ENT AyaSalahEldeen

ENT for medical students
Dr. Adel Adwan
Prepared by:
Aya Abukhalil Salah Eldeen
Al-Quds university
2010/2011
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.
ENT, Dr. Adel Adwan - Al-Quds university

Prepared by: Aya Abukhalil Salah Eldeen
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

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
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.

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).

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.

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).

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.

01
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.

00
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.
Atrophic retrscted with prominent handle of malleus in long standing negative pressure
Secretory or adhesive OM.
Thick with calcification white in color Myringosclerosis (due to recurrent OM or

multiple ear surgeries ).
Perforated: Central / Marginal.
Ear discharge:
o
Brown mass Wax (& can be gold or even black, all are normal).
Moist keratin debri otitis externa
Moist dirty mass Fungus : Candida albicans, Aspergillus flavus, Aspergillus niger (most
common one)
Mucoid or mucoperulent discharge Chronic or acute otitis media.

02
Scanty offensive perulent discharges Cholesteatoma
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.
Bleeding trauma, tumor.
Serosangious discharge Polyp, viral otitis media, and traumatic rupture of tympanic
membrane.
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.
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

03
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
Air conduction (X):

Abnormal
Air-Bone gap < 10 dB

> 90 db (profound hearing loss) is an

indication for cochlear implantation.
04
Mixed hearing loss:
Bone conduction (]):

Abnormal
Air conduction (X):

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.

05
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.

06
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.
2.
It occurs more commonly in psychotic patients.
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.

07
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.

08
& 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.

09
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).

21
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.
2.
3.
4.
5.
6.
7.
8.
9.
Young age
Bottle feeding
Pacifier
Day care attendance
Caretaker smoking
Craniofacial anomalies
Genetics tendency
Allergic disease
Immunodeficiency

20
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
1.
2.
3.
4.
80% bacterial:
S.pneumonia 50%
H.influenzae 25%
M.catarrhalis 12%
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).

22
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.

23
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.
2.
3.
4.
5.
Ear protection from water.

Nasal decongestant to prevent Eustachian tube dysfunction.
Antibiotic for 7 days is controversial.
Wait for 3 months to close spontaneously (90% of heals spontaneously).
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.

24
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 migrainerelated 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 (DixHallpike 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.
4.
5.
6.
7.
8.
Permanent damage due to excessive noise.

Prenatal exposure to Rubella, CMV.
RH incompatibility at birth.
Low birth weight caused by prematurity.
Elevated biliruben levels (jaundice).
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
gap<10DB
SNHL
Bone conduction
abnormal.
Air conduction
abnormal.
Air Bone
gap>10DB
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.

48
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.

49
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.

51
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): Quadrilateral 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.

50
* 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

52
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

53
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
54
Nasal diseases
** The most common nasal mucosal disease is

Allergic rhinitis, affecting app. 30% of people.
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).

55
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.

56
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.
57
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.
58
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 fractured cribriform plate.
How to confirm that this 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.
Inflammations of the external nose & nasal cavity

Vestibulitis:
Purulent inflammation of the hair
follicles. It is an emergency because of
its location in the dangerous triangle
and the risk of retrograde transmission
of the infection through the valveless
emissary veins into the cavernous sinus.
It is caused by Streptococci or
staphylococci so it is treated with ATB
covering gram +ve. However, if furuncle
(abscess) was formed, the patient
should be admitted and started on IV
ATB.

59
Rhinitis:
- Acute (simple) rhinitis:
Infectious rhinitis or common cold, mostly caused by viral infection, but can be caused
by bacterial infection. It is the most prevalent infectious disease.
-
Nonspecific chronic rhinitis:

Etiology:
Can develop due to anatomic changes (e.g., marked septal deviation, septal spur) or
other lesions of the nasal cavity (polyps, tumors) and nasopharynx (adenoids).
Environmental factors such as sustained extreme temperatures or air pollutants can also
bring on this condition.
Symptoms:
Patients present clinically with obstructed nasal breathing and a mucous nasal discharge.
They also complain of frequent throat clearing and occasional hoarseness. Hoarseness
occurs due to post nasal drip causing chronic laryngitis.
Management:
Treat the underlying cause (such as septal deviation, polyp).
Eliminate environmental treiggers/ factors.
Specific chronic rhinitis:

Tuberculosis.
Sarcoidosis .
Rhinoscleroma..
Actinomycosis
Syphilis.
Fungal infections: Aspergillosis, Mucormycosis , Rhinosporidiosis.
Wegener granulomatosis (Wegener disease).
Allergic rhinitis:
Etiology:
Triggered by an immediate IgE-mediated reaction (type 1 hypersensitivity reaction).
classified as seasonal (hay fever) or perennial according to the presence of the allergen
in the environment.
Symptoms:
The clinical manifestations include obstructed nasal breathing and sneezing attacks, a
watery nasal discharge, and itching of the nose and eyes (conjunctivitis).
It may lead to nasal polyps.
** Nasal polyps:
1. Simple: Either inflammatory or allergic.
2. Neoplastic, such as inverted papilloma
which has a high risk of recurrence and
15% risk of malignancy transformation.

61
Management:
Anti-histamines
Local corticosteroids, which cause medical polypectomy as they help in decreasing the
polyps size.
-
Atrophic rhinitis:
It is a chronic form of rhinitis, characterized by dryness of the nasal mucosa & very bad
nasal odor. It can be:
Primary due to fibrosis in submucosal tissue and endarteritis in terminal arterioles of the
nose causing dryness and crustation leading to bad nasal odor.
Secondary due to excessive use of nosal drops, drug abuse (cocaine), or previous
radiotherapy for nasal and sinus tumors. Iatrogenic causes include a botched septoplasty
or an excessive turbinate reduction (conchotomy).
Rhinitis sicca
It is a form of atrophic rhinitis, it affects workers in dry atmospheres.
Rhinitis caseosa
It occurs post acute rhinosinusitis. It is characterized by a cheesy material which is
secreted from the sinuses to the nasal cavity. It is treated with sinus wash out.
Hormonal rhinitis:
It occurs mostly during pregnancy (estrogen-dependent rhinitis).
Rhinitis Medicamentosa
It is caused by long-term use of decongestant nosal drops. It can also result from the use
of certain antihypertensive drugs (e.g., rauwolfia alkaloids, beta-blockers, ACEI), oral
contraceptive use, tegretol (carbamazepine) & other drugs.
Vasomotor rhinitis:
It is a combination of nasal rhinorrhea, sneezing & nasal obstruction with unknown
etiology. It resembles allergic rhinitis in its clinical features, but there is no evidence that
the patient has been previously sensitized. They can be differentiated by taking a smear,
which shows eosinophils in allergic rhinitis but not in vasomotor rhinitis.
Symptoms are related to a temperature change, the consumption of hot liquid or
alcohol, or less specifically to emotional stress.
Symptoms are related to a temperature change, the consumption of hot liquid or
alcohol, or less specifically to emotional stress.
Pathogenesis:
** The greater superficial petrosal nerve (which arises from facial nerve) meets the deep
petrosal nerve (which arises from superior cervical plexus) in the pterigopalatine fossa to
form the nerve of pterigoid canal (vidian nerve), which gives supply to nasal mucosa.
** The greater superficial petrosal nerve is a parasympathetic nerve which causes
increased secretion (rhinorrhea) & vasaodilataion (congestion) in the nasal mucosa.

60
** The deep petrosal nerve is a sympathetic nerve which causes decreased secretion &
vasodilatation in the nasal mucosa.
** Vasomotor rhinitis is thought to result from neurovascular autonomic disturbances in
regulating the tonus of the nasal mucosal vessels, which results in over stimulation of
the parasympathetic input.
Management:
It was used to be treated with vidian neurectomy, but now it is treated the same as
allergic rhinitis.
Nasal surgey
Septum surgery
SMR (Submucosal Resection) of the nasal septum:
It involves extensive removal of deviated cartilaginous part.
It is done for:
- Septal deviation.
- Severe uncontrolled epistaxis.
Septoplasty
It involves correction of the deviated septal part.
It is done for septal deviation.
Turbinate surgery
SMD (Submucosal diathermy)
It involves cauterization of the turbinate causing fibrosis and shrinkage.
It is done for allergic rhinitis.
Conchotomy (turbinotomy)
It involves removal of the mucosal surface of the turbinate.
One of its complications is atrophic rhinitis.
Turbinoplasty/ SMR of the turbinate
Coblation
Using a combination of laser and ultrasound.
CO2 laser
** During surgery, it is important to avoid excessive manipulation of the middle turbinate and
perpendicular plate of ethmoid to avoid CSF leak.
62
2. The paranasal sinuses

Anatomy:
Anterior group:
Maxillary Sinuses.
Anterior Ethmoidal Sinuses.
Frontal Sinuses.
Posterior group:
Sphenoidal Sinuses.
Posterior Ethmoidal Sinuses.
1. Maxillary sinuses:
- 2 in number.
- Lie within the maxilla.
- Pyramidal in shape.
- The roof is formed by floor of orbit.
- The floor is related to the roots of the premolar and molar teeth. This anatomical
relationship explains the pathophysiology of sinusitis of dental origin, which is caused by
anaerobes and occurs most commonly due to 2nd & 3rd molars, either after extraction in the
presence of thin maxillary sinus floor or due to apical granuloma or abscess.
2. Frontal sinues:
- 2 in number.
- Lie within the frontal bone, separated by a bony septum.
3. Sphenoidal sinuses:
- 2 in number.
- Lie within the body of the sphenoid.
4.
Ethmoidal sinuses:
- Anterior, middle, posterior ethmoidal sinuses, called ethmoidal labyrinth.
- Lie within the ethmoid bone.
** The sinuses have small orifices (ostia) that open into the nasal meati. The anterior group of
sinuses opens into the middle meatus at the hiatus semilunaris. However, the posterior group of
sinuses opens into the superior meatus at the spheno-ethmoidal recess which lies above the
superior turbinate.
** Osteomeatal Unit (OMU)/ Osteomeatal complex: anterior ethmoid, opening of the anterior
group of sinuses & middle meatus itself.
** Maxillary sinus is the most frequently to get infected but the ethmoidal sinus is the most
important one. This is because the bulla ethmoidalis "the largest anterior ethmoidal air cell" lies
above the hiatus semilunaris, so its inflammation and enlargement causes obstruction to the
anterior group of sinuses which open into the middle meatus at the hiatus semilunaris.

63
This picture shows the bulla ethmoidalis and its relationship to the hiatus semilunaris.
Function of paranasal sinuses:

1. Act as resonance to the voice.
2. Reduce the weight of the skull.
3. Protect the eye.
Development of paranasal sinuses:

-
Ethmoid sinuses are present and the only pneumatized at birth.

The maxillary presents at birth and become pneumatized at 4 years of age.
The sphenoid sinuses are present by 5 years of age.
The frontal sinuses begin to develop at 7 years of age, and become completely developed at
adolescence.
** Maxillary, sphenoidal and frontal sinuses become developed completely at 18 years of
age.
Sinusitis:
Definition:
Sinusitis is characterized by inflammation of the lining of the paranasal sinuses. Because the nasal
mucosa is simultaneously involved and because sinusitis rarely occurs without concurrent rhinitis,
rhinosinusitis is now the preferred term for this condition.

64
Pathophysiology:
The sinuses are lined by respiratory epithelium mucosa. Superficial viscous layer and
underlying serous layers.
Normal function depends on patent ostia, ciliary function and quality of mucosa.
* The most important pathological process:

Mucosal edema resulting from a viral rhinosinusitis obstruction of natural ostia
hypooxygenation acidosis vasodilation increased secretion by goblet cells ciliary
dysfunction with poor mucous quality retention of secretion and predisposition to bacterial
infection.
Risk factors:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
The common cold: major predisposing factor at all ages.

Cystic fibrosis.
Immunodeficiency, HIV infection.
Nasogastric or nasotracheal intubation.
Immotile cilia syndrome.
Nasal polyps.
Nasal foreign body.
Cold air.
Tumor.
Rhinitis
Anything that blocks mucus from exiting the sinuses predisposes them to inflammation.
Etiolgy:
Ostial obstruction:
Inflammation
- URTI
- Allergy
Mechanical
- Septal deviation
- Turbinate hypertrophy
- Polyps
- Tumors
- Adenoid hypertrophy
- Foreign body
- Congenital abnormalities i.e. cleft palate
Non-ostial obstruction
Immune
- Wegener's granulomatosis
- Lymphoma, leukemia
- Immunosuppressed patients (e.g. neutropenics, diabetics, HIV)
Systemic
- Cystic fibrosis
- Immotile cilia syndrome (Kartagener's)

Triad of:
1. Sinusitis
2. Bronchiectasis
3. Situs invertus
65
Direct extension
Dental
- Infection
Trauma
- Facial fractures
Bacteria causing sinusitis include:
1.
2.
3.
4.
S. pneumoniae
Nontypable H. influenzae
Maroxella catarrhali
Less commonly: S. aureus, other streptococci, and anaerobes.
Indwelling nasogastric and nasotracheal tubes predispose to nosocomial sinusitis, which is

often caused by gram-negative bacteria (Klebsiella and Pseudomonas).
Antibiotic therapy predisposes to infection with antibiotic-resistant organisms.
Sinusitis in neutropenic and immunocompromised persons may be caused by Aspergillus
and the Zygomycetes (e.g., Mucor, Rhizopus).
** Fungal sinusitis is divided into:

1. Invasive: it is usually caused by Mucor, it has a very high mortality rate because it causes
destruction and necrosis to the bone and may reach the brain. It occurs in
immunocompromised patients
2. Non-invasive
Classification:
According to duration:
Acute
Subacute
Chronic
< 1 month.
1-3 months.
> 3 month.
Acute suppurative sinusitis

Definition:
Acute infection and inflammation of the paranasal sinuses.

