibrium between episodes.

- The common etiology is idiopathic or posttraumatic. Other etiologies such as vestibular

neuronitis, Mnire disease, and delayed endolymphatic hydrops are also associated with

BPPV.

- The mechanism of BPPV can be due to canalithiasis (otoconia floating in the endolymph) or

cupulolithiasis (otoconia adherent to cupula).

- The most commonly affected canal is the posterior canal (90% of cases) and, to a lesser

extent, the horizontal canal. The most effective treatment is canalith repositioning from the

affected canal to the vestibular (using Epley, Semont, Lempert, and Hamid maneuvers,

among others). Medications are not effective in the treatment of BPPV.

- The most common complication of the Semont or Epley maneuver is the conversion of the

posterior canal-horizontal canal BBPV, which is treated with the Lempert or Hamid

maneuvers. Less common is undue cervical strain, especially with the Semont maneuver or

with neck hyperextension during the Epley maneuver.

38


Epleys maneuver

39


3. Mnire disease

- Disorder of the inner ear with typical symptoms of episodic vertigo, tinnitus, and hearing

loss.

- If ntreated, severe hearing loss and unilateral vestibular paresis are inevitable.

- Bilateral involvement occurs in about 25% of patients.

- The etiology can be hereditary, autoimmune, infectious, or idiopathic.

- The common pathophysiology is disordered fluid homeostasis in the inner ear, with

endolymphatic hydrops representing a histological footprint rather than an etiology

- More than 80% of patients respond to conservative therapy with salt restriction and

diuretics.

- Corticosteroids, given orally or intratympanically, can be used to stabilize active disease.

- Intratympanic gentamicin (chemical labyrinthectomy) is a minimally invasive procedure that

emerges as an effective method for treating the disabling vertigo of Mnire disease, and it

can be used to reduce vestibular symptoms.

- The role of surgical therapy, such as shunting the endolymphatic sac, is controversial. The

literature demonstrates wide variation in the effectiveness, or lack thereof, of surgery.

4. Autoimmune inner-ear disease

- Typically present with rapidly progressive, bilateral hearing loss with or without vertigo.

- The initial onset may be unilateral.

- However, the rapid progression, bilateral involvement, and response to steroids

distinguishes this disorder from Mnire disease.

- This disease can occur with or without other autoimmune disease or laboratory evidence of

a systemic inflammatory disorder

- Oral and intratympanic corticosteroids are effective in controlling this disease.

- Patients with recurrent symptoms that are steroid responsive may benefit from

methotrexate or other steroid-sparing medications.

- These patients should be treated by a rheumatologist.

Central dizziness

1. Migraine

- Common disorder, affecting 10% of men and 30% of women.

- About 25% of migraineurs have motion intolerance/sickness as opposed to true vertigo.

- The pathophysiology of migraine-associated vestibulopathy is not completely understood.

- Vestibular symptoms usually are dissociated from headaches but sometimes can occur as an

aura or as part of a headache.

- Treatment of migraine-associated vestibulopathy is the same as the treatment of migraine.

- Trigger factors should be eliminated and patients are encouraged to follow common sense

diet and lifestyle.

41


- Prophylactic and abortive medications commonly used in treating migraine should be

tailored to patients with vestibular migraine.

2. Other central causes of dizziness should be excluded:

- TIA

- Stroke

- Multiple sclerosis

- Tumors and malformations of the posterior fossa:

Vestibular schwannoma (acoustic neuroma)

Arachnoid cysts

Chiari malformation:

occurs in a few adults. It is congenital, but often does not become symptomatic

until the age of 20-40 years. Occipital headache precipitated by Valsalva

maneuvers, coughing, exertion, or changing position is common. Dizziness may

occur with the same precipitants.

can be excluded by MRI.

40


Hearing loss

According to the type, it can be due to outer, middle or inner ear disease.

Types of hearing loss:

1. Conductive hearing loss (CHL).

2. Mixed hearing loss (MHL).

3. Sensorineural hearing loss (SNHL).

4. Non-organic hearing loss.

1. Conductive hearing loss (CHL)

It refers to a disruption or mechanical blockage of the movement of sound waves

(vibrations) at some point in the hearing system before they reach the inner ear.

Dysfunction of the outer or middle ear.

