Handbook of Ear, Nose & Throat

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 The Ear

Ear is formed of 3 parts:

a. External ear: Receives and transmits sound waves to tympanic membrane.
b. Middle ear: Transmits movement of the tympanic membrane by three ossicles to
fluid
in the inner ear.
c. Inner ear: Contains receptors for sound and equilibrium.

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a. External Ear
1. The Auricle (Ear pinna): Formed of elastic cartilage covered by thin skin
except the lobule which is the lowest part of the auricle and formed of soft tissues
without cartilage.

Auricle
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2External auditory meatus:
Extent: Short tube extends from the concha to the tympanic membrane.
Direction: It has an S-shaped curve.
Length: 24 mm long
Parts of External Meatus:
- Its lateral ⅓ is cartilaginous and the medial ⅔ is bony.
Lateral cartilaginous part Medial bony part
* It is the lateral ⅓ of the meatus. * It is the medial ⅔ of the meatus.
* 8 mm long. * 16 mm long.
* Skin: Is thick, adherent to the * Skin: Is thin, adherent to the
cartilage. It is rich in hair, bone, no hairs, no glands and
sebaceous and ceruminous rich in nerve endings. It
glands (coiled tubular continues on the outer surface
apocrine). The latter secrete of the tympanic membrane.
cerumen (wax). Hairs and
cerumen limit entry of insects
2. Ear drum (Tympanic membrane):
This oval disc is stretched across the medial end of the external auditory meatus.
Dimensions and Position: It is about 1 cm in diameter and makes an angle of about 55
degrees with the external meatus.
Formed from outside to inside of:
•Thin skin.
•Two layers of collagen and elastic fibers with radial then circular arrangements,
• Simple cuboidal epithelium that is continuous with that lining the middle ear.
Surfaces of the membrane:
• Lateral surface is concave and on examination, it shows a cone of light in its
antero-inferior part.
• Medial surface is convex. The point of maximum convexity is called the umbo
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 produced by the handle of malleus attached to that surface.
• Parts of T.M. :
- The tympanic membrane is formed of a fibrous layer covered externally by
the thin skin of the external meatus and internally by the mucous membrane
of the middle ear
-Its lower large part is called pars tense, has well developed fibrous layer.
-Its upper small part is called pars flacidda and has no fibrous layer

Tympanic membrane

Functions of external ear:

1- Collection of sound by ear pinna to external auditory canal
2- Increase sound pressure at tympanic membrane
3- Ear pinna helps in determining sound localization
4- Protective function:

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b. Middle Ear (tympanic cavity)
• The middle ear is a cavity in the petrous temporal bone
• Communications:
1. Anteriorly: It communicates with the
nasopharynx via the
auditory tube.
2. Posteriorly: It communicates with the
mastoid antrum via the
aditus ad antrum.

Boundaries of the Tympanic Cavity:

I. The Lateral Wall: It is formed by tympanic membrane.
II. The Medial Wall: It separates the middle from the internal ear and has the following
features:
1- Promontory: It is produced by the basal turn of the cochlea.
Upon it, lies the tympanic nerve plexus.
2- The oval window: It lies postero-superior to the promontory and
is closed by the footeplate of the stapes.
3- The round window: It is postero-inferior to the promontory and
is closed by the secondary tympanic membrane. Round
window is covered by a membrane that bulges to relieve
pressure in the cochlea that originates from motion of the
stapes at the oval window
4- Horizontal part of the bony facial nerve canal: above the
promontory and the oval window.
III. The Posterior Wall: It presents three features:
1. Aditus ad antrum: It communicates the tympanic cavity with
the mastoid antrum.
2. Fossa incudes: It contains the short process of the incus.
3. The pyramid: Is a small hollow conical projection. It contains
stapedius muscle.
IV. The Anterior Wall: Has the following features:
• Superiorly: is the opening of the canal for tensor tympani muscle.
• In the middle is the opening of the bony part of the auditory tube.
V. Roof (Tegmental Wall): Is formed by a thin plate of bone called tegmen tympani
VI. Floor (Jugular Wall): Is formed by the jugular fossa of the skull.

Contents of the Tympanic Cavity:

(1) Air: Is very important for proper function of the ear.

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(2) Mucous membrane: It is ciliated columnar epithelium.
(3) Auditory ossicles:
They form a chain from the tympanic membrane to the oval window. They are
malleus, incus, stapes. They are articulating at synovial joints.
(4) Muscles in the Tympani Cavity:
-Tensor Tympani:
• Arises from the cartilaginous part of the auditory tube and adjoining part of the
sphenoid bone →upper end of the handle of malleus.
• N. Supply: mandibular N.
• Action: It tenses the tympanic membrane, restricts its freedom of movement, and
protects the inner ear.
-The Stapedius:
• Arises from the pyramid and is inserted into the neck of stapes. It helps to
dampen very loud sounds thus preventing noise trauma to the inner ear. It is
supplied by a branch from the facial nerve.
(5). Two nerves:
-The chorda tympani nerve is a branch of the vertical part of the facial nerve which enters
the middle ear and runs close to the medial surface of the tympanic membrane between
the handle of malleus and long process of incus. It carries taste from the anterior two
thirds of tongue and supplies secretomotor fibres to the submandibular and sublingual
salivary glands.
-The tympanic plexus lies on the promontory under the mucosa and is formed by (i)
tympanic branch of glossopharyngeal nerve and (ii) sympathetic fibres from the plexus
round the internal carotid artery. It contains sensory fibers to the tympanic cavity and the
drum.

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 Roof, floor, medial walls of the tympanic
cavity

Structures Communicating with the Tympanic Cavity :

I. Auditory Tube (Eustachian tube):
This tube connects the tympanic cavity with the nasopharynx.
Dimensions:
- It is about 36 mm long. Its lateral ⅓ is bony (simple col.ciliated) and its medial ⅔
is cartilaginous (ps.st.col.ciliated)
- It begins at the anterior wall of the tympanic cavity and ends at the pharyngeal
opening in the lateral wall of the nasopharynx.
Muscles Attached to the Auditory Tube:
- Tensor palati. - Levator palati.
- Salpingopharyngeus. - Tensor tympani
Function: It equalizes pressure on both sides of the tympanic membrane.
II. The Mastoid Antrum :
Definition: It is an air-filled sinus, posterior to the tympanic cavity and
communicates with it via the aditus ad antrum.

Its lateral wall is marked by the suprameatal triangle. In the adult, the
antrum is about 15 mm deep the surface. Inferiorly it is continuous
with the mastoid air cells. These are a series of intercommunicating
air cells within the mastoid process.

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- Functions of middle ear:
 It couples sound energy to cochlea to stimulate auditory receptors
‚ Physical protection of cochlea
ƒ Impedance matching:
Sound is conducted from external ear (where it is carried by air which has a low impedance)
to inner ear (which has a much higher impedance) ie the middle ear matches the difference in
impedance, this is carried out through:
1. The tympanic membrane (elastic- tense- a periodic-resonator-damped) is much wider than
the foot of stapes so, the force collected over the tympanic membrane is concentrated over
a small area increasing pressure 17 times
2. The ossicles act as a lever with malleus longer than incus → displacement at stapes is
decreased while force increase 1.3 times
- Thus, sound is magnified 22 times (17 ´ 1.3)

Function of Eustachian tube: It connects middle ear with pharynx

It equalizes air pressure on both sides of tympanic membrane
Normally:
The tube is closed but it opens: During swallowing & yawning
If pressure in middle ear exceeds that of atmosphere by 15 mmHg (as in ascending to high
altitude)
During descent from high altitude, the external pressure pushes the drum inwards, it may
rupture (eg if person is sleeping) unless the person swallows
If the tubes are opened permanently: The noises of breathing, talking will interfere with
hearing
If the tubes are blocked: As in common cold, the tympanic membrane is sucked in due to
gradual absorption of air & auditory acuity is greatly decreased

NB:
Middle ear infection is more in children as Eustachian tube
In children tube is:
 Short
‚ Wide
ƒ Straight
So secretion of nasopharyngeal easily enter the middle ear causing middle ear infection

c. Inner Ear
1. Bony labyrinth:
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 • Filled with perilymph (High Na)
• Comprises:
1. Cochlea.
2. Vestibule.
3. Semicircular canals.