Clinical diagnosis requiring at least 2 major symptoms or 1 major symptom and 2 minor
symptoms
Major symptoms
- Facial pain/ pressure
- Facial fullness/ congestion
- Nasal obstruction
- Purulent/ discolored nasal discharge
- Hypodmia/ anosmia
- Fever

66
Minor symptoms
- Headache
- Halitosis
- Fatigue
- Dental pain
- Cough
- Ear pressure/ fullness
Etiology:
Viral vs. bacterial

Children are more prone to a bacterial etiology than adults, but viral is still more
common
Maxillary sinus most commonly affected
Must rule out fungal causes (mucormycosis) in immunocompromised hosts (especially if
painless, bloodless mucosa on examination)
Organisms:
- Viral (most common): rhinovirus, influenza, parainfluenza
- Bacterial: S. pneumoniae (35%), H. influenzae (35%), M. catarrhalis, anaerobes
(dental)
Clinical features:
Sudden onset:
Nasal blockage/ congestion and/or
Nasal discharge/ posterior nasal drip
facial pain or pressure, hyposmia
Signs more suggestive of a bacterial etiology are erythematous nasal mucosa,
mucopurulent discharge, pus originating from the middle meatus and the presence of
nasal polyps of a deviated septum
Acute viral rhinosinusitis lasts < 10 days. If symptoms increase after 5 days or last longer
than 10 days, consider a bacterial etiology.
Management:
Anterior rhinoscopy
x-ray/ CT scan not recommended unless complications are suspected (i.e. sub-periorbital
abscess or intracranial) spread Pitt's Puffy tumor.
Symptoms improving within 5 days: symptomatic relief "such as decongestant" and
expectant management.
Moderate symptoms that worsen or persist beyond 5 days: institute an intranasal
corticosteroid spray and continue for 14 days if symptomatic relief is noted within 48
hours.
Severe symptoms that worsen or persist beyond 5 days and refractory to intranasal
corticosteroid (INCS): Augmentin (Drug of choice) or clarithromycin therapy INCS
referral to a specialist or if there is a late complication.
Surgery if medical therapy fails:
1. FESS: Opening of the entire osteomeatal complex in order to facilitate drainage
while sparing the sinus mucosa.

67
2. Antral washout: Irrigation of the maxillary sinus through its natural ostium or
through a puncture of the inferior meatus (but 1 cm distance is maintained to avoid
causing injury to the nasolacrimal duct which opens into the inferior meatus and
consequently leading to nasolacrimal duct stenosis causing excessive tearing
"epiphora").
Complications:
Consider hospitalization if any of the following are suspected:
1. Orbital (Chandler's classification)
a. Periorbital cellulitis
b. Orbital cellulitis
c. Subperiosteal abscess
d. Orbital abscess
e. Cavernous sinus thrombosis (The most important sign is pulsating proptosis)
2. Intracranial
a. Meningitis
b. Abscess
3. Bony
a. Subperiosteal frontal bone abscess (Pott's Puffy tumor)
b. Osteomyelitis
4. Neurologic
a. Superior orbital fissure syndrome (CN III/IV/VI palsy, immobile globe,
dilated pupils, ptosis, V1 hypoesthesia)
b. Orbital apex syndrome (as "a" above plus neuritis, papilledema, decreased
acuity)
Potts puffy tumors
Characterized by an osteomyelitis of the frontal bone with frontal

breakthrough.
This results in a swelling on the forehead.
The infection can also spread inwards, leading to an intracranial
abscess.
Although it can affect all ages, it is mostly found among teenagers and
adolescents.

68
Chronic sinusitis
Definition:
Inflammation of the paranasal sinuses lasting > 3 months.
Etiology:
Can result from any of the following:

- Inadequate treatment of acute sinusitis
- Untreated nasal allergy
- Allergic fungal rhinosinusitis
- Anatomic abnormality e.g. deviated septum (predisposing factor)
- Underlying dental disease
- Ciliary disorder e.g. cystic fibrosis, Kartagener's
- Chronic inflammatory disorder e.g. wegener's
Organisms:
- Bacterial: S. pneumonia, H. influenza, M. catarrhalis, S.pyogenes, S.aureus, anaerobes
- Fungal: Aspergillus
Clinical features: (similar to acute, but less sever)
Chronic nasal obstruction

Purulent nasal discharge
Pain over sinus or headache
Halitosis
Yellow-brown post-nasal discharge
Chronic cough
Maxillary dental pain
Sinobronchial syndrome:
Post nasal drip in chronic sinusitis
causing lower respiratory tract
symptoms such as chronic cough
** Allergic fungal rhinosinusitis is a chronic sinusitis affecting mostly young, immunocompetent,

atopic individuals. Treatment options include FESS intranasal topical steroids, antifungals and
immunotherapy.
Diagnosis:
Cultures of the nasal mucosa in not useful.

Sinus aspirate culture is the most accurate diagnostic method but is not practical or
necessary.
Transillumination: show evidence of fluid, difficult to perform in children and is not reliable.
Conventional Radiographs, 4 views:
1. Water's view (Occipitomental view): "with opened mouth" Shows maxillary sinuses,
frontal sinuses, anterior ethmoidal sinuses & via the mouth, the sphenoidal sinuses. Best
for maxillary sinuses.
2. Caldwel view (Occipitofrontal view): Shows frontal, maxillary & anterior ethmoidal
sinuses. Best for frontal sinuses.
3. Lateral soft tissue view: Shows adenoids, sphenoidal sinuses & sella turcica.

69
Lateral soft tissue view of the neck and upper thoracic region is ordered if there is suspicion
of foreign body.
4. Submentovertical view (bucket-handle): Shows ethmoidal sinuses.
Signs of sinusitis on X ray:

1. Air-fluid level
2. Sinus opacity or clouding
3. Mucosal thickening, but it is not specific for sinusitis, it may occur in simple rhinitis.
CT:
The gold standard for sinuses.
MRI
Treatment:
Antibiotics for 3 to 6 weeks for infectious etiology

Augmentin (40-50 mg/kg/day), amoxicillin is the best in children (80-90 mg/kg/day),
macrolide (clarithromycin), fluoroquinolone (levofloxacin), clindamycin, Flagyl TM
Topical nasal steroid, saline therapy
Surgery if medical therapy fails or fungal sinusitis
Removal of all diseased soft tissue and bone, post-op drainage and obliteration of
pre-existing sinus cavity
FESS
Complications:
1. Polyps
2. Mucocele (frontal and ethmoid)

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The oral cavity & Pharynx

1. The oral cavity:
Anatomy:
The oral cavity is bounded anteriorly by the lips, posteriorly by the anterior faucial archs, inferiorly
by the floor of the mouth, and superiorly by the hard and soft palates.
It is divided into 2 parts:
1. Vestibule:
- Between the lips and teeth, contains:
a. The stensen's duct(parotid gland duct) opposite to the second upper molar
tooth.
b. The alveolar precesses.
2. Oral cavity proper:
- Contains:
a. The tongue.
b. Wharton's ducts of submandibular glands.
c. Draining ducts of the sublingual gland:8-20 excretory ducts called the ducts of
Rivinus and the largest duct is the sublingual duct (of Bartholin) which joins the
submandibular duct to drain through the sublingual caruncles located on both
sides of lingual frenulum.
** The epithelial lining of the oral cavity consists of nonkeratinzed stratified squamous epithelium
with subepithelial collections of minor salivary glands.
2. The pharynx:
Anatomy:
It is long muscular tube about 12cm in length, extends
from base of the skull down to level of cervical spine C7. It
is lined with mucosa and is divided into three parts:
1. Nasopharynx: extends from the base of skull down to
the level of soft palate. Anteriorly open in the nose,
inferiorly open in the oropharynx, laterally the
Eustachian tube open on either side. It contains the
pharyngeal tonsil (adenoid). The epithelial lining is
respiratory ciliated and stratified squamous
epithelium, with transitional epithelium area.
2. Oropharynx: extends from the level of soft palate
down to the upper edge of the epiglottis. It is
continuous with the oral cavity through the faucial
isthmus. Its posterior wall is in front the second and
third cervical vertebrae, the lateral wall containing
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the palatine tonsils which are lodged in the tonsillar fossa. The tonsillar fossa lies between
two (anterior & posterior)pillars. The anterior pillar is formed by the palatoglossus muscle
and the posterior pillar is formed by the palatopharyngeus muscle. The epithelial lining
consists of nonkeratinized stratified squamous epithelium.
3. Hypopharynx or laryngopharynx: extends from the upper edge of the epiglottis superiorly to
the lower edge of cricoid cartilage. It opens anteriorly into the larynx and inferiorly it is
continues with esophagus. The epithelial lining consist of nonkeratinized stratified squamus
epithelium.
What is the waldeyer's ring?

-
Palatine tonsils
Pharyngeal tonsil (adenoid)
Lingual tonsil
Tubal tonsils
Subepithelial lymphoid tissue
what is the difference between the adenoids and the palatine tonsils?
Palatine tonsils
Adenoid
Name
Palatine tonsils
Pharyngeal tonsil
Position
Oropharynx
Nasopharynx
Number
Persistence
Remain for life long.
After the age of 10-12 years,

they atrophy.
Capsule
Covered with capsule, so no
Not covered by capsule, there
risk of recurrence post removal
is a risk of recurrence post

removal.

72
Clinical aspects of diseases of the oral cavity and pharynx:
Pain on eating, chewing or swallowing.

Dysphagia.
Globus symptoms.
Burning of the tongue.
Blood in the sputum.
Catarrh.
Oral fetor.
Disorder of salivary secretion.
Disorders of taste.
Respiratory obstruction.
Disorders of speech.
Swellings of the neck, floor of mouth and of the lymph nodes at the angle of jaw and below
the mandible.
Examination:
Palpation: of lips, dental arches, floor of the mouth for swellings ,submandibular area,
submental, TMJs
Inspection: by using tongue depressor, mirror, flexible rigid endoscopy
Look for:
The color, symmetrical mobility of the lips, skin of the lips, mucosa of lips and mouth
vestibule.
The arrangement of the teeth, occlusion, dental caries, temporomandibular joint
mobility.
The shape and mobility of the tongue, the upper surface and inferior surface.
Mucosa of mouth, cheeks are examined for sensation, ulceration, dryness, tumors.
The condition of hard and soft palate; smooth mucosa, mobility of soft palate,
swellings, ulcers.
Examine the parotid duct in the cheek opposite the upper second molar tooth and
the opening of submandibular gland in the floor of the mouth on either side of
frenulum.
Examine the palatine tonsils:- size, crypts, cysts, ulcers or tumor.
Investigations:
Radiography:
Lateral view of the skull: for nasopharynx.

Panorama of jaws: for dental cyst.
Lateral soft tissue view of the neck and upper thoracic region: for hypopharynx, adenoids
and cervical esophagus to show foreign bodies.
Contrast medium: to show pharyngeal pouch, stenosis and swallowing disorders.
CT-SCAN: for skull base larynx.
Carotid angiography: for the highly vascular tumors and in cases of bleeding for possible
embolization of external carotid branches.

73
Microbiology:
Culture for bacteriologic, Mycological and virology examination.
Biopsy:
From any swelling which is not acutely inflamed or suspected highly Vascular.
Diseases of the oral cavity and pharynx:

Oral manifestations of systemic disease:
i.
Gastroenterological diseases
1. Celiac disease
1) Aphthous ulcer like lesion
2) Enamel defects
2. Crohns disease
1) Orofacial Granulomatosis (cheilitis granulomatous )

74
2) cobblestone appearance of the buccal mucosa
3) Irregular superficial ulcers on ventral surface of tongue
4) Aphthous Stomatitis
3. Ulcerative colitis:
1) pyostomatitis vegetans - the most common
Aphthous ulcers are divided into:

2) major or minor aphthae
3) pyoderma gangrenosum on tongue

1. Minor : < 1 cm
2. Major: > 1cm
3. Herpitiform
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4. Chronic liver disease
1) Petechia
2) Jaundice
** GERD:
5. GERD
1) Erosion of the enamel
6. Polyposis disease
Gardner syndrome:
1) Osteoma in the maxilla
Clinical manifestations:
Laryngeopharengeal reflux
Continuous throat clearance
Night cough
Morning hoarsness of voice
Postprandial heart burn
Globus sensation
Chronic laryngitis = reinke's edema
Leukoplakia, which have 20-25% risk
of malignancy transformation.
Diagnosis:
Best diagnostic test is pH metry, in
which a pH meter is introduced 5 cm
above the LES, a pH < 4.1 confirms
the diagnosis.
Flexible pharyngolaryngoscopy:
shows hyperemia & congestion of
the upper surface of the larynx,
hyperemia & edema of the
erytenoid, hyperemia of the upper
surface of the vocal cords;
vestibules; ventricles & laryngeal
surface of the epiglottis.
Treatment:
Anti-reflux therapy: PPI for 3 months
"at least".
2) Supernumerary teeth
3) Multiple odontomas
4) Impacted teeth

76
Petuz-jeghers-syndrome:
1) Perioral pigmented lesions
ii.
Hematological diseases
1. Anemia
Iron deficiency anemia
1) Angular cheilitis
** D.D of angular cheilitis
Anemias
Fungal infection (candida)
Vitamin B2 (Riboflavin)deficiency
2) Atrophic glossitis: smooth and red tongue (may result in burning sensation, taste
loss)
Pernicious anemia
1) Red and smooth dorsum of the tongue with areas of ulcerations

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Sickle cell anemia
1) Mandibular salmonella osteomyelitis
2) Pulpal necrosis (center of tooth)
3) Dentofacial deformities radiographically usually asymptomatic

2. Leukemia
1) Ulcerations
2) Gingival enlargement and spontaneous gingival hemorrhage
3) Tooth loosening
4) Delayed wound healing
5) Candidiasis and herpetic infections are relatively common oral complications of
leukemia.