Middle ear structures are intact.

patients tend to speak with normal or low volume voice

Causes of CHL:

Outer ear:

1. Occlusion/foreign body such as wax impaction.

2. Congenital Atresia.

3. Otitis externa.

Middle ear:

1. Otitis Media

2. TM Perforation

3. Cholesteatoma

4. Ossicular fixation

5. Otosclerosis

6. Ossicular Disarticulation

2. Mixed hearing loss (MHL)

It may be caused by severe head injury with or without fracture of the skull or temporal

bone, by chronic infection, or by one of many genetic disorders.

It may also occur when a transient conductive hearing loss, commonly due to otitis media, is

superimposed on a sensorineural hearing loss.

3. Sensorineural hearing loss (SNHL)

It implies damage to the sensors or nerve fibers which connect the inner ear to the hearing

center in the brain. Since damaged nerve fibers do not regenerate or repair themselves like

some other parts of the body, this damage is permanent.

Middle ear structures are intact.

Possible causes of SNHL are:

1. Hereditary.

2. Drugs.

42


3. Permanent damage due to excessive noise.

4. Prenatal exposure to Rubella, CMV.

5. RH incompatibility at birth.

6. Low birth weight caused by prematurity.

7. Elevated biliruben levels (jaundice).

8. Meningitis, and some infectious diseases such as mumps.

Characteristics of SNHL:

Inappropriately loud voice.

Tinnitus.

Speech sounds distorted.

Background noise makes listening more difficult.

Hearing aids may help.

Sudden onset SNHL (SSNHL)

Definition:

Acute unexplained hearing loss, nearly always unilateral, that occurs over less than a 72 hour period.

Most cases are idiopathic, and the prognosis depends on the severity of the hearing loss.

It's a medical emergency.

Criteria for the diagnosis of SSNHL:

Idiopathic hearing loss of at least 30 dB.

Over at least 3 audiometric frequencies test.

Occurring within 3 days.

** After 14 days, it is not considered sudden, & is not treated !

Epidemiology:

The exact incidence of SSNHL is uncertain. Since recovery is often spontaneous, many affected

people likely never seek medical attention.

Estimates of incidence typically range from 2 to 20 per 100,000 people per year .

SSNHL can occur at any age, MC patients 43 to 53 yr of age.

Similar numbers of men and women are affected.

2% are bilateral.

Etiology OF sudden SNHL:

1. Idiopathic : Most common.

2. Infectious.

- Meningococcal meningitis.

- Herpesvirus (simplex, zoster, varicella, CMV).

43


- Mumps.

- HIV.

- Mycoplasma.

- Cryptococcal meningitis.

- Toxoplasmosis.

- Syphilis.

- Rubella.

pathophysiology: host immune response to the pathologic changes in the membranous

labyrinth and subsequent hearing loss

3. Autoimmune.

- Autoimmune inner ear disease (AIED).

- Ulcerative colitis.

- Relapsing polychondritis.

- SLE.

- Polyarteritis nodosa.

- Cogans syndrome.

- Wegeners granulomatosis.

pathophysiology: vasculitis of vessels supplying the inner ear, autoantibodies directed

against inner ear antigenic protiens, or cross-reacting antibodies

Cogans syndrome

First described by Cogan in 1940.

Autoimmune disease of the cornea and inner ear.

Age of onset 22-29 years.

Presentation interstitial keratitis(IK) and Menieres like episodes of vertigo with

Bilateral Rapidly Progessive SNHL (BRPSNHL).

Associated systemic diseases.

Takayasus like or medium-sized vessel vasculitis.

Aortitis 10%.

Hearing fluctuates with disease exacerbations and remissions.

Majority develop bilateral deafness (67%).

4. Vascular.

- Vascular disease/alteration of microcirculation.

- Vascular disease associated with mitochondriopathy.

- Vertebrobasilar insufficiency.

- Red blood cell deformability.

- Sickle cell disease.

- Cardiopulmonary bypass.

44


pathophysiology: embolic phenomenon, thrombosis, vasospasm, and hypercoagulable or

high viscosity states. An association of genes related to prothrombotic states, and increased

serum levels of fibrinogen and homocysteine in patients with SSNHL microvascular

events as a cause.

5. Neurologic.

- Multiple sclerosis

- Focal pontine ischemia

- Migraine

6. Traumatic.

- Perilymph fistula.

- Inner ear decompression sickness.

- Temporal bone fracture.

- Inner ear concussion.

- Otologic surgery (stapedectomy).

- Surgical complication of nonotologic surgery.

pathophysiology: Traumatic breaks in the membranous labyrinth.

7. Neoplastic.

- Acoustic neuroma.

- Leukemia.

- Myeloma.