2. Membranous labyrinth:
• Filled with endolymph (High K).
• Comprises: Vestibular membrane
1. Cochlear duct.
2. Utricle and saccules.
3. Semicircular ducts.

Basilar membrane

Cochlea:
• It is a bony tube which makes 2½ turns around a central bony axis, the modiolus,
which contains blood vessels, spiral ganglia & cochlear nerve fibers.
• In section, it appears as 5 cavities because the 2 complete turns are cut twice.
• The bony spiral lamina: a bony shelf projecting from the modiolus to the lumen of
cochlea.
• Basilar membrane and vestibular membrane divide the cochlea into 3 compartments.
1. Scala vestibuli: Above vestibular membrane, filled with perilymph, lined by
simple squamous epithelium
2. Scala media (cochlear duct): Filled with endolymph which Is continuous with
endolymph of vestibular labyrinth (semicircular canals, utricle , saccule)
3. Scala tympani: Below basilar membrane, filled with perilymph, lined by
simple squamous epithelium.

• Scala vestibule and Scala tympani contain perilymph & communicate with each other
at the apex of cochlea through helicotrema (perilymph Is derived from CSF)

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 • Medially, the scala vestibuli ends at the oval window (closed with foot plate of
stapes), while scala tympani ends at the round window (closed with secondary
tympanic membrane)
• Perilymph is similar to extracellular fluid with high Na+ & low K+
• Endolymph is similar to intracellular fluid with low Na+ & high K+

Cochlear duct (Scala media):

• In middle part of cochlea, filled with endolymph, triangular in cross section.
• It contains organ of Corti

Organ of Corti:
• It is a neuroepithelial structure
responsible for hearing, found in the
cochlear duct, on the basilar
membrane.
• It is formed of.
Hair cells:
1. Inner hair cells: one row.
2. Outer hair cells: 3-4 rows.
• The hair cells have hair-
like processes
(stereocilia) on their free
surfaces. Their basal
parts are in contact with
the dendrites of the
bipolar nerve cells of the spiral ganglion.

Vestibule:
• Filled with perilymph and contains 2 sacs: utricle and saccule.

The semicircular canals:

• Bony canals that open in the vestibule by 5 openings as 2 of them have a common
opening.
• Each canal has an expanded end called ampulla.
• Each canal contains a membranous duct lined with simple squamous epithelium,
filled with endolymph, has a neuroepithelium for equilibrium in the ampulla called
crista ampullaris.

PHYSIOLOGY OF THE EAR

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The ear has two functions; hearing and equilibrium.

A: Mechanism of hearing
ΠTransmission of sound to inner ear:
- There are three routes by which the sound waves (energy) can be transmitted to the fluid
of inner ear to stimulate the organ of corti
1- Ossicular route: - The normal route
- It is very efficient
- Sound waves are collected by ear pinna, then reaches the
tympanic membrane which vibrates causing ossicles to vibrate
then conducted to fluid of inner ear through oval window
- As sound energy passes from scala vestibuli to scala tympani, it
causes the basilar membrane to vibrate, stimulating the organ of
Corti
- It has the following advantages:
1. Utilization of tympanic membrane (mention its properties)
2. Amplification of sound waves (because tympanic membrane
is 17 times as oval window & ossicles as a lever)
2- Air route: - Not efficient (its sensitivity is 20 dB less than ossicular route)
- Occurs in: - Damage of tympanic membrane
- Auditory ossicles
- Occasionally when Eustachian tube is open
- Sound waves cause vibration of secondary tympanic membrane which
covers round window which cause vibration of inner ear fluid
3- Bone route (Bone conduction): - Not efficient
- Only on testing of hearing
(using the vibrating tuning fork)
 Mechanism of stimulation of organ of Corti & auditory nerve:
1- Propagation of sound waves: To inner ear fluid: Via one of three routes mentioned above
2- Movement of organ of Corti:
- The inward movement of foot of stapes causes perilymph movement in scala
vestibule → endolymph movement In scala media → vibration of basilar membrane
with overlying hair cells → The up and down motion of hair cells (in organ of Corti)
causes the stereocilia to bend back and forth
3- Hair cell potential:
Vibrations of the basilar membrane leads to → vibrations of stereocilia of hair cells
If away from the limbus, K+ channels If towards limbus, K+ channels dose & hair
open → K+ enter & hair cells depolarize cells hyperpolarize
4- Release of synaptic transmitter:
Hair cells depolarization → open Ca++ channels → Ca++ enter → chemical
transmitter is released & auditory nerve is stimulated

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B. Equilibrium:
The vestibular system
The vestibular system is divided into:
(a) Peripheral; which is made up of the membranous labyrinth (semicircular ducts, utricle
and saccule) and the vestibular nerve.
1. Cristae of the three semicircular ducts, their receptors respond to angular acceleration.
2. Maculae in utricle and saccule sense the position of the head in response to gravity and
linear acceleration.
3. Vestibular nerve which is made of the terminal fibres from cristae and maculae.
(b) Central; which is made up of the vestibular nuclei and fiber tracts in the central nervous
system to integrate vestibular impulses with other systems (eyes, joints and muscles) to
maintain body balance.

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Examinations of The Ear
- Clinical examination:
- The auricle for swelling and tenderness.
- Inspection for discharge, swellings and polyps in the external canal.
- The drum by the ear speculum or otoscope.
- The drum mobility is tested by Siegle’s ear speculum.
- The mastoid bone for swelling and tenderness.
- The post-auricular area for previous scars of ear operations.
- Oto-endoscopy: using rigid endoscopes.

- Eustachian tube patency:

-Valsalva’s method: Forced expiration with both mouth and nose closed and monitoring
the drum movement with the otoscope.
-Posterior nasal mirror or flexible and rigid endoscopes for examination of the
nasopharyngeal opening of the Eustachian tube.

- Investigations for ear disease:

1. Tests for hearing and vestibular function.
2. Culture and sensitivity tests for the ear discharge.
3. CT scan and MRI for the petrous part of the temporal bone.
4. Biopsy from ear polyp or tumour.

- Assessment of hearing:
1- Rough methods:
-Whispering voice normally heard at 9 feet.
-Conversation voice normally heard at 9 meters.

2- Tuning fork tests: Mainly to differentiate between conductive and perceptive deafness.
A fork of 512Hz is used.
a) Rinne’s test: Compares hearing by air conduction (AC) with hearing by bone
conduction (BC) in the same ear. The fork is first applied to the
external canal and when the patient can no longer hear its vibration,
the fork is applied to the mastoid bone.
- Normally: AC is better than BC ( Rinne’s +ve).
- In conductive deafness: BC is better than AC ( Rinne’s –ve).
- In perceptive deafness: AC is better than BC but both are reduced than normal.
b) Weber’s test: Compares bone conduction in both ears. The fork is applied to the
forehead. It is useful when there is marked difference in hearing
between the two ears.
- Normally: the sound is heard in the midline or in both ears equally.
- In conductive deafness: the sound is heard better in the diseased ear
(the outside noise masks hearing of the normal ear).
- In perceptive deafness: the sound is heard better in the normal or
better hearing ear.

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 3- Audiometry:
- Subjective audiometry: requires cooperation of the patient.
-Pure tone audiometry.
-Speech audiometry.
- Objective audiometry: does not require cooperation of the patient.
-Impedence audiometry (Tympanometry and stapedial reflex).
-Evoked response audiometry.

- Pure Tone Audiometry (PTA)

-The audiometer produces tones of different frequency and intensity delivered to the ear
through a headphone for air conduction and a vibrator applied to mastoid bone for bone
conduction.
-The test frequencies range from 125 Hz to 8000 Hz, at intensities from -10 to 120
decibel (dB).
-The threshold of hearing for air and bone conductions are recorded on a graph.
-The audiogram is interpreted as conductive, sensorineural or mixed deafness and the
degree of hearing loss as mild, moderate, severe and profound.