78
3. Lymphoma
1) Nodular non-Hodgkin's lymphoma in a patient with AIDS
4. Langerhans cell histiocytosis

1) Radiologic findings demonstrate characteristic "floating teeth".
2) Letterer siwe form : large ulcerations , Ecchymosis ,gingivitis , Periodontitis , And
subsequent tooth loss.
3) Hand-schuller christian form: irregular ulcerations of the the hard palate , which
may be the primary manifestation of the disease , gingival hyperplasia , difficulty in
chewing , and foul-smelling breath may also occur.
iii.
Endocrine diseases
1. DM
1) Periodontal disease (occurs more frequently and progress rapidly than in normal
patients).
2) diabetic sialadenosis (diffuse bilateral enlargement).
3) oral candidiasis
4) migratory glossitis
5) xerostomia
2. Hypothyroidism
1) Thickenning of the lips (accumulation of glyosaminoglycans.
2) Macroglossia (accumulation of glyosaminoglycans.
3) Failing of teeth eruption (childhood).
3. Addison's disease
1) Diffuse or patchy brown macular pigmentation of the oral mucosa caused by excess
melanin ( oral melanosis ).

79
4. Acromegaly
1) Enlargement of facial soft tissues (coarse facial appearence)
2) Mandibular prognathism as a result of the increased growth of the mandible
(spacing of the teeth)
3) Macroglossia
iv.
Metabolic diseases
1. Amyloidosis
1) Macroglossia (12 -40 % of patients and may appear as diffuse or nodular
enlargement of the tongue).
2) Amyloid nodules of the oral mucosa or of the lips (sometimes associated with
ulceration and submucosal hemorrhage).
** Biopsy of gingival tissue or labial salivary gland is alternative specimen sources for
diagnosis of amyloidosis.
v.
Connective tissue & rheumatologic diseases

1. Rheumatoid arthritis
1) TMJ arthritis
2) Cricothyroid & cricoarytenoid subluxation
2. Behcets disease
1) Recurrent oral ulcers
3. Sjogren syndrome
1) Pached appearance of the mouth and oral mucosa due to profound dryness.

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2) Dryness of the mouth and inadequate saliva formation result in a tendency to
dental caries.
3) Parotid enlargement
4. Kawasaki disease
1) Erythema or fissuring of the lips
2) Strawberry tongue- pathognomonic for kawasaki disease.
3) Diffuse injection of oral and pharyngeal mucosa

5. Pulmonary
Wegener's granulomatosis
1) Strawberry gingivitis: gingivae take on a characteristic swollen, reddened, and
granular appearance.
Sarcoidosis
1) Multipe, nodular , painless ulcerations of the gingiva , buccal mucosa , labial mucosa,
and palate .
** Biposy reveal noncaseating granuloma surrounded by multinucleate giant cells
along with lymphocytic infiltrate.
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2) Rarely sarcoidosis may involve the tongue with swelling ,and enlargement.
vi.
Mucocutaneous diseases
1. Lichen planus
1) Reticular: fine, lacy appearance on buccal mucosa (Wickams striae).
2) Hypertrophic: resembles leukoplakia
3) Atrophic or erosive: painful

2. Psoriasis
1) Geographic tongue.
2) Fissured tongue.
vii.
HIV
1) Candidiasis (90% of pts, first presenting).
** HIV infection should be considered with repeated oral candidiasis in absence of
other risk factors.
2) Herpes simplex: more aggressive, prolonged, and diffuse

** Any oral ulcers should be evaluated for HSV in HIV patient.

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3) Hairy leukoplakia (white plaques commonly on the lateral portions of the tongue.
4) Kaposi sarcoma (KS): most common malignancy in HIV patients. Purple, red patches
or papules on the hard palate, mucosa, and gingiva.
5) aphthous like ulceration etc

83
Apnea
Definition
RDI(Respiratory Disturbance Index): is used in reporting polysomnography (sleed study)findings,
according to the number of apnea episodes( cessation of breathing >10 seconds for each) in a
period of 7 hours sleep.
-
If <10 episodes: mild apnea
10-30 episodes: moderate apnea
>30 episodes: severe apnea
So, definition of severe apnea: more than 30 episodes of apnea each more than 10
seconds in a period of 7 hour sleep.
Types of apnea
1) Central
2) Peripheral or obstructive: any obstruction above the vocal cords.
Causes of apnea
** The most common cause in children is adenotonsillar hypertrophy, while in adults is obesity.
Causes of obstruction according to site:
Nose:
1. Any type of rhinitis
2. Foreign body (rhinolith)
3. Nasal polyposis
4. Tumors
Nasopharynx:
1. Adenoid hypertrophy
2. Foreign body
3. Tumors, such as angiofibroma: characteristically found in males and never in
females, if you found this tumor in a female do karyotyping!
Oropharynx:
1. Tonsilllar hypertrophy
2. Foreign body
3. Enlarged tongue, retrognathia or micrognathia, in syndromes such as down
syndrome, Treacher-Collins syndrome.
4. Tumors
Hypopharynx:
1. Tumors
2. Webs

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Adenoid face:
Due to adenoid hypertrophy
Characteristics
-
Mouth breather
Snoring
Obstructive sleep apnea
High arch palate (V-shaped palate)
Protruded mandible (Prognathia)
Recurrent chest infections

85
Tonsillitis
Definition
-
Tonsillitis is an infection and swelling of the tonsils.

The tonsils are lymph nodes, located on both sides of the throat
that are part of the body immune system.
Q: which muscle is present in the

bed of the tonsils?
A: Superior constrictor muscle.
Tonsil function
Prevent infections in two ways:
1. They act like filters to trap bacteria, viruses, and other materials that enter the body through
the mouth and sinuses.
2. They also produce antibodies to help fight off infections.
Types
1. Acute tonsillitis (< 1 month) can either be bacterial or viral in origin
2. Subacute tonsillitis (1-3 months) is caused by the bacterium Actinomyces
3. Chronic tonsillitis (> 3 months), which can last for long periods if not treated, is mostly
caused by bacterial infection.
Prevalence
-
Acute tonsillitis can occur at any age but is most frequent in children under 9 years.
Spread is by droplet infection.
In infants under 3 years of age with acute tonsillitis, 15% of cases were found to be
streptococcal; the remainder were probably viral. In older children, up to 50% of cases are
due to streptococcus pyogenes.
It is commonest in winter and spring.
Etiology
1. Group A streptococcal bacteria resulting in strep throat.
2. Viral tonsillitis such as the Epstein-Barr virus (the cause of infectious mononucleosis )or the
Adenovirus.
3. Sometimes ,tonsillitis is caused by a superinfection of spirochaeta and treponema, in this
case called Vincent's angina or Plaut-Vincent angina.
Clinical features
Symptoms:
1. Severe sore throat (which may be experienced as referred pain to the ears)
2. Painful/difficult swallowing
3. Headache, fever and chills.
Signs:
1. Red, swollen tonsils which may have a purulent exudative coating of white patches )i.e. pus).
2. Enlarged and tender neck cervical lymph nodes.

86
Grading of tonsil hypertrophy:
Grade 0: Tonsils are entirely within the tonsillar fossa.
Grade 1+: Tonsils occupy less than 25 percent of the lateral dimension of the oropharynx as
measured between the anterior tonsillar pillars.
Grade 2+: Tonsils occupy less than 50 percent of the lateral dimension of the oropharynx.
Grade 3+: Tonsils occupy less than 75 percent of the lateral dimension of the oropharynx.
Grade 4+: Tonsils occupy 75 percent or more of the lateral dimension of the oropharynx
(kissing tonsils).
Investigations
-
Inflammatory parameters: The CBC shows leukocytosis, and

(ESR) and (CRP) are elevated.
Bacteriologic testing: A bacterial culture is rarely taken from
throat smears because it usually takes 23 days to obtain a
definitive result, by which time treatment should already be
initiated. It is better to perform a rapid immunoassay, which
can identify the causative organism as a group A streptococcus in just 10 minutes.
Differential Diagnosis
-
Infectious mononucleosis: Caused by EBV, called glandular fever. Presents with

splenomegaly, severe membranous tonsillitis.
Scarlet fever
Diphtheria
Agranulocytosis
HIV

87
Treatment
-
Restthe patient will usually prefer to be in bed.

Soluble aspirin or paracetamol held in the mouth and then swallowed eases the discomfort.
Remember that aspirin should not be given to children under the age of 12 years because of
the risk of Reyes syndrome.
Encourage the patient to drink
Antibiotics in severe cases. Penicillin by injection followed by oral treatment remains the
treatment of choice.
It is recommended that treatment be continued for 10 days to reduce the risk of
reactivation.
Macrolides or oral cephalosporins can be used in patients allergic to penicillin.
Complications of tonsillitis
-
Acute otitis media (the most common complication).

Peritonsillar abscess (quinsy).
Pulmonary infections (pneumonia, etc.).
Acute nephritis IgA nephropathy.
Acute rheumatism.
Hypertrophy of the tonsils can result in snoring, mouth breathing, disturbed sleep, and
obstructive sleep apnea .
Indications for tonsillectomy

Absolute indications:
-
Severe apnea
Suspected malignancy for biopsy
Relative indications:
-
Recurrent tonsillitis : > 6 times yearly, 5 times in 2 consecutive years or 3 times in 3

consecutive years.
Mild and moderate obstructive sleep apnea.
2nd attack of peritonsillar abscess (Quinsy).
2nd attack of febrile convulsions due to acute otitis media.
Chronic tonsillitis:
1. Asymmetric tonsils. However, symptomatic tonsils regardless of being
symmetric or asymmetric are also considered an indication for tonsillectomy.
2. Cryptic tonsils( each tonsil contains 11-17 crypti, when they become more wide
and more deep, the tonsils are called cryptic)
3. Tonsillolith
4. Intratonsillar pussy cyst
5.
Jugulodigastric LAP
6. Congested anterior pillar (dilated vessels)

-
Complicated tonsillitis: Rheumatic fever,glomerulonephritis.

88
As part of some surgery, such as UPPP(uvulopalatopharyngoplasty)
Recurrent otitis media
Contraindications for tonsillectomy(all are relative)

-
Patient's medical condition
Acute tonsillitis
Coagulopathy
Obesity
Methods of tonsillectomy
-
Dissecting
Ligation
Blood supply to the pharynx(the vessels that are ligated):
The dorsal branches of the lingual artery, a branch of the external carotid artery.
The tonsillar and the ascending palatine arteries, which are branches of the
facial artery, a branch of the external carotid artery.
The ascending pharyngeal artery, a branch of the external carotid artery.
The descending palatine artery, a branch of the third portion of the maxillary
artery which is one of the terminal branches of the external carotid artery.
** The facial and the ascending pharyngeal arteries are ligated together, the dorsal
lingual artery is ligated by one clip and the descending palatine artery is ligated by a
third clip.
-
CO2 laser tonsillectomy
Coblation: US+ co2 laser
Galotine method(by a snare)
Complications of tonsillectomy
-
Bleeding:
1. Primary: within 24 hours after surgery, either bad surgeon or bad patient.
2. Reactionary: within 1-5 days
3. Secondary: after the 5th day till day 14, usually because of infection.
Velo pharyngeal insufficiency:

Because of injury to the posterior pillar(palatopharyngeus muscle), this will result in
nasal tone speech:
Rhinolalia aperta
Rhinolalia calusa

89
Drooling
Definition
Drooling is the salivary incontinence or the spillage of saliva over the lower lip, it reflects inefficient;
uncoordinated swallowing and poorly synchronized lip closure. It is also known as ptyalism in
pregnancy.
Silaorrhea: an increase in salivary flow which can lead to drooling.
Functions of the saliva
1.
2.
3.
4.
5.
Moistening of food bolus

Prevention of dental caries
Protection of mucosa from desiccation
Medium for lysozyme, secretory IgA, salivary peroxidase
Digestion by emulgation of food and enzymatic cleavage of starch by -amylase.
Salivary glands
They are divided into:
- Minor salivary glands: 1% of daily salivary flow.
- Major salivary glands:
1. parotid glands: 25% of daily salivary flow, serous.
2. Submandibular gland: 70% of daily salivary flow, mixed serous and mucinous.
3. Sublingual gland: 5% of daily flow, mucinous.
4. Minor salivary glands 1%.
** The most salivary glands to secrete saliva (saliva flow) is submandibular glands.
** The most salivary glands to secrete salive in response to stimulus is parotid glands, which are
supplied by glossopharengeal nerve.
** Salivary glands are controlled by the autonomic nervous system, primarily, the parasympathetic
nervous system.
Parotid gland
Innervated by parasympathetic fibers
originating in the inferior salivary
nucleus in medulla CN IX
(Glossopharyngeal nerve) Petrosal
ganglion Lesser superficial petrosal
nerve Otic ganglion
Auricotemporal nerve
Submandibular & sublingual glands
Innervated by Preganglionic PS fibers
originating in the superior salivary
nucleus in medulla Nervus
intermedius CN VII (Facial nerve)
Chorda tympani Lingual nerve
Submandibular ganglion.