- Metastasis to internal auditory canal.

- Meningeal carcinomatosis.

Associated with gradually progressive hearing loss

8. Other causes:

- Endocrine disorders: Hypothyroidism

- Medications : Aspirin, antibiotics: aminoglycosides; vancomycin; erythromycin, loop

diuretics, antimalarials, cisplatin.

- Excessive noise, such as chronic exposure to loud music or other sounds.

- Presbycusis sensory hearing loss (PSHL): Senile hearing loss.

Presbycusis is sensorineural hearing loss that probably results from a combination

of age-related deterioration and cell death in various components of the hearing

system and the effects of chronic noise exposure.

Consonant sounds are the most important sounds for speech recognition. For

example, when shoe, blue, true, too, or new is spoken, many people with

presbycusis can hear the oo sound, but most have difficulty recognizing which

word has been spoken because they cannot distinguish the consonants.

45


History:

Time-course: 1/3 cases upon first awakening in the morning.

Associated symptoms:

Vertigo/dizziness: in 1/2 cases.

Aural fullness: a sense of air pressure in the middle ear.

Tinnitus.

Hx of ototoxic drug use.

Symptoms of URTIs.

Hx of head trauma, straining, sneezing, nose blowing, intense noise exposure.

Hx of flying or diving.

Past medical Hx:

Autoimmune disorders.

Vascular disease.

Malignancies.

Neurologic conditions.

Hypercoagulable states.

Sickle cell disease (African Americans).

Past surgical Hx : stapedectomy or other otologic surgeries.

Physical examination:

Complete Head & Neck exam.

Ears: Rule out effusions, cholesteatoma, cerumen impaction

Cerumen (earwax) accumulation is the most common cause of treatable hearing

loss, especially in the elderly. Foreign bodies obstructing the canal are sometimes a

problem in children, both because of their presence and because of any damage

caused during their removal.

Weber's & Rinne's tests.

Neurologic exam cerebellar findings:

Romberg

Nose to finger, heel to shin

Vestibular Dix-Hallpike test.

Diagnosis:

Patients who complain of sudden hearing loss or awaken with new hearing loss, it is due to a

conductive or sensorineural problem Weber's and Rinne's tests.

1. Weber's test:

The patient may hear the sound:

- Equal in both ears = normal.

- Better in the diseased ear = conductive hearing loss.

- Better in the normal ear = sensory neural hearing loss.

2. Rinne's test:

+ Rinne positive:

AC > BC = Normal or Sensorineural hearing loss.

46


- Rinne negative:

BC > AC = Conducive hearing loss.

Diagnostic Testing

Audiogram

Diagnostic and prognostic.

Subjective method of testing hearing.

Audiogram

Bone conduction within normal.

Air conduction abnormal.

Air Bone gap>10dB

CHL

Bone conduction abnormal.

Air conduction abnormal.

Air Bone gap10DB

MHL

Laboratory testing :

CBC

ESR, CRP

Chemistry

Cholesterol/triglycerides

T3/T4, TSH

HIV

Lyme titer

Antigen-specific cellular immune tests

Lymphocyte transformation test (LTT)

Western blot

Imaging study:

MRI:

Any patient presenting with SSNHL, it is mandatory to do MRI with contrast to Rule out:

47


Cerebellopontine angle tumors (Acoustic neuroma).

** 1% of SSNHL patients have acoustic neuroma.

** 10-19% of acoustic neuroma patients present with SSNHL.

Multiple sclerosis.

Ischemic changes.

Treatment:

** SNHL is an emergency !!

Treat underlying condition if there is a known cause.

In idiopathic SSNHL, there is a high spontaneous recovery rate (47% to 63%).

We use:

Anti-inflammatory/immunologic agent as:

- Steroids

- Prostaglandin

- Cyclophosphamide

- Methotrexate

Diuretics

Antiviral agents: Acyclovir,Valacyclovir

Vasodilators

Calcium antagonists: Nifedipine

Antioxidants: Vitamin A

Plasmapheresis (in autoimmune cases)

Cochlear implantaion: in bilateral progressive deafness & Profound hearing loss (>90 dB).

Prognosis

It is depend on:

Time since onset:

The sooner the patient was seen and therapy initiated, better the recovery.

Age:

The average age for those recovering totally was 41.8 years.

Age < 15 years & > 60 years: poorer recovery rates.

Associated symptoms:

Vertigo: worse outcome.

Audiogram:

Patients with profound hearing loss significantly decreased recovery rates.