Normal Conductive Sensorineural

AUDIOGRAM

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- Impedance audiometry
- Tympanometry:
- The compliance of the middle ear is monitored on a graph while the pressure in
external auditory canal is gradually changed from - 200 H2O to + 200 H2O.
- The compliance is at maximum when air pressure on both sides of the drum is equal.
- The graph shows characteristic changes in different middle ear conditions
- Normal ear: Symmetrical graph (Type A).
- Eustachian tube obstruction: -ve peak tympanogram curve (Type C).
- Secretory otitis media: Flat tympanogram curve (Type B).
- Ossicular disconnection: Hypermobile tympanogram curve (Type Ad).
- Otosclerosis: Restricted tympanogram curve (Type As).

Tympanogram
A.Normal B. Seretory otitis media C. Eustachian dysfunction
As, Otosclerosis. Ad. Ossicular disconnection

- Stapedial reflex:
Normally, the two stapedius muscles contract when a sound of 80dB is applied to one
ear. The stapedial reflex threshold (SRT) is the minimum intensity required to evoke
this reflex:
- Normal ear: SRT at 80 dB.
- Conductive deafness: SRT is absent.
- Nerve deafness: SRT is above 80 dB.

- Evoked respose audiometry

- Auditory brainstem response (ABR): Is an auditory evoked potential extracted from
ongoing electrical activity in the brain and
recorded via electrodes placed on the scalp. The
resulting recording is a series of 5 positive
waves. It is used for threshold detection in
infants and uncooperative adults..

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- Hearing assessment in children:
1-Subjective:
a) Under 2 years: Distraction tests: The child blinks or turns head or body in response
to sound (Moro reflex).
b). Between 2 – 5 years: Co-operative tests: The child picks up toys when he hears
sound.
2- Objective:
a) Impedence audiometry.
b) Evoked response audiometry.

- VESTIBULAR FUNCTION TESTS

The eyes are examined for the presence of nystagmus which is an involuntary, oscillatory
movement of the eye ball by:
- Direct observation or through Frenzel’s glasses which worn by the patient to magnify
his eyes and to abolish visual fixation.
- Electronystagmography (E.N.G):
Recording nystagmus on a graph using a battery of tests including:
1. Spontaneous nystagmus: patient is looking straight ahead.
2. Gaze test: patient is looking to right, left, up and down.
3. Rotation test: Nystagmus to the opposite direction when rotation stops
4. Positional test: Nystagmus in certain position.
5. Caloric test:
The patient lies supine; his head is flexed forwards at 30° angle to bring the
lateral semicircular canal into a vertical position to be maximally stimulated.
Each ear is irrigated with water 7° C above and 7°C below normal (30° C
and 44 °C) for 40 seconds.
- Normally: Nystagmus occurs and lasts for 2 minutes.
- Hypo function of the labyrinth: Nystagmus duration is diminished, e.g.
one minute.
- Dead labyrinth: No response.
4. Fistula test:
Air compression in the external canal by Siegle’s speculum causes
momentary vertigo and nystagmus. This indicates the presence of a fistula
between the middle ear and the inner ear in the lateral SSC caused by
cholesteatoma and that the labyrinth is still alive.

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Diseases of The External Ear
Congenital Anomalies of The External Ear
I. Auricle:
1. Anotia: Absent auricle.
2. Microtia: Small deformed auricle.
3. Macrotia: abnormally large auricle.
3. Bat ear (protruding auricle): commonest congenital anomaly.
4. Pre-auricular fistula: A tiny opening in front of auricle.
5. Accessory auricle: periauricular remnants formed of skin and cartilage.

II. External auditory meatus:

Atresia of the external auditory meatus due to failure of canalization during the first
trimester of pregnancy leads to conductive deafness. It is commonly associated with
congenital anomalies of the auricle and the middle ear.
- Investigations:
1-Audiological: ABR to assess the type and degree of hearing loss.
2- Radiological: C.T Scan to evaluate the middle and inner ear state.
- Treatment:
1- Unilateral cases: no treatment or auriculoplasty for cosmetic reasons.
2- Bilateral cases: * Hearing aid: early to help speech development.
*Reconstruction: late at 6 years (Meatoplasty).

Trauma of the external ear

I. Trauma to the auricle:
- Hematoma of the auricle: Is due to collection of blood between the cartilage and the
perichondrium. It is due to closed blunt trauma eg,. Boxing.
If this hematoma becomes infected, it leads to perichondritis
of the auricle.
- Clinical picture: Painful, swollen and bluish auricle.
- Treatment: Antibiotics and aspiration of the collected blood with tight bandage to
prevent recollection.

- Perichondritis of the auricle: Is due infection, suppuration and necrosis of the auricular
cartilage leading to cauliflower auricle.
- Causes: Infected hematoma, septic incisions or furunculosis.
- Clinical picture: Painful, swollen, reddish and tender auricle. The auricle is swollen,
red, hot and tender.
- Treatment:
-Antibiotic injections.
-Multiple incisions to drain the pus and remove the necrosed cartilages.

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II. Trauma to the external auditory meatus:
Foreign bodies, fracture base of skull and scratching with nails or pins.
Foreign Body (F.B) Common in children
- Types of F.B: - Animate: flies, mosquitoes and larvae (myasis).
- Inanimate: seeds, beans, beads and buttons.
- Complications:
- Acute otitis externa and otitis media.
- Injury of the external canal, the drum and the ossicles during unskilled
attempts of removal.
- Treatment: Ear wash or hocks remove most foreign bodies which could be done
under general anesthesia in children.

Inflammations of The External Ear Canal

External Otitis (Otitis externa)
1. Bacterial Infections:
A) Localized otitis externa (Furunculosis):
It is a staphylococcal infection of a hair follicle in the skin of the cartilagenous external canal.
- Symptoms:
-Pain: severe on mastication because the skin is adherent to the cartilage.
-Deafness follows if the canal is occluded by the swelling.
-Scanty, purulent discharge if the furuncle bursts.
- Signs:
-Tenderness on moving the auricle or pressing the tragus.
-Localized lymphadenitis (pre and postauricular).

Treatment:
-Systemic antibiotics, ear drops and analgesics.
-Test for diabetes in recurrent cases.
B) Diffuse external otitis:
It is a diffuse inflammation of the external canal skin due of Staphylococcus
infection (swimmer's ear).
- Causes:
-Scratching the ear with dirty fingers or unsterile pins.
- Sepsis from ear wash.
-Humidity in summer (excess sweating).
- Symptoms:
-Pain on mastication. -Scanty discharge. -Slight deafness.
- Signs:
-The canal shows diffuse red swollen skin with narrow lumen.
-Tenderness on moving the auricle or pressing the tragus.
- Localized lymphadenitis (pre and postauricular).
- Treatment:
-Systemic antibiotics, ear drops and analgesics.

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Staphylococcus aureus:
Gram-positive spherical bacteria that occur in grape like-clusters. It causes a wide
range of suppurative infections (pus-forming) and toxic shock syndrome.

Source of infection: Either endogenous from skin and nasal normal flora or
exogenous by contact.

Laboratory diagnosis: Specimen: pus.

1. Direct microscopic examination: Gram positive cocci in grape like clusters.
2. Culture: on blood agar: complete (beta) hemolysis.
Prevention:
1- Cleanliness, and frequent hand washing, and aseptic management of lesions
2- Reduce persistent nasal colonization by intranasal application of muporicin.
3- Cefazolin is used preoperatively to prevent staphylococcal surgical-wound
infections.
C) Malignant otitis externa:
It is a pseudomonas infection in elderly, diabetic or immune-compromized patients.
The infection and granulations starts at the junction of the cartilagenous and bony
portions of the external ear canal leading to osteitis, osteomyelitis and extensive
granulations.
- Clinical picture:
-Pain is severe and resistant to analgesics.
-Serosanguinous discharge (serous &blood).
-Infection and granulations may involve:
* Stylomastoid foramen leading to facial paralysis.
* Jugular foramen leading to paralysis of the last four cranial nerves.
* Sigmoid sinus and meninges leading to fatal outcome.
- Investigations: 90% diabetic, Radionuclide scanning (Gallium).
- Treatment:
-Topical gentamycin and antibiotic injections.
-Control of diabetes and improve immunity.