91
Etiology of drooling
-
Acute:
o Epiglottitis causef by H.ifnleunzae.
o Neoplasm.
o Peritonsillar abscess.
Chronic:
o Neurological: CP, strokes, perkinosons disease.
o Medication effect: tranquilizers, anti convulsants, anti cholynesterase.
o Indirect: nasal obstruction, malocclusion, large tongue,emotional state, adenoid
hypertrophy.
History
-
Estimated quantity of saliva, use of bibs, clothing changes.

Nasal obstruction secondary to adenoid hypertrophy, rhinitis, sinusitis, nasal deformities
Extent of underlying neurologic disease
Hearing loss may be tumor in the middle ear affecting chorda tympani
-
Head posture.
Sores on lips or chin.
Dental problems.
Tongue control.
Swallowing control.
Consider: audiogram, barium swallow, modified barium swallow "using video
esophagoscopy".
The severity of drooling can be classified with the following scale:

- Dry - Never drools
- Mild - Only lips wet
- Moderate - Lips and chin wet
- Severe - Clothing soiled
- Profuse - Clothing, hands, and tray moist and wet
The frequency of drooling can be quantitated based on the following scale:
- Never drools
- Occasional drooling - Not every day
- Frequent drooling - Every day
- Constant drooling
Measurement of Drooling
Thomas-Stonell & Greenberg
- Grade 1 Dry, no drooling
- Grade 2 Mild: humid lips only
- Grade 3 Moderate: humid lips and chin
- Grade 4 Severe: clothing begins to be affected
- Grade 5: - Profuse: clothes, hands & objects wet

90
Treatment options
1. Speech therapy:
- Goals: improve jaw stability and closure, increase tongue mobility and strength, improve
lip closure, decrease nasal regurgitation.
- Usually disappointing results unless started in infancy.
- Severely retarded patients and those who drool profusely get little benefit.
2. Behavioral therapy:
- Incorporates cuing, positive and negative reinforcement, overcorrection.
- Can be fairly successful in patients with adequate intelligence.
- Regression is common.
3. Radiation therapy:
- Has been used to control drooling in patients with amyotrophic lateral sclerosis with
success.
- Decrease drooling with few side effects in this terminally ill population.
4. Medications:
- Glycopyrrolate: 70-90% response rates; 30-35% will discontinue medication due to side
effects (excessive dry mouth, constipation, urinary retention, decreased sweating,
irritability).
- Trihexyphenidyl: efficacy and side effects similar to glycopyrrolate; may be useful in
dystonic CP due to tone reduction.
- Scopolamine patch can also be used and has the advantage of only needing to be
changed every three days.
5. Botulinum Toxin:
- Several recent small series report success with intraglandular injection of botulinum
toxin.
6. Surgery:
- Duct rerouting procedures:
- Parotid Duct Relocation: parotid duct relocation to tonsillare fossa produced
unsatisfactory results. Submandibular gland excision was added with success,
however, there was 35% complication rate, including: cysts, parotid duct
stenosis, fistulas, wound dehiscince, parotid swelling, suppurative parotitis,
xerostomia, increase dental & gingival infection.
-
Submandibular Duct Relocation: Submandibular duct relocation was performed

with good results, however, complicated by ranula and lateral neck cysts.
Addition of sublingual gland excision yielded good results with no ranula
formation. This is the best treatment.
Excision of salivary glands.
Ligation of salivary gland ducts

- Parotid duct ligation is technically easy with few complications, however
associated with 50% re-fistulization rate.
- Submandibular duct ligation is not advised as saliva constituents (viscous,
alkaline, high Ca+2, phosphate) are more prone to form stones especially as the
route of the duct is uphill.

92
-
Combinations of all the above.
Transtympanic Neurectomy
- 80% success rate.
- Lift tympanomeatal flap, locate and divide chorda tympani which supplies the
submandibular & sublingual salivary glands.
- Few complications.
Laser photocoagulation of parotid gland ducts

- Showed improvement in drooling.
- Few complications.
Conclusion
-
Noninvasive modalities should be attempted first.

A trial of medication is warranted if noninvasive methods fail.
Surgery is a final option for those patients with severe drooling problems not adequately
addressed by noninvasive means or medication.

93
Congenital diseases
Cleft lip and palate
-
Cleft lip and palate is the most common congenital malformation involving the head and
neck, and it presents long-term multidisciplinary management problems.
Cleft lip and palate occurs in 1 in 1,000 births; cleft palate alone occurs in 1 in 2,000 births.
There are both syndromic and nonsyndromic clefts.
Lip and palate embryologic development occurs in two phases, the first beginning at 4 to 5
weeks (lip, nose, premaxilla) and the second at 8 to 9 weeks (secondary palate).
Cleft lip:
Due to abnormal development of the medial nasal and maxillary processes at the time that they
bulge downwards in front of and below the nasal pit and when their surfaces should touch, the
epithelium over them fuse and then break down.
Cleft palate:
Due to failure of fusion of the two palatine processes or ,in the case of soft palate due to a merging
process to carry the union backwards from the site of initial fusion.
Cleft classification:
Clefts of the lip alone
Either right or left-unilateral or bilateral, complete (with extension into the nasal floor) or incomplete
(anything from a slight muscle diastasis with intact epidermis to a small bridge of tissue connecting
the medial and lateral lip elements or Simonarts band).
Example:
1.
2.
3.
4.
5.
6.
7.
8.
Left complete cleft lip.

Right complete cleft lip.
Bilateral complete cleft lip.
Left incomplete cleft lip.
Right incomplete cleft lip.
Bilateral incomplete cleft lip.
Left complete & right incomplete cleft lip.
Right complete & left incomplete cleft lip.
Clefts of the palate

Palatal clefts also may be:
1. Unilateral (the palatal process of one side is fused with the septum, resulting in
communication of the oral and nasal cavities on one side only) or bilateral (no connection
between either palatal process and the septum).
2. Primary (anterior to incisive canal) and secondary (posterior to incisive canal including also
bifid uvula, midline diastasis of the levator muscles, and loss of the posterior nasal spine or
notching).

94
3. Complete cleft palate refers to a cleft of both the primary and secondary palates and is
nearly always associated with a cleft lip.
4. Incomplete cleft palate is synonymous with a cleft of the secondary palate or may be used to
describe a palatal cleft with an area of intact mucosa associated with a cleft lip.
Prevalence of cleft types in the cleft population:
-
Clefts of the lip, alveolus, and palate, about 45%.

Clefts of the lip only, or lip and alveolus, about 25%.
Clefts of the secondary palate, about 30%.
Cleft lip occurs in males > females.
Cleft palate occurs in females > males.
Common syndromes with facial clefts:

-
Aperts syndrome.
Ectodermal dysplasia syndrome.
Orofacial-digital I syndrome.
Orofacial-digital II syndrome.
Sticklers syndrome.
Treacher Collins syndrome.
Van der Woudes syndrome.
Waardenburgs syndrome.
Pieree Robin sequence: Retrognathia/ micognathia, glossoptosis (posterior displacement of
the tongue), upper airway obstruction, cleft palate.
Cleft lip & palate are associated with:

-
Nasal deformity.
Disturbance of facial growth.
Otitis media with hearing loss. Otitis media occurs due to Eustachian tube dysfunction
(previously mentioned!).
Cleft lip repair:

The rule of tens of lip repair is performed when the infant is at least 10 weeks old, weighs 10
pounds, and has a hemoglobin of 10 g.
Cleft palate repair:
Cleft palate repair often is performed at 10 to 12 months of age when a lip repair has been
performed earlier.
In many cases, further therapeutic intervention will be required that may include surgical correction
of secondary lip and nasal deformities, dental and orthodontic care, speech therapy (and possible
correction of velopharyngeal incompetence), otologic and audiologic care, and orthognathic surgery.

95
The larynx
Larynx anatomy
The skeleton
-
The larynx extends from the

root of the tongue to the
trachea. It is an organ of
phonation and breathing.
It is situated from the level of
C3-C6 or C7.
In pediatric age group, it
extends from C1-C4, and that
explains why they are obligate
nasal breathers as the epiglottis
is high in location and makes a
sort of obstruction to the air
entering from the mouth.
Anteriorly it is covered by the
skin, the fascia, and the
infrahyoid muscles.
The thyroid gland is attached to
and covers the side of the larynx
from the cricoid cartilage to the
level of the oblique line of the
thyroid cartilage.
Hyoid bone:
-
Not strictly considered part of the larynx, but as a

point of attachment for muscles and ligaments it is
essential for laryngeal functions.
It is intimately attached to the larynx by the
thyrohyoid and the thyroepiglottic ligaments and
the extrinsic muscles of the larynx.
Thyroid cartilage:
This is the largest cartilage of the larynx

composed of two flat wings, the laminas (alas)
& two posterior processes; horns or cornu
(two greater cornu & two lesser cornu).
The lower 2/3's of the flattened laminas are
fused anteriorly in the midline forming an

96
angle of 90 degrees in the male (forming the Adam's apple) and 120 degrees in the female.
The upper 1/3's of the laminas are not fused and form the thyroid notch.
Cricoid cartilage:
This cartilage is shaped like a signet ring, the narrow part of ring
faces anteriorly (the cricoid arch) while the broad signet part faces
posteriorly (cricoid lamina). It is the only complete cartilagenous
ring in the upper airway.
Epiglottis:
-
This leaf shaped cartilage is composed mainly of elastic cartilage (unlike

the remaining laryngeal cartilages, most of which are hyaline) and thus it
is very flexible.
** All cartilages of the larynx are hyaline

cartilage except the epiglottis which is
elastic cartilage.
** Laryngomalacia which is the most
common cause of stridor in children
occurs most commonly in the epiglottis
because of its hyaline cartilage.
Artenoid, Cuneiform,
Corniculate:

97
-
Artenoid cartilage: Two pyramidal-shaped structures which sit on the lateral part of the superior
border of the lamina of the cricoid cartilage(the cricoarytenoid joints).
Cuneiform cartilage: Small, paired, nodular structures found in the posterior part of the
aryepiglottic folds. They articulate with the summit of the arytenoid cartilages.
Corniculate cartilage: Small, paired, rodlike structures embedded in the margin of the
aryepiglottic folds. They are found superio-anteriorly to the corniculate cartilages.
** That's how they look all together:

98
The joints
** The cricoid cartilage may be regarded as the base and support for the entire larynx. It articulates
with the thyroid cartilage via the cricothyroid joints and with the arytenoids via the cricoarytenoid
joints. Both of these are true synovial joints (so any disease that affect the synovial joints will affect
these joints as well. This explains why RA patients may present with hoarseness of voice, stridor or
difficulty breathing).
Cricothyroid Joint:
-
Location : Located between the facet on the

posterolateral sides of the cricoid cartilage and the
facet on the medial surface of the inferior cornua of
the thyroid cartilage.
Movement : It permits the thyroid cartilage to rotate

anteriorly or posteriorly on the cricoid cartilage. When
the thyroid cartilage is rotated anteriorly, the anterior
arch of the cricoid will come in closer proximity to the
lower border of the thyroid cartilage.
Cricoarytenoid joint:
-
Location : It is the articulation point between the inferior

surface of the arytenoid cartilages and the posterosuperior surface of the cricoid lamina.
Movements : This joint permits 2 types of movements:

1. Rotation of the arytenoid around an axis that runs obliquely from the dorsomediocranial to
the ventrolaterocaudal position, permitting movement of the vocal process medially or
laterally. The rotation in which the anterior vocal process deviates medially causes adduction
of the vocal folds, whereas a lateral rotation causes abduction.
2. Medial and lateral sliding of the arytenoid
- Medial sliding causes adduction of the vocal folds, whereas lateral sliding causes
abduction.
- The cricoarytenoid joints are bilateral (work in unison) but operate independent of one
another.