Syndromes associated with hearing loss:

Alport's syndrome.

Mondani syndrome: Partial aplasia of cochlea.

Michel aplasia: Total aplasia of cochlea.

Common cavity syndrome.

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Goldenhar syndrome.

Waardenburg syndrome.

Treacher collins syndrome.

Alexander syndrome.

Usher syndrome.

Referred otalgia Pain referred from structures whose nerve supply also sends branches to the ear.

Sensory innervations of the ear:

1. Auriculotemporal nerve, a branch of mandibular division of trigeminal nerve. It causes referred otalgia of trigeminal origin. Patient may have dental caries, gingival abscess, TMJ problem, sinusitis

2. Arnold nerve, auricular branch of vagus nerve. It causes referred otalgia of vagal origin. Patient may have MI, peptic ulcer or most commonly, laryngitis with hoarseness of voice.

3. Jacobson nerve, tympanic branch of glossopharengeal nerve. It causes referred otalgia of glossopharengeal origin. Patient may have

4. Greater auricular nerve (C2) & Lesser occipital nerve (C3). It causes referred otalgia of cervical origin. Patient may have muscle spasm, spondylosis or disc herniation in the neck.

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The nose & Paranasal sinuses

1. The nose:

Nose anatomy:

** Face is divided into 3 parts:

1. Upper third: From the hair line to the bridge of the nose.

2. Middle third: From the bridge of the nose to the nasolabial angle

(the angle between the columella & philtrum).

3. Lower third: From the nasolabial angle to the chin.

Nose is a pyramidal structure, located in the middle third of the face with the base at the upper lip

and the apex between the orbits (root of the nose). It is composed of: bridge, dorsum, 2 lateral

surfaces, tip, columella, 2 ala nasi & 2

nostrils. It is divided into two parts :

a. External nose:

1. Bony part: forms 2/3 of nose anatomy,

composed of:

Nasal bone.

Ascending (frontal) process of

maxilla.

Nasal process of frontal bone.

The skin over the bony part is very thin due to

the absence of sebaceous glands, hair follicles

& sweat glands. So, this thin skin is the one

used for flaps rather than the thick skin.

2. Cartilaginous part: forms 1/3 of nose

anatomy, composed of:

Upper lateral cartilage.

Lower lateral cartilage.

The skin over the cartilaginous part is very thick

because there are sebaceous glands, hair

follicles & sweat glands. It needs deep suture if

being used for flaps, that's why the thin skin is

preferred.

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b. Internal nose:

= Nasal cavity proper which extends from nostrils

in front to conchae behind. It has 6 walls:

i. Anterior wall: Anterior nares/nosetrils.

ii. Posterior wall: Posterior nares/ choana.

** Choanal atresia in the pediatric age group is

an emergency & has a mortality risk because

they are obligate nasal breathers.

iii. Medial wall: Septum, it divides the nose into

right & left. It has 3 parts:

1. Membraneous part: Columella with skin.

2. Cartilaginous part (anteriorly): Quadri-

lateral cartilage which is the most

common site of septal deviation.

In the anterior part of the cartilage locates

the Little's area that contains the

kiesselbach plexus which is the most

common site of epistaxis(75-90%).

Kiesselbach plexus: 5 arteries,

- 3 from the external carotid artery:

Sphenopalatine artery, a branch of

maxillary artery;

Greater palatine artery, a branch of

maxillary artery

Superior labial artery, a branch of facial

artery

- 2 from the internal carotid artery:

Anterior ethmoidal artery

Posterior ethmoidal artery, both

branches of ophthalmic artery

3. Bony part (posteriorly): Vomer "backward

downward" and perpendicular plate of ethmoid bone "backward upward". During

surgery, surgeons should avoid moving the perpendicular plate of ethmoid because of

the risk of fracture & causing CSF leak.

iv. Lateral wall: 3 turbinates or conchae(three

bony projections below each of them lies a

meatus).

The superior and middle turbinates are parts of

the ethmoid bone while the inferior turbinate is

a separate one.

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* During surgery, surgeons should avoid excessive movement of the superior and middle

turbinates because of the risk of CSF leak.

The inferior meatus receives the opening of the nasolacrimal duct which lies 1cm

posteriorly to the anterior tip of the inferior turbinate.

*1 cm posterior to the inferior turbinate lies the pharyngeal orifice of the Eustachian

tube behind of which lies a small recess, the pharyngeal recess or fossa of

Rosenmller which is the most common site of nasopharyngeal carcinoma.