2. Fungal Infections (Otomycosis):

Fungal infections are caused by Aspergillus niger or Candida albicans.
- Symptoms:
-Itching may be the only symptom.
-Pain when secondary infected.
-Deafness caused by the fungal mass when it obstructs the external ear
- Signs:
White mass with black spots (fungus mass), which appears as wet newspaper
in the external meatus.
- Treatment:
-Ear wash to remove the fungus mass.
-Antifungal ear drops as mycostatin or canesten.

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Wax Accumulation
It is abnormal accumulation of ear wax (cerumen: a mixture of secretions of both ceruminous
and sebaceous glands) which are present in the outer cartilagenous part of the external canal.
- Symptoms: Deafness and tinnitus if the wax completely obstructs the meatus.
- Treatment:
-Removal by forceps or ear wash.
- If hard, glycerin bicarbonate drops will soften it for two or three days before wash.

EAR WASH
- Indications:
- Wax causing deafness.
- Foreign body (not impacted).
- Fungus mass (Otomycosis).
- Aural toilet for discharge of chronic suppurative otitis media.

- Contraindications:
- Dry or traumatic perforation.
- Impacted foreign body.
- Otitis externa.
- Fistula from the middle ear to the inner ear.
- Technique:
The fluid used is sterile, isotonic saline or water at body temperature.
The ear canal is straightened by pulling it upwards and backwards.
The sterile nozzle of the syringe is put on the posterior wall and the flow of water is
directed posteriorly to avoid rupture of the drum.

Ear wash
- Complications:
- Trauma to the drum or injury of the external canal.
- Infection: Acute otitis externa or acute otitis media.
- Reflex cough or syncope due to vagal stimulation.
- Vertigo: Caloric reaction from hot or cold fluid used.

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Diseases Of The Middle Ear
- Congenital Anomalies
- Dehiscence of the bony facial canal (horizontal part) predisposes to facial paralysis
during attacks of acute otitis media, cholesteatoma and ear surgical trauma.
- Fixation or absence of ossicles causing conductive deafness.
- Dehiscence of the floor of the tympanic cavity predisposes to injury of the jugular bulb
during tympanoplasty leading to severe hemorrhage.

- Trauma of the middle ear

1. Traumatic rupture of the drum:
- Causes:
Indirect trauma: Slap, blast or otitic barotrauma.
F.B. or during its removal, clumsy ear wash, fracture base of the skull.
- Symptoms:
-Slight pain.
-Mild deafness and tinnitus.
-Minimal bleeding.
- Signs and Differential Diagnosis:
Traumatic perforation Pathological perforation
1. History Of trauma Of common cold
2. Site Central and antero-inferior Central, marginal or attic
3. Size Any size Usually large
4. Shape Any shape, with sharp edge Rounded, oval or kidney-shaped
5. Edges Thin, irregular, hyperaemic, Thick, regular, smooth, surrounded by
surrounded by blood clots pus
6. Rest of drum Normal Congested
7. Discharge Usually absent Usually present

- Treatment:
- Keep the ear dry: no drops and water.
- Antibiotics, analgesics and nasal decongestive drops.
- The perforation usually heals in three to six weeks.
- Myringoplasty after three months if the perforation fails to heal.

2. Otitic Barotrauma
Non infective inflammation of the middle ear due to relatively negative intratympanic
pressure caused by Eustachian tube obstruction.
- Predisposing factors:
- Eustachian tube pathology e.g. allergy, inflammation, or adenoids.
- Eustachian obstruction due to rapid descent in a no pressurized airplane or sea divers.
- Pathology:
- Congestion and effusion in the middle ear due to negative pressure.
- Symptoms:
- Deafness, tinnitus, pain and auto-phony (patient hears his voice loud).

21
 - Signs:
- Retracted congested drum.
- Fluid and bubbles in the middle ear.
- The drum may be traumatically perforated.
- Prophylaxis:
- Avoid flying when having upper respiratory infection.
- Avoid sleeping during flight descent (Eustachian tube is closed at rest).
- Opening the Eustachian tube by nasal drops, chewing gum and auto-inflation by
performing Vasalva's method.
- Treatment:
- Antibiotics, analgesics and nasal decongestive drops.
- Myringotomy to allow air in and drain fluid out.

3. Fracture Base of Skull

- Longitudinal fracture passes in the long axis of the petrous temporal bone through the
middle ear, drum and external ear. It causes conductive
deafness, bleeding from the ear and cerebrospinal otorrhea. It is
more frequent than the transverse fracture.
- Transverse fracture (at right angle to the long axis of the petrous bone) usually affects
the inner ear and the facial nerve. It causes sensorineural
deafness, vertigo and facial paralysis.

4. Ossicles disconnection
- Disconnection of ossicles following head injury, fracture skull base, ear surgery or
impacted foreign body. It causes conductive deafness and the drum may be intact. The
incudostapedial joint is the most commonly affected.
- Treatment: Middle ear exploration and Ossiculoplasty.

22
INFLAMMATIONS OF THE MIDDLE EAR
- Acute Otitis Media (AOM)
- Definition: An acute inflammation of the mucosal lining of the middle ear cleft.
- Causative organisms:
- Bacterial as Haemophilus influenza, streptococci and staphylococci.
- Viral as influenza.
- Routes of infection:
- Through the Eustachian tube: extension of infection from:
- Acute rhinitis, acute sinusitis.
- Adenoiditis, common cold.
- Milk regurge during suckling in infants.
- Through a drum perforation: During swimming and bathing.
- Clinical picture:
A) Before perforation:
- Fever which is higher in children, throbbing pain, deafness and tinnitus.
- On examination: bulging of the drum, conductive deafness.
B) After perforation:
- Necrosis of the drum anywhere causes perforation.
- Discharge, deafness, fever and pain diminish.
- On examination: Perforated drum, mucopurulent or purulent discharge and
conductive deafness.
- Treatment of acute otitis media:
- General: Antibiotics, analgesics and nasal decongestive drops.
- Surgical: Myringotomy to allow drainage before perforation.
- Sequelae of acute otitis media:
- Healing: Arrest of discharge, normal drum and normal hearing.
- Non-resolution: Is due to inadequate treatment, virulent organisms and low
resistance of the patient.
This may manifest by:
A) Residual deafness due to:
- Secretory otitis media: Fluid collects in the middle ear due to Eustachian
tube obstruction or mild infection. Treated by
myringotomy, aspiration of the fluid and insertion
of ventilation tube (Grommet's tube).
- Residual perforation: Treated with myringoplasty.
B) Residual discharge due to: Persistence of the cause: Treated with tonsillectomy
and adenoidectomy.

23
 Acute otitis media in infants and children
Otitis media is more common in infants than in adults because children are more
susceptible to infection than adults due to their low resistance as a result of teething,
gastrointestinal troubles and artificial feeding.
- Causes of A.O.M. is more frequent than in adults:
a) Adenotonsillitis and recurrent upper respiratory tract infections.
b) Milk regurge during suckling enters the Eustachian tube when the child
suckles in the supine position.
c) The Eustachian tube is shorter, more horizontal and wider than in adults.
- Symptoms: Mainly general.
-Fever, vomiting and diarrhea.
-Child cries, restless, moves his head and pulls his ears.
- Signs: The drum is congested. Bulging is late as the drum is thicker and more
oblique than in adults.
- Treatment:
- Antibiotics, analgesics and nasal decongestive drops.
-Myringotomy under general anesthesia is done if not resolved.