99
Ligaments and Membranes:

** The laryngeal membranes and ligaments can be divided into two
subgroups:
The extrinsic ligaments (containing the thyrohyoid

membrane, thyrohyoid ligaments, thyroepiglottic ligament,
hyoepiglottic ligament, cricothyroid ligament, and
cricotracheal ligament)
The intrinsic ligaments (containing the quadrangular
membrane, vestibular ligament, conus elasticus, and vocal
ligament).
The extrinsic ligaments:

Thyrohyoid Membrane:
-
Median thyrohyoid ligament, which is pierced on each

side by the superior laryngeal artery and vein and the
internal branch of the superior laryngeal nerve.
The tips of the superior horns of the thyroid cartilage are
connected to the greater cornua of the hyoid bone by
the lateral thyrohyoid ligaments, which are also
thickenings of the thyrohyoid membrane.
Cricothyroid Membrane:
-
This broad membrane is attached from the superior

border the cricoid to the inferior surface of the thyroid cartilage. It is pierced laterally on
each side by the external branch of the superior laryngeal nerve and recurrent laryngeal
nerve.
It is the site where emergency cricotomy or thyrotomy done.
Thyroepiglottic Ligament:
-
Attaches the anterior lower part of the epiglottis to the thyroid cartilage.
Hyoepiglottic Ligament:
-
Attaches the anterior upper part of the epiglottis to the hyoid bone.

011
Cricotracheal Ligament:
-
The inferior border of the cricoid cartilage is joined to the first ring of the trachea by this
ligament.
The intrinsic ligaments:

Quadrangular Membrane:
-
It extends from the lateral

margins of the epiglottis
within the aryepiglottic fold
and attaches to the
arytenoid and corniculate
cartilages. The inferior free
edge is thickened to form
the vestibular ligament
(false vocal cord). The
superior edge is also free
and it is covered with
aryepiglottic fold of mucosa.
* So, its:
- Upper edge:
Aryepiglottic fold
- Lower edge: Vestibular ligament (False vocal cord)
Conus Elasticus (Cricothyroid or the Cricovocal

Membrane):
-
This membrane arises from the inner surface of the cricoid

arch and it consists of two distinct parts:
The anterior or superficial part, also called the medial
cricothyroid ligament, extends from the upper border of the
cricoid cartilage to the lower border of the thyroid cartilage.
The lateral part of this membrane extends from the superior
inner border of the cricoid cartilage to the inner surface of
the thyroid angle and posteriorly to the tip of the vocal
process of the arytenoid cartilage. The superior edge of the this part of the conus elasticus is
free and thickened between its two attachments, the angle of the thyroid lamina and vocal
process of the arytenoid cartilage, and forms the vocal ligament (true vocal cord).
* So, its:
- Upper edge:
Vocal ligament (true vocal cords).
010
Lower edge:
Inner surface of cricoid.
** Between the vestibular

ligament (false vocal
cord)superiorly & the vocal
ligament (true vocal cord)
inferiorly is the ventricle.
** Between the tongue
superiorly and the epiglottis
inferiorly is the volecule.
Spaces:
The various membranes, ligaments and
skeletal structures of the larynx have been
shown to delineate several potential
spaces and compartments. The internal
cavity of the larynx is divided into:
Supraglottic space
(vestibule):
Superior border: free margin of the
epiglottis and aryepiglottic folds
Inferior border: lower margin of the
ventricular (false vocal folds).
Glottic space:
Superior border: ventricular folds (false
vocal cords).
Inferior border: vocal cords.
Subglottic space:
Superior border: vocal cords.
Inferior border: lower border of cricoids cartilage.

012
Nerve supply:
** The nerve supply to the larynx is derived from the motor nuclei in the medulla oblongata in the
brainstem. The vagus (cranial nerve X) is the main nerve innervating the larynx and it arises from the
nucleus ambiguus (branchiomeric nucleus) and the dorsal motor nucleus of vagus (autonomic,
parasympathetic nucleus). The vagus reaches the larynx via the internal and external branches of the
superior laryngeal nerve, as well as by the recurrent laryngeal nerve. It is important to note that the
innervation of the larynx is mainly from the parasympathetic nervous system, however, the
sympathetic fibers arising from the superior cervical ganglion also innervate the larynx.
** Superior laryngeal nerve: it is divided into 2 branches:
1. Internal branch: supplies sensation above the vocal cords.
2. External branch: supplies cricothyroid muscle, which cause tension of the vocal cords, and
constrictor muscle.
** Recurrent laryngeal nerve: supplies sensation below vocal cords & intrinsic muscles of the
larynx except the cricothyroid muscle.
Blood supply:
The arterial blood supply of the larynx is derived from the
laryngeal branches of superior and inferior thyroid
arteries and to a small extent from the cricothyroid. Most
of the arteries anastomose freely with each other.
** Superior thyroid artery is a branch of the external
carotid artery.
** Inferior thyroid artery is a branch of the thyrocervical
trunk which is a branch of the subclavian artery.
Venous drainage:
The venous drainage is supplied by the superior and
inferior laryngeal veins, which essentially follow the
arteries in their course (see arterial blood supply). The
superior drainage joins the superior and middle thyroid
veins and then the internal jugular. The inferior drainage
joins the middle thyroid vein and the inferior thyroid vein,
which empties into the superior vena cava.

013
Lymphatic drainage:
The larynx is very well supplied with lymphatics, with the
exception of the free margins of the vocal folds
themselves. The lymphatics of the larynx are divided into a
superior and an inferior group.
Superior group: The area of the larynx above the vocal
cords is drained into the superior (level II)and middle
jugular nodes (level III).
Inferior group: The area of the larynx below the vocal cords
is drained into the middle (level III) and inferior jugular
nodes (level IV) as well as to the paratracheal lymph
nodes.
Muscles:
** The laryngeal musculature can be divided into two groups:
A. The intrinsic muscles
B. The extrinsic muscles
The intrinsic muscles:

-
cricoarytenoid muscles
a. Lateral cricoarytenoid muscle
b. Posterior cricoarytenoid muscle
Interarytenoid muscles
a. Transverse arytenoid muscle
b. Oblique arytenoids muscle
Thyroarytenoid muscle
thyroepiglottic muscle
Cricothyroid muscle
** All the intrinsic muscles of the larynx are supplied by

the recurrent laryngeal nerve except the cricothyroid
muscle which is supplied by the external branch of the
superior laryngeal nerve.
** The most important intrinsic muscles are:
- Lateral cricoarytenoid muscle which causes adduction of vocal cords.
- Psterior cricoarytenoid muscle which causes abduction of vocal cords. It may be
considered the most important muscle in the human body to its function. It is also called
posticus muscle.
- Cricothyroid muscle which causes tension of vocal cords.

014
The extrinsic muscles:

** The extrinsic muscles, also called the strap muscles,
are capable of moving the larynx up or down during
deglutition, respiration and phonation.
** They are divided into 2 groups:
1. Suprahyoid muscles:
- Digastric muscle (anterior & posterior belly).
- Geniohyoid muscle.
- Mylohyoid muscle.
- Styhyoid muscle.
- Stylopharyngeus muscle.
- Thyrohyoid muscle.
2. Infrahyoid muscles:
- Omohyoid muscle.
- Sternohyoid muscle.
- Sternothyroid muscle.
- Thyrohyoid muscle.
** Stylopharyngeus muscle is the only muscle

innervated by the glossopharyngeal nerve.
Vocal Fold Microstructure

** There are 5 histologically discrete layers. These layers
vary in composition and mechanical properties.
** 5 histologic layers from most superficial to most deep
are:
Epithelium squamous epithelium.

Lamina propria (3 layers):
- Superficial layer composed of loose fibrous
matrix, composition described as soft gelatin. It
is known as reinke's space, and here occurs
reinke's edema in chronic laryngitis, e.g. in
GERD.
- Intermediate layer composed of elastic fibers
and has slightly more mass.
- Deep layer denser still, composed of
collagenous fibers.
Vocalis muscle- Main body of the vocal fold, it provides stability and mass.
** Tissues of 3rd & 4th layers together are known as the vocal ligament. The vocal ligament
develops throughout childhood until the larynx reaches full maturity (puberty).
015
** Quink edema: It is type I hypersensitivity reaction. occurs in anaphylactic shock & angioedema. The
edema occurs mainly in the superficial layer of lamina propria. It is an emergency which requires
management with adrenalin, intubation or even tracheostomy.
** Angioedema: two types:
1. Congenital: C1 esterase inhibitor deficiency. So, any patient presenting with angioedema should
be investigated for C1 esterase inhibitor level.
2. Acquired: Allergy to specific drugs (e.g. ACEI), certain foods, insect bites or even emotional
stress. Patient presents with difficulty breathing, edema and swelling of the lips, tongue,
oropharynx, soft palate, uvula, epiglottis & arytenoids.
Functions of the larynx:

1. Phonation.
2. Respiration.
3. Protection of the lower airway:
- Closure of the aditus.
- Closure of the glottis.
- Reflex respiratory arrest.
- Cough reflex.
4. Fixation of the thorax aided by glottic closure.
5. Function of Macula Flava: Hypothesized to protect the membranous portion of the vocal
folds during vibration from mechanical damage.
Protective mechanisms of the larynx:

1. Epiglottis.
2. False vocal cords (vestibular folds).
3. Vocal cords The strongest

016
Clinical aspects of laryngeal diseases:

Symptoms:
-
Hoarseness
Stridor: Inspiratory type.
Irritative cough
Dysphagia
Pain in the neck, which may radiate to the ears
Examinations of the larynx

Inspection of the larynx
Normally, the thyroid prominence can only be seen in men. It moves upward on
swallowing; absence of this movement indicates fixation of the larynx by infection or
tumor.
- Indrawing of the suprasternal notch on inspiration combined with inspiratory stridor points to laryngotracheal obstruction by foreign body, tumor, odema, etc.
-
Palpation
- The laryngeal skeleton and neighboring structures are palpated during respiration and
swallowing, paying attention to the following: The thyroid cartilage.
The cricothyroid membrane and the cricoid cartilage.
The carotid artery with the carotid bulb which must not be confused with
neighboring cervical lymph nodes; the palpating picks up pulsations.
The simultaneous movement of the larynx and thyroid gland on swallowing.
- Laryngeal click: Normally it is present and you feel click sensation by moving the larynx
side to side. But when lost it means there is increase in the thickness of prevertebral soft
tissue. This is present in post cricoid carcinoma, edema or abscess.
Laryngoscopy
- Indirect laryngoscopy: - inspection by means of mirror or telescopic system 90 degree.
- Direct laryngoscopy:- Rigid - Flexable
By all the above methods examine the following areas: Base of the tongue, both vallecule, lingual surface of the epiglottis, piriform sinus,
glossoepiglottic and aryepiglottic folds, epiglottis, vestibular folds, vocal cords,
anterior and posterior commissures. The normal colour of vocal cords is whitish,
surface is smooth, and closed in the mid line when patient say's eeeeeeeeeeeee
Investigations:
-
Radiography
Plain views in the sagittal or lateral plane for foreign body.
CT scan.
Laryngography.
Stroboscopy.
Biopsy.

017
** Important radiological signs:
1. Thumb printing sign, on lateral view, is seen in epiglottitis.
2. Steeple sing () , on frontal view, shows tracheal narrowing and suggestive of the
diagnosis of croup.
Vocal cord polyps

Polyp: is an edematous or pedunculated or over pouching of mucosa.
Most common site: between anterior one third & middle one third.
Treatment:
Medical: Anti histamine, corticosteroids & speech physiotherapy.
Surgical removal.
Vocal cord nodule:
hyperkeratinization of mucosa, occurs mostly in people who talk loudly, e.g, singers, teachers.
Patients complain of hoarseness of voice.
Treated with speech physiotherapy then surgical excision.

018
Tracheostomy
Definition
It is a surgical procedure to open a direct airway through an incision in the trachea.
Procedure
The operation should be carried out under GA + ETT.

The neck extended, the head straight (not turned to one side).
A transverse incision is preferable to vertical incision.
*In elective Horizontal incision.

*In emergency / Pediatric age Vertical incision .
The incision should be centered midway between the cricoid cartilage and sternal notch .
The strap muscles are identified and retracted laterally and the thyroid isthmus is divided.
The cricoid must be identified by palpation and the tracheal rings counted.
An opening is made into the trachea, centred on the third and fourth rings .
Indications
1. Obstruction of the upper airway like foreign body, trauma, infection, laryngeal tumours and
facial fractures.
2. Impaired respiratory function (head trauma lead to unconsciousness, bulbar poliomyelitits).
3. To assist weaning from ventilation support in pt in the ICU.
4. To help clear secretions in the upper airway.
5. Prophylaxis.
Immediate complications
1. Heamorrhage.
019
2.
3.
4.
5.
6.
Apnea.
Trauma to recurrent laryngeal nerve and great vessles.
Damage to esophagus.
Pneumothorax.
Subcutaneous emphysema.
Early complications
The critical period is the first 48 hrs.
1.
2.
3.
4.
5.
6.
7.
Tube obstruction or displacement.

Bleeding from tracheostomy site.
Infection (Tracheitis, Cellulitis).
Aspiration.
Plugging with mucus .
Subcutaneous emphysema .
Atelectasis.
Late complication
1.
2.
3.
4.
5.
6.
Tracheal stenosis.
Fistula formation (tracheocutaneous or trachea esophagus or trachea-innominate).
Airway obstruction with aspiration.
Bleeding.
Scarring.
Tracheomalacia.
Decannulation
-
When ventilation or suctioning no longer needed, and patient can control their own airway
and not be at risk for aspiration.
Can occur when patient has:
Good cough.
Good ABGs (relative, for the patient).
Clear lungs.
No pathogens in sputum.
Contraindications
-
No absolute contraindications!
A strong relative contraindication to discrete surgical access to the airway is the anticipation
that the blockage is a laryngeal carcinoma.