The middle meatus contains the opening of the anterior group of sinuses (maxillary,

frontal & anterior ethmoidal sinuses) at the heatus semilunaris.

** Osteomeatal Unit (OMU)/ Osteomeatal complex: anterior ethmoid (Bulla

ethmoidalis), opening of the anterior group of sinuses & middle meatus itself.

The superior meatus receives the openings of the posterior group of sinuses

(posterior ethmoidal & sphenoidal sinuses) at the spheno-ethmoidal recess which

lies above the superior turbinate.

v. Floor: formed by the palatine process of the maxilla and the horizontal plate of the palatine

bone.

vi. Roof: dorsum of the sphenoid, cribriform plate of the ethmoid, nasal bone, upper and lower

lateral cartilages.

Mucous membranes of the nasal cavity: Respiratory mucosa: Pseudostratified ciliated columnar epithelium.

Below the middle turbinate, the mucosa is pinkish Respiratory mucosa.

Above the middle turbinate, the mucosa is yellowish Olfactory neuroepithelium

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Nose examination:

External nose examination inspect the skin for swellings, ulcers, deviations humb, scars and

abnormal colouration. Palpate for tenderness on the bony nose ,floor of frontal sinus and

maxillary sinuses.

Internal nose examination- rise the tip with your finger and look inside the nose to see the skin

of vestibule and part of nasal mucosa, then with nasal speculum examine the left and right nasal

cavities, look for:-

Colour of mucous membrane

Normal: smooth glistening reddish white.

Acute rhinitis: congested red smooth.

Chronic rhinitis: congested red non smooth.

Allergic rhinitis: bluish/ Purple mucosa.

Amount, color and consistency of secretions

Normal: minimal amount of clear mucous.

Acute rhinitis: profuse amount of mucous or mucopurulent discharge.

Chronic rhinitis: mucoperulent discharge.

Allergic rhinitis: profuse clear mucous discharge with swelling.

Clear water discharge: CSF.

Bloody discharge: tumor (eg: Juvenile angiofibroma)or grannuloma.

Fresh blood: epistaxis.

Nasal septum deviation.

Inferior and Middle turbinate: Look for congestion or hypertrophy.

Floor of the nose: because it is the functional area of the nose for breathing.

Inferior and middle meatus.

Presence of abnormal growth.

Anterior and posterior Rhinoscopy

Nasal Endoscopy

Specific diagnostic methods:

a) Nasal endoscopy

b) Biochemical and immunologic investigation of the secretions

c) Cytology and bacteriology

d) Allergic investigation

e) Biopsy

To complete examination of the nose, the naso pharynx should be examined with endoscopy

through the nose or with mirror through the mouth.

X-Ray conventional for sinuses and nasal bones in case of trauma, but CT is much more

diagnostic.

Clinical aspects of nasal disease:

Nasal obstruction.

Nasal discharge

Fetor

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Epistaxis

Smell disturbance

Facial pain

Facial deformity

Differential diagnosis of nasal airway obstruction

Acute and chronic rhinitis (e.g., allergic, atrophic)

Sinusitis

Deviated septum (congenital, acquired)

Nasal pyramid fracture

Septal perforation

Nasal polyps

Cephalocele / Meningiocele

Adenoids (Pharengeal tonsils)

Tumors of the nose, paranasal sinuses, and nasopharynx

Foreign bodies (especially in small children)

Drugs

Adverse effects: oral contraceptives, antihypertensive

agents (e.g., reserpine, propranolol, hydralazine), antidepressants

(e.g., amitriptyline)

Drug abuse: imidazoline derivatives (e.g., oxymetazoline

hydrochloride, xylometazoline hydrochloride)

Causes of olfactory disturbances:

** Hposomia: Decreased sense of smell.

** Anosmia: Absent sense of smell.

Transport of odorants

Nasal obstruction Deviated septum

Mucosal swelling, polyps, tumor

Scar tissue occluding the olfactory groove

After intranasal surgery

Perception: damage to the olfactory epithelium caused by:

Toxic substances SO2, NO, ozone,heavy metals, varnishes

Drugs

Viral infections, e.g: Influenza

Radiotherapy (rare)

Stimulus conduction and processing

Avulsion of fila olfactoria due to skull base fracture.

Aplasia of the olfactory bulb (rare).

Kallmann syndrome: Hypothalamic hypogonadism, anosmia, SNHL.