- Chronic Otitis Media

- Chronic suppurative otitis media:
1. Tubotympanic (Safe ear).
2. Attico-antral (cholesteatoma)(Unsafe ear).
- Chronic non-Suppurative otitis media:
1. Secretory otitis media (Middle ear effusion or glue ear).
2. Middle ear atelectasis and adhesive otitis media.
3. Tympanosclerosis.
- Chronic Suppurative Otitis Media (C.S.O.M)
Chronic inflammation of the middle ear: causing conductive deafness and discharge
from a perforated drum.

- Clinical types:
1. Tubotympanic disease: Safe ear
It is a safe mucosal affection of Eustachian tube and tympanic cavity. It is due
to inefficient treatment, inadequate drainage and low resistance of the patient
or high virulence of the organism in cases of repeated attacks of acute otitis
media.
2. Attico-antral (Cholesteatoma): Unsafe ear
It is unsafe bony affection of the attic, antrum and bony walls of the mastoid
air cells.

24
 Cholesteatoma:
Cholesteatoma is a bag-like, cystic, foul smelling mass. It is formed of
keratinizing desquamated squamous epithelium, pus, cholesterol crystals and
proteolytic enzymes.
It erodes bone by chemical (proteolytic enzymes) and bacterial action
(secondary infection). The abnormal presence of the squamous epithelium in
the middle ear is either congenital or acquired:
a) Congenital cholesteatoma arises from embryonic epithelial rests in
of the petrous bone. It could be arise at
cerebellopontine angle (CPA) or middle
ear. In CPA, it may present with facial
nerve paralysis, nerve deafness and
vertigo while in the middle ear it leads to
conductive deafness behind an intact
drum.
b) Acquired cholesteatoma may be due to:
- Primary acquired cholesteatoma:
- No previous suppurative otitis media
- Invagination of the pars flaccida into middle ear due to
repeated prolonged Eustachian tube obstruction. The flaccid
part of the drum (weak, no fibrous layer) is sucked into
middle ear and is separated as a sac filled with squamous
epithelium in the attic (attic retraction pocket).
- Secondary acquired cholesteatoma:
Theories:
- Migration of epithelium of the skin of the external canal to the
middle ear through a marginal perforation.
- Metaplasia of the flattened epithelium of the middle ear by
recurrent infection into stratified squamous epithelium..

- Clinical picture:
Signs Safe ear Unsafe ear
1. Deafness Conductive and not severe Conductive and severe
2. Discharge Mucopurulent,profuse,odourless Purulent, scanty, foul odour
3. Perforation Central Marginal or attic
4.Cholesteatoma Not present Peasent

-Investigations:
- X-ray and CT scan of the mastoids.
- Culture and sensitivity test for the discharge.
- Audiological assessment.

- Treatment:
-Tubotympanic type: (Safe type)
Tympanoplasty in done after trials to make the ear dry by conservative
treatment using antibiotics, suction, ear drops and removal of the source of
infection as tonsils and adenoids.

25
 -Atticoantral Cholesteatoma: (Unsafe type)
a) Atticotomy when it is limited to the attic.
b) Modified radical mastoidectomy if it is localized to the attic and antrum.
c) Radical mastoidectomy for extensive cholesteatoma or the presence of
complications.

COMPLICATIONS OF CHRONIC SUPPURATIVE OTITIS MEDIA

I.ACUTE MASTIODITIS
Extension of infection from the inflamed mucosa of middle ear to the bony septa of the
mastoid air cells in the course of suppurative otitis media.
Symptoms:
-Fever and pain, deafness, recurring middle ear discharge.
-A swelling appears behind the ear.
Signs:
-Swelling over the mastoid: forming a postauricular mastoid abscess pushing the auricle
forwards, downwards and outwards.
-Sagging of the posterosuperior meatal wall by swelling edema of the skin of the bony canal
(area related to the mastoid antrum).
-Positive reservoir sign: discharge is profuse mucopurulent and recurs after removal from the
external canal.
-Drum is congested or perforated.

Mastoid abscess

Investigations:
- PTA: Conductive deafness (due to necrosis of ossicles).
-CT scan shows haziness of the mastoid air cells and loss of cell walls.
Treatment:
- I.V antibiotics and analgesics.
-If no improvement after 48 hours cortical mastoidectomy is indicated.

26
II.OTOGENIC LABYRINTHITIS
Progress of the disease and clinical picture:
During the course of otitis media and due to erosion of the lateral semicircular canal by
cholesteatoma, the patient complains of intermittent attacks of vertigo, nausea and vomiting
which is accompanied by deafness and tinnitus. Pressure changes in external auditory canal
produce vertigo and nystagmus (positive fistula sign). The symptoms become worse disabling
the movement of the patient. The patient falls to the opposite side. With progression of the
disease, all symptoms fade away as the sensory cells in the labyrinth become destroyed and
compensation of vertigo occurs from the healthy side.
Treatment:
-Antibiotics, antivertigenous drugs.
-Mastoidectomy for removal of cholesteatma and repair of the fistula.
-In persistent cases, labyrinthectomy to drain the affected labyrinth.

III.OTOGENIC FACIALPARALYSIS
Causes:
1- Acute suppurative otitis media if the bony facial canal is congenitally deficient.
2- Chronic suppurative otitis media due to erosion of the facial canal by
cholesteatoma.

3-Ear surgery injury:

-Cortical or radical mastoidectomy and during stapedectomy
-Long postauricular incision in children where the facial nerve is superficial.
Treatment:
-In acute suppurative otitis media: Antibiotics and myringotomy.
-In chronic suppurative otitis media: Antibiotics, mastoidectomy and decompression of the
facialnerve.
-In surgical injury: The nerve is grafted from the greater auricular nerve, or the lateral
cutaneousnerve of the thigh.

27
Non-Suppurative Otitis Media
- Secretory Otitis Media (Middle ear effusion)
Accumulation of a non-purulent effusion in the middle ear cleft. It may be serous or mucus
(glue). The disease is common in children.
- Causes:
- Eustachian tube pathology due to: allergy, inflammation, adenoids, nasopharyngeal
cancer and cleft palate.
- Unresolved acute otitis media due to inefficient treatment.
- Symptoms:
-Deafness and tinnitus.
-Bubbling sounds in the ears.
- Signs:
1. Commonest cause of conductive hearing loss in children (CHL).
2. Otoscopic examination shows: The drum is intact, but retracted. A fluid level forms
a hair line due to interruption of the fluid by the handle of malleus.
- Diagnosis:
-Tuning fork test: Conductive deafness.
-Pure tone audiometry: Air bone gap (CHL).
-Impedence audiometry: Flat curve (Type B) with absent stapedial reflex.
- Treatment:
-Medical: Nasal drops, antiallergic, steroids and mucus dissolvent.
-Surgical: When medical treatment fails: Myringotomy with fluid aspiration and
insertion of ventilation tubes (Grommet's tube).
- Surgery of the causative factor e.g. removal of adenoids.

- Otosclerosis
It is a heredo-familial disease characterized by conductive deafness due to fixation of the
footplate of the stapes in the oval window by the formation of new spongy bone of greater
thickness, celullarity and vascularity which replaces the normal compact bone of the bony
labyrinth.
- Incidence:
- Deafness usually starts between 20 and 30 years of age.
- Positive family history in more than 50% of the cases.
- Females (pregnancy) are more commonly affected between 20-40 years.
- Bilateral in most cases.
- Symptoms:
-Deafness and tinnitus. Deafness increases during pregnancy.
-Paracusis: The patient hears better in noisy places as the speaker spontaneously raises
his voice.

28
 - Signs:
- Conductive deafness with normal drum and patent Eustachian tube.
- Schwartz's sign: flamingo red color of the drum reflecting dilated blood vessels of
the promontory indicating active disease.
- Cochlear otosclerosis is due to invasion of the cochlea causing sensorineural hearing
loss.
- Investigations:
1. Tuning fork test: conductive deafness in stapedial otosclerosis.
2. Pure tone audiometry:
- Air bone gap with Carharts notch (at 2000Hz).
- Mixed hearing loss in combined otosclerosis (stapedial & cochlear).
- Sensorineural hearing loss in cochlear otosclerosis.
3. Impedance audiometry: restricted curve (As) with absent stapedial reflex due to
fixation of the stapes.
- Treatment:
- Sodium fluride is ineffective, may be used in active stage of the disease.
- Stapedectomy and replacement of the stapes by prosthesis.
- Hearing aid is indicated in severe mixed deafness or if the patient refuses the
operation.