001
Head & Neck

Headache & facial pain
Introduction
-
Major reason for seeking medical care.

90% is vasculr headache.
10% is mixture of inflammation, traction or dilatation of pain sensitive structures:
dura of base of skull
cerebral artries
venous sinuses
cranial nerves 5, 9, 10, C2 , C3
Pathophysiology
Pain
Referred pain
Pattern of referred pain
Clinical assessment
History
Hx of present illness( 1st occurrence, time, quality, treatment,symptoms, precipitating
factors).
Past medical hx ( head injury, infections, surgeries, medications: anti hypertensive,
vasodiators, alcohol, tobaco).
Family hx
Social hx
Complete head & neck examination
cranial nerves
TMJ & muscles
scalp vessels
trigger points
Neurological examination
Diagnostic tests:
EEG
CT & or MRI
EMG
TMJ radiography
Cervical spine film
labs
Clinical features suggesting serious cause
Crescendo
Early morning
Vomiting
Fever
Seizures & other neurological symptomes
Worst headache in my life

000
Known malignancy
Tenderness
1. Facial pain
Typical Neuralgias
1) Trigeminal neuralgia
Characterized by recurring paroxysmal severe pain,

brief duration (seconds) in the territory of the
trigeminal nerve, spontaneously or initiated by
chewing, talking, touching the affected side of the
face.
Unknown aetiology, an arterial loop pushing on the
sensory root in the posterior fossa.
Females affected more than males.
Treatment: Start with paracetamol, then NSAIDs,
then carbamazepine, then surgical division of the
nerve.
2) Glossopharyngeal neuralgia
Unknown cause
Equal both sexes
Severe, sudden episodes of pain in the tonsil region one side only, ipsilateral ear.
Pain - severe for 1-2 hours, recur daily
Treated like trigeminal neuralgia.
** Eagle syndrome is considered a type of glossopharyngeal neuralgia. Eagle syndrome
is characterized by recurrent pain in the oropharynx and face due to an elongated styloid
process or calcified stylohyoid ligament, with consequent compression or stretching of
the vascular and nervous structures contained in the retrostyloid compartment (in
particular, the glossopharyngeal nerve and perivascular carotid sympathetic fibers).
3) Sluders neuralgia and Vidian neuralgia
Intractable pain in the nose, eye, cheek and lower jaw.

Could be due to lesion of the sphenopalatine ganglion, or vidian nerve.
Treatment: Analgesics, vidian neurectomy
4) Posttraumatic neuralgia
1. Neuroma.
2. Parietal & occipital.
3. 90% recovery.
Atypical facial pain
Pain felt over the cheek, nose, upper lip or lower jaw.
Usually bilaterally symmetrical.

002
Aching, shooting, burning, accompanied by reddening of the skin and lacrimation or

watering of the nose & that's what differentiates it from the typical facial pain.
Lasts for hours, days or weeks.
Occurs mostly in females.
Treatment: Psychological consultation, analgesics.
Symptomatic neuralgias
Intracranial lesions
1) Central lesions
Tumours of the brain stem, M.S., thrombotic lesions, metastasis, occult nasopharyngeal ca.
No precipitant, sensory loss.
2) Post herpetic neuralgia
Herpes zoster may affect trigeminal nerve ganglion

Vesicular rash covers one division commonly the 1st with severe pain.
Extracranial lesions
1) Nasal :
-
Malignant tumours of nose & sinuses.

Infection : acute & chronic sinusitis.
Its site depends on the affected sinus.
It is more severe in the morning.
Increased by coughing, straining, leaning forwards.
NB: vaccum headache: caused by obstruction of frontal recess which is the opening of
frontal sinus as in: frontal sinusitis & deviated septum. Characterized by periodic attacks(
start in the morning, increased in mid day, subside by the end of the day, it is due to
absorption of air in the sinus).
NB: contact headache: Caused by contact of septum & middle turbinate.

003
2) Aural:
-
Infections: otitis externa, ASOM, complicated OM.

NB: CSOM (Chronic Suppurative OM) is never painful except in : complication ,acute
exacerbation or rarely malignant transformation.
Tumours: glomus, acuostic neuroma, carcinoma.
3) Ocular:
-
Infections: orbital cellulitis or abscess.

Tumours: orbital tumour.

004
-
Errors of refraction & glaucoma.

NB: ocular headache is more severe by the end of the day
4) Dental:
-
Infection: dental caries or peri-apical abscess.

Trauma: post extraction neuralgia.
NB: dental caries is the most common cause of facial pain.
5) Temporomandibular joint pain
TMJ arthritis
Costen's syndrome:
TMJ pain
Deafness
Tinnitus
6) Cervical:
Cervical spondyolosis
2. Headache
Headache is one of the commonest symptoms in medical practice.
Etiology:
1) Raised intracranial pressure.
Due to tumours, abscesses, subdural haematoma, brain haemorrhage.
2) Inflammation of the brain and meninges
e.g. meningitis, cerebritis, others.
3) Migraine
Congenital predisposition
Triggered by hunger, certain foods, sleep - too much or too little, hormonal
variations, stress.
Pathology-vascular dilatation
Females affected more than males
? Proceeded by aura usually visual, paraesthesiae of hands, weakness
Headache is unilateral or bilateral, affects any area of the head, aching or throbbing
often accompanied by nausea and vomiting
Diagnosis - by history alone
Treatment - prevention by avoiding precipitating factors, appropriate medication.
4) Tension headache
More common in adult females
Positive family history (40%)
Maybe associated with migraine
Produced by persistent contraction of the muscles of the neck, head and face
005
Caused by emotional tension, secondary to other headaches, posture habit

Treated by analgesics, muscle relaxants, physiotherapy
5) Cluster headache
90% are men
Age 20 - 30
Attacks occur in groups, no aura
Caused by vascular dilatation of branches of external carotid
Triggered by histamines, alcohol
Treated by analgesics, anti-histamine, steroids
3. Pains from head and neck muscles

Pain from temporalis muscles
-
Can arise from grinding teeth at night (bruxism), impacted wisdom teeth,
temporomandibular joint dysfunction, anxiety when the patient clenches the jaws too
tightly.
Treatment: Refer to interested dental surgeon.
Pain from upper neck muscles

-
Can radiate over the head.

Treatment by physio-therapist or rheumatologist.
Pain from frontalis muscles

-
Usually due to bad posture at work or while driving.

Treatment: physio-therapy.
Cervical spondylosis
-
Pain mediates upwards from the neck to the occiput or vertex to the front of the head,
down to the shoulders.
Due to cervical discs prolapse.
Diagnosis - x-ray.
Treatment: Physio-therapy, referral to rheumatologist.
Temporal arteritis
-
Due to acute inflammation of the artery, the cause unknown, affects men and women over
the age of 60.
Pain over the temples and frontal region, intense, throbbing, tenderness over the scalp,
swelling and redness of the overlying skin with general malaise, partial or complete loss of
vision.
ESR Elevated.
Treatment: Cortisone, analgesics.
Psychologic headache
-
Usually accompanied by depression, anxiety.

No organic lesion.

006

007
Temporal bone fractures:

There are 2 types of fractures:
1. Longitudinal fracture (80%):
- Fractures line goes via the middle ear cavity, tympanic
membrane & external auditory canal.
-
Clinical presentation:
- Lacerations at the external auditory canal.
- Conductive hearing loss (CHL).
- Vertigo.
- Tinnitus.
- Hemotympanum.
- Perforated ear drum.
- CSF leak.
- Facial palsy ! because of the relation of the
tympanic segment of facial nerve.
Diagnosis: CT scan.
Management:
- Admission to neurosurgery ward for 24
hours for observation & to exclude epidural/
subdural hematoma.
- Audiometry (PTA) is mandatory!
If CHL, just observation.
Hemotympanum is basal skull

fracture until proven otherwise.
** Signs of basal skull fracture:
1. Periorbital Ecchymosis
(Raccoons Eyes).
2. Mastoid Ecchymosis
(Battles Sign).
3. Hemotympanum.
2. Transverse fracture (20%):

- Farcture line goes through the internal auditory canal &
labyrinth.
- Patient comes complaining of:
- Sensorineural hearing loss (SNHL).
- Vertigo.
- Tinnitus.
- Hemotympanum.
- Facial palsy.
-
Diagnosis: CT scan.
Management:
- Admission to neurosurgery ward for 24 hours for observation & to exclude
epidural/ subdural hematoma
- Audiometry (PTA) is mandatory!
If SNHL, give corticosteroids.

008
Maxillofacial trauma
Definition:
-
Maxillofacial trauma refers to any injury to the face or jaw caused by physical force, foreign
objects, or burns.
Maxillofacial trauma includes injuries to any of the bony or fleshy structures of the face.
The maxillofacial region is divided into 3 parts:

1. First part (upper face): Fractures involve the frontal bone and sinus.
2. Second part (the midface): is further divided into:
o The upper midface: where maxillary Le Fort II and Le Fort III fractures occur and/or
where fractures of the nasal bones, nasoethmoidal or zygomaticomaxillary complex,
and the orbital floor occur.
o
3.
The lower midface: where Le Fort I fractures occur.
Third part (the lower face): Fractures are isolated to the mandible.
Causes of maxillofacial trauma:

-
Road traffic accident (RTA) in 35-60% of cases.

Fight and assault (interpersonal violence).
Sport and athletic injuries.
Industrial accidents.
Domestic injuries and falls.
In RTA:
Mandible (61%)
Maxilla (46%)
Zygoma (27%)
Nasal (19.5%)
Complications:
-
60% of patients with severe facial trauma have multisystem trauma and the potential for
airway compromise.
20-50% concurrent brain injury.
1-4% cervical spine injuries.
Blindness occurs in 0.5-3%.
25% of patients with severe facial trauma will develop Post Traumatic Stress Disorder.

009
Anatomy:

021
Fractures:
Frontal Sinus/ Bone Fractures:
-
Results from a direct blow to the frontal bone with blunt object.
Associated with: intracranial injuries, injuries to the orbital roof and dural tears.
Caldwell view best evaluates the anterior wall fractures.
Naso-Ethmoidal-Orbital Fracture
-
Fractures that extend into the nose through the ethmoid bones.
Associated with lacrimal disruption and dural tears.
Suspect if there is trauma to the nose or medial orbit.
Patients complain of pain on eye movement.
Clinical findings:
Flattened nasal bridge or a saddle-shaped deformity of the nose.
Widening of the nasal bridge (telecanthus)
CSF rhinorrhea or epistaxis.
Tenderness, crepitus, and mobility of the nasal complex.
Intranasal palpation reveals movement of the medial canthus.
- Imaging studies:
Plain radiographs are insensitive.
CT of the face with coronal cuts through the medial orbits.
Nasal Fractures
-
Most common of all facial fractures & it is the most common fracture in head & neck region.
3 types:
4. Depressed
5. Laterally displaced
6. Nondisplaced
- Clinical findings:
Nasal deformity
Edema and tenderness
Epistaxis
Crepitus and mobility

020
-
Diagnosis:
History and physical exam.
Lateral or Waters view to confirm your diagnosis.
Management:
In managing nasal trauma, first check for septal hematoma (which is an emergency
& need to be drained), then if there is NO edema, do nasal bone reduction.
However, if there is edema, follow up after 5-14 days till the edema & swelling
resolve then do nasal bone reduction.
In cases of noncompliance and late follow up, the bone will be already healed and
nasal bone reduction would not be done, instead, cranioplasty after 6 months will
be the appropriate management.
Orbital Blowout Fractures

-
2 mechanisms of injury:
1. Blunt trauma to the globe.
2. Direct blow to the infraorbital rim.
Clinical Findings
Periorbital tenderness, swelling,

ecchymosis.
Enopthalmus or sunken eyes.
Impaired ocular motility.
Infraorbital anesthesia.
Step off deformity
Imaging studies
Radiographs.
CT of orbits.
CT Head to rule out intracranial injuries.
Zygoma Fractures
-
Two types of fractures can occur:

1. Arch fracture (most common)
2. Tripod fracture (most serious): consist of fractures through:
a. Zygomatic arch

022
b. Zygomaticofrontal suture
c. Inferior orbital rim and floor
Maxillary Fractures/ LeFort

-
Classified as LeFort fractures.
LeFort I
-
Definition:
Horizontal fracture of the maxilla at the

level of the nasal fossa.
Separates the alveolar process and hard

palate from the rest of maxilla.
Allows motion of the maxilla while the

nasal bridge remains stable.
Clinical findings:
Facial edema.
Malocclusion of the teeth.
Motion of the maxilla while the nasal

bridge remains stable.
LeFort II
-
Definition:
Pyramidal fracture
Maxilla
Nasal bones
Medial aspect of the orbits
Clinical findings:
Marked facial edema
Nasal flattening
Traumatic telecanthus
Epistaxis or CSF rhinorrhea
Movement of the upper jaw and the nose.
LeFort III
023
-
Definition:
Fractures through:
Maxilla
Zygoma
Nasal bones
Ethmoid bones
Base of the skull
Clinical findings:
Dish faced deformity or donkey face.
Epistaxis and CSF rhinorrhea.
Motion of the maxilla, nasal bones and zygoma

open book facial fracture, craniofacial
dissociation.
Severe airway obstruction.
Mandible Fractures
-
Mandibular fractures are the third most common facial fracture.
Assaults and falls on the chin account for most of the injuries.
The most common direction for dislocation is anteromedial.
** The most common site of mandibular fracture is condyle process (subchondylar).