Injury to olfactory centers: Contusion or hemorrhage due to head injury

Neurodegenerative diseases: Alzheimer disease, Parkinson disease, diabetes mellitus

Olfactory hallucinations After epileptic seizures, in schizophrenia

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Nasal diseases

Choanal atresia

Embryology of choanal atresia

The choanae are the posterior openings that connect the nasal cavities with the nasopharynx.

They develop between the third and seventh embryonic weeks, following rupture of the vertical

epithelial fold between the olfactory groove and the roof of the primary oral cavity (pronasal

membrane).If this process is disturbed, rupture of the oronasal membrane will be absent or

incomplete, resulting in the partial (stenosis) or complete closure (atresia) of one or both

choanae.

Classification:

Unilateral / Bilateral

Bony / Membraneous

Complete (atersia) / Incomplete (stenosis)

** Complete bilateral choanal atresia in neonates is an emergency because they are obligate

nasal breathers.

Nasal deformities

Deformities of the external nose:

Crooked nose Humped nose Saddle nose Broad nose

Management:

Rhinoplasty

Deformities on the internal nose:

Nasal septal deviation

- 70% of the population have nasal septal deviation !

- Require surgical repair if causing complications, such as: nasal obstruction,

snoring, recurrent sinusitis or rhinitis.

Classification:

Bony / Cartilaginous.

Traumatic / Non-traumatic (congenital).

** The most common nasal mucosal disease is

Allergic rhinitis, affecting app. 30% of people.

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Types of deviation:

C-shape with sharp angle.

C-shape.

S-shape.

Management:

Septoplasty.

SMR: Submucosal Resection.

Complications of surgery:

Perforation.

Saddle nose.

Retrobulbar hematoma.

Adhesions.

Fracture of cribriform plate and CSF leak.

Septal perforation

Etiology:

Local causes:

- Traumatic: surgery / Pick ulcer.

- Snuff takers.

- Chrome ulcer: affects workers in chrome factories.

- Neglected foreign body.

- Rhinolith

Systemic causes:

- SLE.

- Wegener's granulomatosis.

- Other vasculitis syndromes.

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Epistaxis

Causes:

Local causes:

- Traumatic: Surgery, picking, foreign body

- Neoplastic: Any tumor can cause epistaxis but angiofibroma is the most one.

- Inflammatory: Any acute rhinitis can cause epistaxis.

- Environmental: especially coldness and dryness.

- Idiopathic.

Systemic causes:

- Increased venous pressure: such as in right-sided HF, whooping cough, pneumonia.

Retro columellar vein is the most common site of bleeding when the cause is

increased venous pressure.

- Blood and blood vessels disease: Any cause of bleeding tendency, such as, Vitamin K

deficiency, Hemophilia, Leukemia, Von willebrand disease, Christmas disease

(Hemophilia B), Liver failure.

** Hypertension is NOT a cause of epistaxis, but epistaxis is more severe and more prolonged

in hypertensive patients and they need admission. Moreover, there is a theory that seeing

the blood coming out of the nose causes an increase in blood pressure !

Sites of bleeding:

- The most common site of

bleeding is Little's area

Kiesselbach's plexus,

accounting for 75-90% of

cases.

- Bleeding above middle

turbinate, mostly due to

ethmoidal artery.

- Bleeding posteriorly, mostly

due to sphenopalatine artery.

Management:

1. Trotter position: Place patient in an upright position, leaning forward to reduce venous pressure. Tell the Patient to firmly grasp and pinch his entire nose between the thumb and fingers for at least 10 minutes.Compress the soft outer portion of the nose against the midline septum for about 5-10 minutes continuously.

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2. Application of ice. 3. Anterior packing: Gauze packing inside the nose for anterior epistaxis.

4. Posterior packing: for 24-48 hours for posterior epistaxis

5. Cauterization: using silver nitrate.

6. Ligation of the arteries. 7. Embolization: using angiography 8. SMR: for recurrent epistaxis from little's area.

Nasal bone fractures:

Classification: - Open. - Closed.

Diagnosis:

- Inspection.

- Intranasal inspection.

- Palpation.

- Radiographic evaluation.

Management:

if there is NO edema, do nasal bone reduction.

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if there is edema, wait for 1-2 weeks, then do nasal bone reduction.

** Look for septal hematoma, why is it an

emergency?!

Cartilage receives its blood supply from the

perichondrium, so the presence of the

hematoma deprives the cartilage from its

blood supply leading to necrosis, saddle

nose or septal perforation. So, it should be

evacuated by incision and drainage.

CSF leak

The most common site for CSF leak is through fra

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