Diseases of The Inner Ear

- Congenital anomalies
- Aplasia: Complete absence of the inner ear.
- Hypoplasia: Incomplete development of the inner ear.
The cochlea is 1.5 turns instead of 2.5 turns.
- Dysplasia: Absence of organ of Corti.
- Clinical picture: Sensorineural hearing loss since birth.
- Investigations:
- CT scan to determine the state of the inner ear.
- ABR to determine the level of hearing.
- Treatment:
-Hearing aids.
-Cochlear implantation.

- Trauma of the inner ear

1. Acoustic trauma
It is an irreversible damage of the cochlear sensory end organ due to exposure to loud
noise.
- Causes:
Acute: like gunshots and blasts.
Chronic: as in factories, airports and disco parties.

29
 - Clinical picture: Sensorineural hearing loss and tinnitus.

- Treatment: Hearing aids.

2- Transverse temporal bone fracture

- Etiology: Due to car accidents or fall from a height. The fracture line is
perpendicular to the long axis of the petrous part of temporal bone.
- Clinical picture: Sensorineural hearing loss, vertigo, tinnitus and facial paralysis.
- Treatment: vestibular sedatives, surgical repair of facial nerve and hearing aids.

- Inflammations of the inner ear

- Labyrithitis:
-Inflammatory labyrinthitis: as a complication of chronic suppurative otitis media.
-Toxic labyrinthitis:
a) Endogenous: Diabetes mellitus, uremia and hypothyroidism.
b) Exogenous: Ototoxic drugs Streptomycin, Neomycin and Salicylates.
- Clinical picture: Deafness, tinnitus and vertigo.
- Treatment: vestibular sedatives and hearing aids.

- Meniere's Disease
Distension of the membranous labyrinth due to increased volume of endolymph of unknown
etiology (Endolymphatic hydrops).It is a common cause of peripheral labyrinthine vertigo
and usually unilateral but may become bilateral.
- Etiology: Endolymphatic hydrops may be due to:
a) Hyper secretion from the stria vascularis
-Local disturbance of salt and water balance causing edema of the
endolymph.
-Auto-immune disturbance of the endolymphatic system.
-Sympathetic over activity leading to allergy of the inner ear causing
edema.
-Vascular disturbance of the inner ear, especially of the stria vascularis.
B) Hypo-absorption of the endolymph may be due to disturbance of the
endolymphatic duct or sac causing interference with its absorption.
- Symptoms:
It is a triad of recurrent sudden attacks of: vertigo, deafness and tinnitus.
Hearing loss and tinnitus are initially reversible (fluctuating) but later on they
become permanent and progressive. The attack is usually accompanied by nausea
and vomiting.
- Signs:
1. Pure tone audiometry: Shows low tone SNHL, later affects all tones.
2. Electronystagmography (ENG) shows hypofunction of the labyrinth.

30
 - Treatment:
Medical:
- Vestibular sedatives: Cinnarzine.
- Labyrinthine vasodilators: Betahistine.
- Labryrinthine decompressants: diuretics and salt restriction.
Surgical: If the medical treatment fails and vertigo persists.
1. If hearing is serviceable:
a) Vestibular neurectomy serving the cochlear nerve.
b) Decompression of the endolymphatic sac.
2. If hearing is not serviceable:
A) Labyrinthectomy: Destruction of the membranous labyrinth
through an opening of the lateral S.C.C.
b) Intratympanic injection of ototoxic drugs (gentamycin)
which are absorbed by the round window to destroy the
labyrinth.

- Benign paroxysmal positional vertigo

It is repeated episodes of positional vertigo as a result of degeneration of the vestibular
sensory end organs. The otoconia are dislodged from their usual position within the utricle
and they migrate over time into one of the semicircular canals (the posterior canal is most
commonly affected due to its anatomical position). The utricle may have been damaged by
head injury, infection, or because of advanced age. It is the commonest cause of vertigo.
- Clinical picture:
-Recurrent sudden attacks of vertigo in certain head positions
-Hearing is normal.
- Investigations:
Electronystagmography: Positional nystagmus.
- Treatment:
-Medical: vestibular sedatives.
-Repositioning procedure (Epley maneuver).

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Facial Nerve Paralysis
- Causes of facial paralysis:
- Central:
Lesions above the nucleus: Upper motor neuron lesion (UMNL): Vascular lesions
(hemorrhage or thrombosis), multiple sclerosis and brain
tumours.

- Peripheral:
Lesions at or below the nucleus: lower motor neuron lesion (LMNL).
1. Intracranial causes:
a) Brainstem lesions as vascular lesions or multiple sclerosis
b) Cerebellopontine angle lesions as acoustic neuroma, meningioma and congenital
cholesteatoma.
2. Cranial causes (Temporal):
a) Idiopathic: Bell’s palsy is the commonest cause.
b) Traumatic: Fracture base, mastoid operations.
c) Inflammatory: otitis media, herpes zoster oticus and malignant otitis externa.
3. Extracranial causes:
a) Parotid gland tumour and its surgery.
b) Cut wounds of the face, birth injury.

- Diagnosis of facial nerve paralysis

Lower motor neuron (LMNL) or upper motor neuron lesion(UMNL):
- In LMNL:
- Upper and lower parts of the face are paralyzed.
- Paralysis of voluntary and emotional muscles.
- No hemiplegia.
- In UMNL:
- The upper part of the face is not paralyzed because it is supplied by pyramidal
fibres from both sides.
- Emotional expressions (smiling and crying) are intact because they are controlled
by extrapyramidal fibres.
- Hemiplegia of the other side is common.

3. Instigations:
a) Radiological: CT scan and MRI for brain and temporal bone.
b) Electrodiagnosis (EMG): To evaluate the condition of the nerve and muscles.

32
 Cranial and extracranial facial nerve

- BELL'S PALSY
(Idiopathic Facial Paralysis)
It is a sudden facial nerve paralysis of unknown etiology. It is the commonest cause of facial
paralysis. It commonly follows exposure to cold air currents.

- Etiology:
-Vascular theory: Edema pressing on the nerve in its bony canal.
-Viral theory: Reactivation of a dormant herpes virus in the geniculate ganglion.

- Clinical picture:
1. Sudden facial paralysis of LMNL (partial or complete).
2. Ear and other cranial nerves are normal.
3. Pain is often present.

- Site of lesion:
At the geniculate ganglion.

- Treatment of Bell's palsy:

- Medical:
Steroids, vasodilators, antiviral (acyclovir), short wave physiotherapy.
- Surgical: (only in cases of permanent disfigurement)
-Hypoglosso-facial or facio-facial anastomosis.
-Tarsorrhaphy to protect the cornea.
-Plastic surgery (facial slings) in late cases with fibrosed muscles.
- Prognosis:
85-90% of the patients recover fully within 6 weeks, while10-15% recover
incompletely. Prognosis is good in incomplete Bell's palsy (95% complete
recovery).

33
Symptoms of Ear Diseases
- DEAFNESS
- Types:
-Conductive deafness. (CHL)
-Perceptive deafness (Sensorineural Hearing Loss) (SNHL).
-Mixed (conductive and perceptive deafness).
-Functional (psychogenic and malingering) deafness.

- Conductive Deafness
Conductive deafness is caused by diseases of the external or middle ear.
A) External ear:
1. Congenital: Atresia.
2. Wax: Accumulation (commonest cause)
3. Foreign body: Impaction.
4. Inflammatory: Otitis externa, big furuncle and fungal mass.
B) Middle ear:
A) Drum: Perforation.
b) Trauma: - Haemotympanum (fracture base)
- Otitic barotraumas
c) Inflammatory: Acute and chronic suppurative otitis media
- Non-suppurative otitis media. .
-Ossicles:
a) Congenital: Absence or fixation.
b) Trauma: Dislocation.
c) Inflammation: Necrosis.
d) Otosclerosis.
-Eustachian tube:
a) Inflammation: Salpingitis.
b) Allergy: Causing edema.
c) Mechanical obstruction: By adenoids or nasopharyngeal tumours.