** the least common site of mandibular fracture is coronoidal process.
Mandibular pain.
Malocclusion of the teeth

Clinical findings
024
Separation of teeth with intraoral bleeding
Inability to fully open mouth.
Preauricular pain with biting.
Positive tongue blade test.
Radiographs:
Panoramic view is the view of choice for mandible fractures.
Treatment
Nondisplaced fractures:
1. Analgesics
2. Soft diet
3. oral surgery referral in 1-2 days
Displaced fractures, open fractures and fractures with associated dental trauma:
Urgent oral surgery consultation.
** All fractures should be treated with antibiotics and tetanus prophylaxis.

025
Facial palsy
Facial nerve
The facial nerve is the seventh (VII) of twelve
paired cranial nerves.
It emerges from the brainstem between the pons
and the medulla.
Nuclei:
1. Facial nucleus - Special Visceral Efferent
(SVE).
2. Superior salivatory nucleus - General
Visceral Efferent (GVE).
3. Lacrimatory nucleus - General Visceral
Efferent (GVE).
Facial nerve is a mixed nerve, having 2 roots:
1. Medial motor root.
2. Lateral sensory root (nervus intermedius),
which contains sensory &
parasympathetic fibers.
Function:
1. Motor function:
Muscles of facial expression.
Posterior belly of digastrics muscle.
Stylohyoid muscle.
Stapedius muscle of the middle ear.
2. Sensory function:
- Taste sensations from the anterior two-thirds of the tongue.
- Oropharynx above the palatine tonsil.
3. Secretomotor function (parasympathetic innervation):
- Submandibular & sublingual salivary glands.
- Lacrimal glands.
- Nasal glands.

026
Course:
The motor part arises from the facial nerve nucleus in the pons while the sensory part arises from
the nervus intermedius. The two roots emerge from the anterior surface of the brain between the
pons and Medulla oblongata. They pass laterally & forward in the posterior cranial fossa to opening
of the internal acoustic meatus. At the bottom of the meatus, the nerve enters the facial canal &
runs laterally above the vestibule of the labyrinith until it reaches the medial wall of the tympanic
cavity. Here, the nerve expands from the sensory geniculate ganglion to give:
Branches inside the facial canal:
1. Greater petrosal nerve : provides parasympathetic innervation to lacrimal gland, as well as
special taste sensory fibers to the palate via the nerve of pterygoid canal (Vidian Nerve).
2. Nerve to stapedius : provides motor innervation for stapedius muscle in middle ear.
3. Chorda tympani : provides parasympathetic innervation to submandibular gland, sublingual
gland and special sensory taste fibers for the anterior 2/3 of the tongue.
Then it descends in the posterior wall of the middle ear, behind the pyramid, then through the
stylomastoid foramen & passes through the parotid gland. Though it passes through the parotid
gland , it doesnt innervate it.
Branches distal to stylomastoid foramen:
1. Posterior auricular nerve: controls movements of some of the scalp muscles around the ear.
2. Branch to Posterior belly of Digastric and Stylohyoid muscle.

027
As the facial nerve runs forward within the substance of the parotid gland, it divides into its 5
terminal branches:
1. Temporal branch
2. Zygomatic branch.
3. Buccal branch.
4. Mandibular branch.
5. Cervical branch.
** Mastoid surgery (mastoidectomy) to remove cholesteatoma carries a risk of facial paralysis.

Testing the facial nerve:
Voluntary facial movements, such as:
Wrinkling the brow
Showing teeth
Frowning
Closing the eyes tightly
Pursing the lips
Puffing out the cheeks
028
There should be no noticeable asymmetry.
Facial paralysis:
Pathology:
-
IF 6TH / & 7TH N not functioning:-lesion within the pons.

If 8th/ 7th N not functioning:-lesion in internal acoustic meatus.
If excessively sensitive to sound in one ear:- lesion involving n. to stapedius.
Loss of taste:-lesion proximal to the point where it gives of the chorda tympani.
UMN lesion:
In an UMN lesion, called central seven, only the lower part of the face on the opposite side will be
affected, due to the bilateral control to the upper facial muscles.
LMN lesion:
LMN lesions can result in Bell's palsy, manifested as both upper and lower facial weakness on the
same side of the lesion.
Bell's palsy
-
The most common cause of unilateral facial paralysis. Bell palsy is an acute, unilateral,
peripheral, lower-motor-neuron facial-nerve paralysis that gradually resolves over time in 8090% of cases.
The cause of Bell palsy remains unknown, though it appears to be a polyneuritis with possible
viral, inflammatory, autoimmune, and ischemic etiologies. Increasing evidence implicates
herpes simplex type I and herpes zoster virus reactivation from cranial-nerve ganglia.
Treatment of Bell palsy should be conservative and guided by the severity and probable
prognosis in each particular case. Studies have shown the benefit of high-dose corticosteroids
for acute Bell palsy. Although antiviral treatment has been used in recent years, evidence is
now available indicating that it may not be useful.
House brackmann facial nerve grading system:

Grade
Description
Characteristics
Normal (100%)
Normal facial function in all

areas
II
Mild dysfunction (75-99%)
III
Moderate dysfunction (50-75%)
- Gross: slight weakness on

close inspection, may have
minimal synkinesis.
- At rest: normal symmetry &
tone.
- Motion:
Forehead: moderate to good
Eye: complete closure with
minimal effort.
Mouth: slight asymmetry
- Gross: obvious but not
disfiguring difference between
two sides; noticeable but not
severe synkinesis, contracture,

029
and/or hemifacial spasm.
- At rest: normal symmetry and
tone.
- Motion:
Forehead: slight to moderate.
Eye: complete closure with
effort.
Mouth: slightly weak with
maximum effort.
IV
Moderately severe dysfunction

(25-50%)
- Gross: obvious weakness

and/or disfiguring asymmetry.
- At rest: normal symmetry and
tone.
- Motion:
Forehead: none.
Eye: incomplete closure.
Mouth: asymmetry with
maximum effort.
Severe dysfunction (0-25%)
- Gross: barely perceptible

motion.
- At rest: asymmetry.
- Motion:
Forehead: none.
Eye: incomplete closure.
Mouth: slight movement.
VI
Total paralysis (0%)

No movement
031
Neck
The upper border of the neck runs along the inferior border of the mandible through the apex of the
mastoid process to the external occipital protuberance. Inferiorly, the neck ends in a plane formed
by the suprasternal notch, the clavicles, and the spinous process of the seventh cervical vertebra.
Neck triangles:
1. Posterior triangle
It is subdivided into:
- Occipital triangle.
- Suprasternal triangle.
2. Anterior triangle
It is subdivided into:
Submandibular triangle.
Submental triangle.
Carotid triangle.
Muscular triangle.
Neck zones:
Zone I: Suprasternal notch to cricoid cartilage.
Zone II: Cricoid cartilage to angle of mandible.
Zone III: Angle of mandible to base of skull.
Deep neck lymph nodes:

Level 1: Submental & submandibular lymph nodes.
Level 2: Upper jugular group (from base of skull to hyoid bone
anatomacilly or from base of skull to bifurcation of common
carotid artery surgically).
Level 3: Middle jugular group (from hyoid bone to omohyoid
muscle).
Level 4: Lower jugular group (from omohyoid muscle to
clavicle).
Level 5: Posterior triangle group.
Level 6: Anterior compartment group.
Level 7: Mediastinal group.

030
Deep neck infection
Cervical fascia:
1. Superficial fascia: forms a thin layer that encloses platysma muscle, superficial veins &
superficial lymph nodes
2. Deep cervical fascia:
1. Superficial layer of deep cervical fascia (investing layer):
It covers:
a. Muscles: trapezius & SCM muscles.
b. Glands: parotid and submandibular salivary glands.
c. Spaces: posterior triangle & suprasternal space.
2. Middle layer of deep cervical fascia (pretracheal layer):
It covers:
a. Muscles: infrahyoid muscles.
b. Viscera: pharynx, larynx, esophagus, trachea.
c. Glands: thyroid gland
3. Deep layer of deep cervical fascia:
Splits into 2 layers:
a. Alar layer: Posterior to visceral layer of middle fascia & anterior to
prevertebral layer.
b. Prevertebral layer: It encloses vertebral bodies & deep muscles of the neck.
032
Carotid sheath:
-
It is formed by the 3 layers of deep fascia.

It contains:
a. common & internal carotid arteries.
b. Internal jugular vein.
c. Vagus nerve.
Deep neck spaces (described in relation to hyoid bone):
1. Entire length of neck:

a. Superficial space:
- Surrounds platysma.
- Involved with cellulitis and superficial abscess.
- Treated with incision along langers line (tension line) with drainage and ATB.

033
b. Retropharyngeal space:
- Anterior border is pharynx and esophagus (buccopharyngeal fascia).
- Posterior border is alar layer of deep fascia.
c. Danger space.
- Anterior border is alar fascia.
- Posterior border is prevertebral layer.
- Extend from skull base to diaphragm.
- Danger because of risk of mediastinitis.
d. Prevertebral space.
- Anterior border is prevertebral fascia.
- Posterior border is vertebral body and deep neck muscles.
- Extends along the entire length of vertebral column (so complications can reach
sacrum).
e. Visceral vascular space.
- Carotid sheath = Lincolins highway.
- Can become secondarily involved with any other deep neck space by direct
spread.
2. Suprahyoid
a. Submandibular space.
- Superior border is oral mucosa.
- Inferior border is superficial layer of deep fascia.
b. Parapharyngeal space
(Pharyngomaxillary
space)
- Medial border is
buccopharyngeal
fascia.
- Lateral border is
superficial layer of
deep fascia.
c. Peritonsillar space.
- Medial border is capsule of palatine
tonsil.
- Lateral border is superior pharyngeal
constrictor.
- Superior border is anterior tonsil pillar.
- Inferior border is posterior tonsil pillar.

034
d. Masticator space (dental abscess)
e. Temporal space.
f. Parotid space.
3.
Infrahyoid:
a. Anterior visceral space.
Deep neck infection (DNI)

- Spread of infection can be from the oral cavity, face or superficial neck to deep neck space
via lymphatic system.
- Infection can also spread to the deep neck space by the path of communication b/w spaces.
- Direct infection may occur by penetrating trauma.
- Often a rapid onset and may progress to fatal complications.
- Most common cause of DNI in pediatrics is tonsillitis and adenitis.
- Most common cause of DNI in adults is odontogenic origin by the 2nd and 3rd molar
because their roots extend below mylohyoid muscle, so below the mouth floor.
Etiology
1. Dental infection
2. Tonsillar and peritonsillar infection
3. Retropharyngeal lymphadenitis
4. Potts disease
5. Sialadenitis
6. Upper respiratory tract infection
7. Trauma
8. Foreign body
9. Instrumentation
10. Spread from superficial infection
11. Unknown (20%)
Bacteriology:
- Usually mixed aerobic and anaerobes that represent the flora of the oral cavity, upper
respiratory tract, and certain parts of the ears and eyes.
- The most common is:
- Strept viridians
- S. aureus
- Klebsiella
- Anaerobes
Clinical features:
- Sore throat or pain and trismus.
- Dysphagia and odynophagia.
- Stridor and dyspnea.
- Late findings may include dysphonia and hoarseness.
- Swelling of the face and neck, erythema.
- Asymmetry of the oropharynx with purulent oral discharge.
- Lymphadenopathy.

Trismus means the pterigoids

(mostly, the medial pterigoid) are
involved and airways will become
inceasingly hard to access which is a
red flag.
035
Diagnosis
- X-ray (lateral cervical soft tissue view): we find air in
unusual places.
- US.
- CT.
- MRI.
Treatment
1. Secure the airway.
2. ABC.
3. Surgical drainage.
4. ATB: Maximum doses of IV systemic antimicrobials regimens according to the site of infection
(Ampicillin or Augmentin,, metronidazole or clindamycin).
Retropharyngeal abscess:
50% usually in children (6-12 months of age).
90% before 6 years of age.
Clinical manifestation:
- In children: fever, irritability, LAP, drooling, stridor, sore throat, torticollis due to edema or
compression on SCM muscle.
- In adults: pain, dysphagia, snoring and nasal obstruction.
On exam:
- lateral posterior oropharyngeal wall bulge.
- Usually unilateral due to fascia between 2 spaces which differentiate it from the danger
space which is usually bilateral bulging.
- The abscess is limited to one side of the midline by the median raphe of buccopharyngeal
fascia, which is firmly attached to the prevertebral fascia
- Extension b/w spaces could occur.
Causes:
- In pediatrics: suppurative process in LN of nose (retropharyngeal lymphadenitis), tonsillitis,
adenoiditis and sinusitits.
- In adults: trauma, instrumentation, extension from other spaces.
Clinical features
1. Retropharyngeal space abscess forms abscess lateral to midline while prevertebral space
abscess forms abscess in midline.
2. Mediastinitis signs & symptoms: Dyspnea, chest pain, tachycardia, fever.
Investigation
1. Lateral neck film
- C2 > 7 mm in both children
and adults.
- C7 > 14 mm in children.
> 22 mm in adult.