- Perceptive (Sensorineural) Deafness

Sensorineural hearing loss is caused by diseases of the inner ear, cochlear nerve or brain.
A. Cochlear lesions:
1- Congenital:
a) Genetic: Consanguinity (marriage of relatives).
b) Prenatal: German measles affecting the mother during the first trimester of
pregnancy and intake of ototoxic drugs.
2- Trauma:
a) Head injuries: Fracture skull base.
b) Acoustic trauma: Acute as blasts or chronic as in factories due to long
exposure to loud noise.

34
 3- Inflammatory: (labyrinthitis)
a) Viral: Measles, mumps and influenza.
b) Bacterial: Meningitis, typhoid, tuberculosis, syphilis and complications of
chronic suppurative otitis media.
4- Toxic: (ototoxicity)
a) Endogenous: Diabetes mellitus, uraemia and hypothyroidism.
b) Exogenous: Streptomycin, neomycin, kanamycin and quinine.
5- Vascular:
Spasm, hemorrhage or thrombosis of the internal auditory artery.
6- Miscellaneous:
1. Senile deafness (Presbycusis) is the most common cause of SNHL in adults.
2. Menière’s disease and cochlear otosclerosis
B. Cochlear nerve lesions:
Tumours: acoustic neuroma.
C. Brain lesions:
1- Vascular: vertebrobasilar insufficiency.
2- Tumours.
3- Multiple sclerosis.
4- Epilepsy.

- Deaf-Mutism
A deaf infant becomes a dumb child because he does not hear; so he will not develop
speech. This is either due to congenital mal-development, or acquired diseases such as
meningitis, measles or mumps.
It is treated by a powerful hearing aid, cochlear implantation, lip reading and auditory
training.

- Ear Discharge (Otorrhoea)

a) Watery discharge (C.S.F.):
- Fracture skull base.
- Surgical trauma if the dura is injured, perilymph fistula.

b) Bloody discharge:
1. Trauma:
- Fracture skull base.
- Injury of the external ear or traumatic drum perforation.
2. Inflammatory:
- Acute otitis media when drum perforates.
- Chronic otitis media with granulations.

c) Mucoid or mucopurulent discharge:

Chronic suppurative otitis media (safe type).

d) Purulent discharge:
Furunculosis, Cholesteatoma (offensive due to bone osteitis).
35
- Pain in The Ear (Earache)
- Causes:
- Local in the ear:
1. Inflammatory: acute otitis externa, malignant otitis externa and acute otitis media
before perforation.
2. Traumatic conditions of the external and middle ear.
3. Cranial and intracranial complications of chronic otitis media.
- Referred pain:
From diseased organs sharing the same nerve supply with the ear.
- 5th cranial nerve:
1. Sinusitis.
2. Post adenoidectomy.
3. Impacted wisdom tooth and dental caries.
4. Temporomandibular joint arthritis.
5. Salivary calculi.
th
- 9 cranial nerve:
1. Tongue, pharyngeal ulcers and cancer.
2. Acute tonsillitis and Quinsy.
3. Post tonsillectomy.
- 10th cranial nerve:
Tuberculosis of the larynx or cancer larynx.
- 2 and 3rd cervical nerves:
nd

1- Cervical disc lesion (spondylosis).

2- Myositis of neck muscles.

36
Operations of The Ear
- Myringotomy
It is a surgical incision of the drum in the postero-inferior segment to drain the middle ear.

- Indications:
a) Acute suppurative otitis media: (ASOM)
1. ASOM with bulging drum about to perforate.
2. ASOM in children not responding to medical treatment.
3. ASOM with cranial or intracranial complications.
b) Secretory otitis media: To drain the middle ear and to insert ventilation tubes
(Grommet's tube).
c) Otitic barotrauma: To drain fluid out and to let air into the middle ear.

- Advantages:
- Restores normal hearing in cases of secretory otitis media.
- Prevents adhesive otitis media.

- Complications:
- Dislocation of incudo-stapedial joint.
- Hemorrhage from a congenitally high uncovered jugular bulb.

37
- Cortical Mastoid Operation
The operation is performed to remove all the diseased mastoid cells to obtain drainage and
eradicate infection.

- Indications:
- Acute mastoiditis and mastoid abscess after failure of medical treatment.

- Complications:
Injury of: Facial nerve, lateral sinus, dura mater.

Cortical mastoidectomy

38
- Radical Mastoid Operation
Removal of the mastoid air cells together with the posterior bony meatal wall and the
middle ear contents except the stapes. The operation is done to give a dry safe ear and
prevent complications with no attempts of reconstruction of the hearing mechanism.

- Indications:
1. Chronic suppurative otitis media with:
a) Cholesteatoma.
b) Cranial or intracranial complications.
2. Tumours of the middle ear.

- Complications:
1. Injury of the facial nerve, lateral sinus, dura and inner ear.
2. Infection leading to labyrinthitis or meningitis.

Radical mastoidectomy

- Tympanoplasty
A plastic operation designed to eradicate infection in the middle ear cleft and reconstruct
hearing mechanism.

- Indications:
Tubotympanic type of C.S.O.M with conductive deafness.
- Grafting the drum perforation by Temporalis fascia, or perichondrium or cartilage
(Myringoplasty).
- Reconstruction of ossicles (Ossiculoplasty)

- Complications:
1. Injury of the facial nerve, lateral sinus, dura and inner ear.
2. Infection leading to labyrinthitis or meningitis.

39
Ossiculoplasty

40
- Stapedectomy
Surgical treatment of otosclerosis by replacement of the fixed stapes by a prosthesis.
(Teflon piston, Teflon wire)

- Indication:In cases of otosclerosis with large air bone gap (30-60 dB).
- Contraindications:
- Small air bone gap.
- Cochlear involvement.
- If the affected ear in the only hearing ear.

- Complications:
1. Injury of facial nerve (if the canal is dehiscent).
2. Failure: Persistent conductive deafness (slipped prosthesis).
3. Postoperative vertigo and SNHL (perilymph fistula).

Stapedectomy

41
Anatomy of the Nose & Paranasal Sinuses
The nose is divided into external nose and nasal cavity.

External Nose
- Its framework is formed by bones and cartilages, which are covered by skin.
- The bones include :
• Nasal bones (the bridge of the nose)
• Frontal processes of maxillae.
- The cartilages includes :
• Upper nasal cartilages (Rt., Lt.)
• Lower nasal cartilages (Rt., Lt.)
• Anterior border of the septal cartilage : it projects between the upper and lower nasal
cartilages to support them.
• Small alar cartilages : lateral to the anterior naris (it is the ala of the nose).

External nose

42
Nasal Cavity:

Boundaries of the Nasal Cavity:

(1) The Roof : Formed by the 2 nasal bones, cribriform plate of the ethmoid bone and the
inferior surface of the body of the sphenoid.
(2) The Floor : Is formed by the hard palate
(3) The Medial Wall (the nasal septum) :
- It is formed by 3 structures :
• Perpendicular plate of ethmoid : Above
• Vomer : Below and behind.
• Septal cartilage : Below and anterior.

(4) The Lateral Wall :

- It is formed: mainly by the medial wall of maxilla and shows three bony projections called
conchae or turbinates covering the three meatuses and named after them:

1. Superior meatus: drains the posterior ethmoidal sinuses.

2. Middle meatus: (osteomeatal complex), drains the:
a) Frontal sinus anteriorly.
b) Maxillary sinus posteriorly.
c) Anterior and middle ethmoidal sinuses in the middle.
3. Inferior meatus: drains the naso-lacrimal duct.
Spheno-ethmoidal recess: is a recess above the superior
turbinate and drains the sphenoidal sinus.