036
2. Chest film (detection of mediastinitis, widened
mediastinum).
Retropharyngeal abscess
Treatment
- Antibiotics should be given in full doses.
- Incision of the abscess should be carried out without delay. General anaesthesia is
advisable but requires great skills.
Danger space infection:
- Presentation and exam like above.
- Bilateral bulging
- Extension from retrophryngeal, prevertebral and parapharyngeal spaces.
Prevertebral space infection:
- Back, shoulder and neck pain.
- Dysphagia or dyspnia.
- Causes: Potts abscess, trauma and osteomyelitis.
Submandibular space infection
Most common cause: Dental caries
Anterior teeth & first molar: infection enters sublingual space.
Second & third molars: infection enter submaxillary space.
Clinical features
(True Ludwigs angina)
- Starts unilaterally and progresses bilaterally
037
-
Induration of submandibular region and floor of mouth (severe cellulitis).

Tongue trusted posteriorly and superiorly (causes airway obstruction).
Drooling, odynophagia, trismus, fever.
No purulence(due to no time to developed).
Ludwigs angina
- It is cellulitis not abscess.
- It is limited to submandibular space & its
compartments, sublingual & submaxillary spaces .
- It is an emergency.
Parapharyngeal abscess
Most common cause: Peritonsillar infection
Typical findings:
1. Trismus, drooling, torticollis.
2. Swelling of angel of mandible.
3. Medial displacement of lateral
pharyngeal wall.
4. Others: fever, limited neck
motion, neurologic deficit (C.N
9,10,12, Horners syndrome).
Peritonsillar Space infection.

- The most common one.
- Fever, malaise.
- Dysphagia, odynophagia.
- Hot-potato voice, trismus, bulging of superior tonsil pole
and soft palate, deviation of uvula.
- Cause: extension from tonsillitis.
Parotid space infection
Most common cause: Bacterial retrograde from oral cavity.
Clinical features
High fever, weakness, mark swelling and tenderness of parotid gland,fluctuation,pus at stensens
duct.

038
Descending necrotising mediastinitis (DNM) and lincolns highway
- Suppurative mediastinitis .
- Mortality rate 40% despite aggressive medical and surgical interventions.
- Deep neck infections can spread easily into the mediastinum & pleural cavities commonly
through the carotid sheath.
- Carotid space surrounded by the carotid sheath that descends into the chest and continues into
the mediastinum to fuse with the pericardium has been considered a possible conduit for
infection.
- In recurrent DNM think of congenital abnormalities as 2nd branchial cleft cyst, thyroglossal
cyst or lymphangioma.
Complications
- Carotid artery erosion-rupture.
- Airway obstruction (need tracheostomy, endotracheal intubation).
- Internal jugular vein thrombosis (Lemierres syndrome): can cause pressure on vagus,
internal carotid artery and lead to syncope). Since vagus nerve is involved, the patient may
have referred otalgia of vagal origin.
- Cavernous sinus thrombosis.
- Neurological deficits.
- Grisel syndrome: atlanto-axial subluxation in association with inflammation of adjacent soft
tissues.
- Osteomyelitis.
- Mediastinitis.
- Aspiration.
- Sepsis.
- Pulmonary edema.
- Pericarditis.
Emergencies
- Loss of airway
- Septic shock
- Carotid blowout
- Internal jugular vein thrombosis

039
Embryology of the Neck & Neck Masses

Neck Masses
A mass in the neck is a common clinical finding.
-
Benign Neoplasm
Malignant Neoplasm
Infectious
Congenital
An appreciation for the embryological development of the cervical structures must be made to
competently understand and treat the disorders of the neck.
Embryology and Anatomy

-
Branchial System: 6 pairs of pharyngeal arches separated by endodermally

lined pouches and ectodermally lined clefts.
Each arch consists of a nerve, artery, and cartilaginous structures

(skeleton).
The remaining neck musculature gains contributions from cervical somites.
Branchial system
1. First Branchial arch

-
It is also known as mandibular or maxillary arch/ Meckel's arch.
Nerve: Trigeminal nerve
Artery: Maxillary artery
Skeleton: Malleus, incus, mandible, sphenomandibular

ligament and anterior malleolar ligament.
** Patient with hypoplasia in

mandible is suspected to have
anomalies in the malleeus & incus!!
Muscles: Muscles of mastication (medial & lateral pterigoid, masseter, temporalis muscles),
mylohyoid, anterior belly of digastrics, tensor tympani and tensor veli palatine.
Anamoly in first branchial cleft produces cyst, sinus or fistula. First branchial cleft cysts are
divided into type I and type II.
Type I is preauricular. If it is a fistula, its internal opening is in the middle ear.
Type II is post-auricula, at the angle of the mandible. If it is a fistula, its internal

opening is in the external auditory canal.

041
2. Second branchial arch

-
It is also known as facial arch/ Reicherts arch.
Nerve: Facial nerve.
Artery: Stapedial artey.
Skeleton: stapes, the upper half & lesser cornu of the hyoid, the
** Ant. Belly of digastrics is

supplied by a branch of
trigeminal nerve & post. Belly
of digastrics is supplied by a
branch of the facial nerve, &
this applies to the rest of
muscles according to which
branchial arch they are derived
from!
styloid process and stylohyoid ligament.

-
Muscles: platysma, muscles of facial expression, posterior belly

of digastric, stylohyoid, and stapedius.
Anamoly in second branchial cleft produces cyst, sinus or fistula on anterior margin of SCM
muscle between the first one third and second one third. If it is a fistula, its internal opening
is in the tonsillar fossa.
3. Third branchial arch

-
It is also known as glossopharyngeal arch.
Nerve: Glossopharyngeal nerve.
Artery: Common carotid and proximal portions of the internal and external carotid.
Skeleton: Lower body of the hyoid and greater cornu.
Muscles: Stylopharyngeus muscle.
Third branchial pouch: Inferior parathyroids, thymus gland
Stylopharyngeus muscle is the only

muscle that is supplied by the
glossopharyngeal nerve.
and thymic duct.

-
Anomaly in third branchial cleft produces cyst, sinus or fistula on anterior margin of SCM
muscle. If it is a fistula, its internal opening is in the piriform fossa.
** How to differentiate between second & third branchial cleft cyst ?

It is second branchial cleft cyst until proven otherwise, because it accounts for 90% of cases.
Fistulogram can be done to confirm that.
4. Fourth branchial arch

-
Nerve: Superior laryngeal nerve.
Artery: Right Subclavian artery and ortic arch.
Muscles: cricothyroid muscle.
Fourth branchial pouch: Superior parathyoid glands and parafollicular thyroid cells
Rarely to have cysts or fistula. However, if there is a fistula its external opening is in the neck
and its internal opening is in the thymus.

040
5. Fifth branchial arch

-
The fifth arch only exists transiently during embryologic growth and development. It
disappears before birth.
6. Sixth branchial arch

-
Nerve: Recurrent laryngeal nerve.
Artery: Pulmonary artery and ductus arteriosus.
Muscles: Intinsic muscles of larynx.
** Fourth and Sixth Branchial arches fuse to form the laryngeal cartilages.

042
Principles of Diagnosis and Treatment Head & Neck Cancer

Benign\Malignant Tumor
Benign proliferation of cells without control
Slow growing tumor
Capsule
No metastasis
No mortality
Malignant (cancer):
Invasion of adjacent tissues
Metastasis
Rapid growth
Mortality
Histopathology:
1. Squamous Cell Carcinoma:
-
Most common Head & Neck tumor (90%).

Risk Factors: major aetiological factors.
o Tobacco
o Alcohol
More common in men than women.
Tumor of adults (mostly).
Possibility of second primary (recurrence).
Tumor develops from skin or mucosa.
Ulceration.
Exophitic.
Bleeding.
Pain.
Growth.
Induration on palpation.
Squamous Cell Ca of floor of mouth
Squamous Cell Ca of tongue

043
Squamous Cell Ca of larynx
Squamous Cell Ca of nasopharynx
2. Adenocarcinoma:
-
Tumors of glands
Salivary glands
Skin
Sweat gland, Sebaceous gland, Hair follicles

044
Bulging under normal mucosa or skin.

May ulcerates the mucosa and the skin.
Adenocarcinoma of major salivary glands
Adenocarcinoma of minor salivary glands
3. Lymphoma:
-
Origin: lymphoid tissues.

Waldeyer ring:
Palatine tonsils
Pharyngeal tonsil (adenoid)
Lingual tonsil
Tubal tonsils
Subepithelial lymphoid tissue
Cervical lymph nodes.

045
Lymphoma of the tonsil
4. Sarcoma
- Fibrosarcoma
- Ostesarcoma
- Chondrosarcoma
- Liposarcoma.
5. Melanoma
6. Metastasis
Etiology:
-
Tobacco
Alcohol
Radiation (thyroid) Tinea capitis
Hardwood dust (adenocarcinoma of sinuses)
Viruses (EBV: nasopharyngeal carcinoma)
Chemical
Trotter's triad of nasopharyngeal

carcinoma:
1. Unilateral secretory OM.
2. Trigeminal neuralgia.
3. Soft palate immobility &
trismus.
Progressive Signs and symptoms Indicating Head & Neck Cancer:

-
** Angiofibroma, occurs
Dysphonia
characteristically in young males
Dysphagia
(9-19 years). If found in a female, it
Odynophagia
is an indication to do karyotyping !
Weight loss
Loose dentition
Trismus: Most common muscle to be involved is medial pterigoid.
Otalgia
Neck mass
Serous otitis media: The first sign of nasopharyngeal carcinoma is unilateral
serous/secretory OM.
Nasal obstruction
Epistaxis

046
-
Facial pain
Cranial Neuropathies
Airway obstruction
Bulging of mass
Oral Fetor
Physical Examination:
-
Laryngoscopy
Imaging:
-
CT
MRI
Scintigraphy
FNA
Endoscopy
Biopsy:
TNM Classification of larynx CA:

T1: Tumor is limited to 1 region without impairment of mobility & without extension to other region.
T2: Tumor extension to other region.
T3: T2 + impairment of vocal cord mobility.
T4: Invasion of surrounding organs such as cartilage or skin.
Nx: Regional lymph nodes cannot be assessed.

N0: No regional lymph nodes.

047
N1: Single ipsilateral lymph node 3 cm.
N2: Ipsilateral or bilateral single or multiple lymph nodes < 6 cm.
N3: Ipsilateral or bilateral single or multiple lymph nodes > 6 cm.
Neck dissection (ND):

-
Removal of lymph nodes tissue from the neck.

Elective vs. theraputic ND
Types:
Radical ND: Removal of all lymph node groups & functional structures: SCM
muscle, accessory nerve & internal jugular vein.
Modified Radical ND: Removal of all lymph node groups & one or two of the
functional structures (Preservation of some functional structures).
Functional ND: Removal of all lymph nodes only. (Preservation of the functional
structures).
Selective ND: Selective lymph node removal.


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ENT for medical students

Dr. Adel Adwan

ENT, Dr. Adel Adwan - Al-Quds university

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

ENT, Dr. Adel Adwan - Al-Quds university

Composed of middle ear cleft which contains:

ENT, Dr. Adel Adwan - Al-Quds university

There are joints between the ossicles:

Foot plate is attached to the oval window

Eustachian Tube (Auditory tube):

Connects middle ear and nasopharynx.

Protection from nasopharyngeal secretions

ENT, Dr. Adel Adwan - Al-Quds university

The vestibular system

It lies in the otic capsule in the petrous

The vestibular fluids:

ENT, Dr. Adel Adwan - Al-Quds university

The otolith organs: Utricle & Saccule

** The sensory organs of the utricle

When stereocilia bend to the direction of

ENT, Dr. Adel Adwan - Al-Quds university

Conversely, bending of stereocilia in the opposite

When the head is upright, the hairs project upward

ENT, Dr. Adel Adwan - Al-Quds university

The semicircular canals

Lateral or horizontal, Anterior or

Nerve fibers send impulses to the brain cerebellum

Analysis of information allows the brain to predict the

ENT, Dr. Adel Adwan - Al-Quds university

Each semicircular canal works in

ENT, Dr. Adel Adwan - Al-Quds university

Palpate the auricles for:

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

Perforated: Central / Marginal.

Moist keratin debri otitis externa

Mucoid or mucoperulent discharge Chronic or acute otitis media.

ENT, Dr. Adel Adwan - Al-Quds university

Scanty offensive perulent discharges Cholesteatoma

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

Bleeding trauma, tumor.

Tuning fork tests:

ENT, Dr. Adel Adwan - Al-Quds university

Subjective method of testing hearing. It is performed

Conductive hearing loss:

Bone Conduction (]) :

Air conduction (X):

Air-Bone gap > 10 dB

Sensorineural hearing loss:

Bone conduction (]):

Air conduction (X):

Air-Bone gap < 10 dB

ENT, Dr. Adel Adwan - Al-Quds university

> 90 db (profound hearing loss) is an

Mixed hearing loss:

Bone conduction (]):

Air conduction (X):

Air-Bone gap > 10 dB

Objective method of testing middle ear pressure, TM

ENT, Dr. Adel Adwan - Al-Quds university