43
Arterial Blood Supply :
1- Anterior ethmoidal and posterior ethmoidal arteries (of ophthalmic artery).
2- Sphenopalatine, greater palatine and anterior superior alveolar arteries (of maxillary artery).

Nerve supply :
1- Anterior ethmoidal nerve (of ophthalmic nerve).
2- Nasal + greater palatine branches of the pterygopalatine ganglion (maxillary nerve)
3- Anterior superior alveolar nerve (of maxillary n).

44
Venous Drainage of the Nasal Cavity :
Veins form a plexus beneath the mucous membrane. It is drained anteriorly into the facial V.
and posteriorly into the pterygoid venous plexus.

Clinical Anatomy :
• On the lower part of the nasal septum, there is anastomosis between the septal
branches of the facial and spheno-palatine arteries. This is known as Little’s area
which is a common site of bleeding from the nose (epistaxis).
• The autonomic nerve supply reaches the nasal cavity through the nasal branches
derived from the pterygopalatine ganglion. The sympathetic supply is responsible for
the nasal congestion and the parasympathetic for the mucoid discharge seen in the
common cold and allergic rhinitis.

Lateral wall of the nasal cavity

Histology of the Nasal Cavities

The nasal cavities can be subdivided into two regions: the respiratory [non-olfactory]
and the olfactory regions.

• Respiratory region: consists of

• Vestibule: The entrance of nasal cavity lined by skin with short coarse hairs
• 2 Nasal cavities separated by nasal septum
Middle and inferior conchae are covered by
o Respiratory epithelium
(pseudostratified columnar ciliated epithelium
with goblet cells)
o Underling a highly vascular C.T. that contains
mucous and serous glands → warming,
moisture and catching dust.

45
 [Superior conchae is covered by olfactory epithelium]

Olfactory region: Extends over superior

conchae and about 1 cm
down nasal septum. It is
covered by olfactory
epithelium resting on CT
corium.

• Olfactory epithelium:
Tall pseudostratified columnar epithelium
(no cilia, no goblet cells) composed of 3 types of cells;

1. Olfactory cells (neurons):

• Bipolar neurons that respond to odors.
• A single dendrite extends to the surface to form a swelling, the olfactory vesicle,
from which stereocilia extend over the surface to increase surface area exposed to
odours.
• The axon passes to CT corium to form olfactory nerve.

2. Supporting (sustentacular) cells :

• Tall columnar cells.
• Narrow base wide apex.
• Microvilli on the apex.
• Nucleus oval near apex.
• Cytoplasm contains yellow pigment
that gives the olfactory mucosa
yellow color.
• Support olfactory cells.

3. Basal cells :
• Short pyramidal cells.
• Nucleus rounded near base.
• Cytoplasm basophilic.
Serve as reserve cells for the olfactory and supporting cells.

• The CT corium (lamina propria): connective tissue layer contains Bowman’s glands:
• Serous glands.
• Tubuloalveolar.
• Their secretion dissolves odorous gases to stimulate the cilia.

46
Physiology of Smell = Olfaction
- It is important in regulating behavior in all animals
- It is weak in man compared to animals
- It determines flavors of food
- It is essential for GIT functions
- It has a role ill sexual behavior
- Smell & taste trigger long term memory

« Olfactory receptors:
- Are located in specialized nasal mucosa called olfactory mucosa which is located in
superior nasal concha (need for sniffing)
- They are bipolar nerve cells, in between, there are supporting cells
- The distal ends of olfactory cells form hairs covered by:
- Mucus &
- their axons form the olfactory nerve

« Properties of olfactory receptors:

1- They are distant receptors
2- They are chemoreceptors & their hairs contain odorant binding proteins (OBP)
3- They are highly sensitive
4- They can discriminate high number of odorants (10000)
5- Discrimination of intensity is tow
6- Adaptation is very rapid
7- They generate receptor potential on stimulation
8- There is no stimulus specificity ie a receptor can respond to many odours
9- Electroolfactrogram: It is the electrical response recorded from olfactory mucosa on
stimulation

« Odorant material must be:

1- Volatile
2- Slightly H2O soluble, dissolve in mucus
3- Slightly lipid soluble to dissolve in the lipid membrane of olfactory cells

« Stimulation of olfactory receptors:

1- The membrane of cilia of hair cells (receptors) contains odorant binding proteins
(OBP).
2- Odorous material binds to OBP → this complex activates G-protein → activates
adenyl cyclase → activates cAMP → opens Na+ channels → leading to
depolarization.

47
Paranasal air sinuses

The Frontal Sinus :

Site : It lies between the outer and inner tables of the frontal bone
Drainage of the sinus: By the fronto-nasal duct into the anterior end of the hiatus
semilunaris..

The Ethmoidal Sinuses :

Site: They are anterior, middle and posterior groups of intercommunicating air cells
which lie within the ethmoidal labyrinth .
Drainage of the sinuses :
* Anterior group: Opens by the ethmoidal infundibulum into the anterior end of
the hiatus semilunaris.
* Middle group: Bulge the bulla ethmoidalis and opens on its upper part.
* Posterior group: Open in the superior meatus.

Sphenoidal Sinus :
Site : Within the body of the sphenoid, separated from the opposite by a septum.
Relations :
* Superiorly: Is related to optic chiasma and the pituitary gland in the sella turcica
* On either side: It is related to the cavernous sinus with its contents.
* Inferiorly: Roof of the nasal cavity.
Drainage of the sinus : Into the spheno-ethmoidal recess of the nasal cavity.

The Maxillary Sinus :

Site : It is a pyramidal space within the body of the maxilla.
Relations: Its floor is formed by the alveolar process of maxilla. It is about 1.25 cm
below the floor of the nasal cavity. The upper premolars and molars project
into the floor of the sinus in the form of conical projections. Infection of
these teeth may spread into the sinus.
Drainage of the sinus: By 2 openings into the posterior part of hiatus semilunaris

48
Examinations of The Nose
- History of nasal symptoms:
1- Obstruction.
2- Nasal discharge.
3- Headache.
4- Sneezing.
5- Affection of olfaction.

- External examination:
For deformity, swelling or tenderness.
- Anterior rhinoscopy:
By nasal speculum: To inspect the septum, middle and inferior turbinates.
- Posterior rhinoscopy:
By the posterior nasal mirror: To inspect the posterior choanae, Eustachian
tube openings and to examine the nasopharynx
for swellings or adenoids.
- Nasal endoscopy:
Rigid nasal endoscopy and flexible nasopharyngoscopy help to evaluate
inaccessible areas of nasal cavity.
- Radiology:
- Plain X- ray: Lateral and occipitomental veiws.
- CT scan: For nose and paranasal sinuses: Coronal and axial views; for
opacities, fluid level, sinusitis, polypi, fracture nasal bone and tumours.
- Culture and sensitivity test: Of the nasal discharge.
- Biopsy: from nasal masses.

49
Diseases of The Nose
- Congenital Anomalies
- Choanal atresia
Atresia of the posterior nares due to persistence of bucconasal membrane.

- Symptoms and signs: it may be bony or membranous atresia.

A) Unilateral: May not be noticed until late in childhood.
1. Unilateral nasal obstruction.
2. Unilateral glue-like discharge.
B) Bilateral:
1. Asphyxia in newly born as oral respiration is not yet developed.
2. Respiratory distress and difficult suckling in infants.

- Diagnosis:
- Mirror test: No condensation of air from anterior nares on cold mirror.
- A rubber catheter cannot pass to the nasopharynx.
- Radio-opaque material cannot be detected in nasopharynx in X- ray.
- CT scan to determine the thickness of the bony atresia.

- Treatment:
1. In emergency cases of bilateral atresia: Intubation or oral airway.
2. Trans-nasal endoscopic removal: For unilateral or bilateral cases.
3. Trans-palatal excision: Old method or if endoscopic removal fails.

- Trauma of The Nose

- Foreign Body
Usually children insert foreign bodies in their nose.
Commonly beans, papers, gums, buttons or animate foreign bodies.
RHINOLITH: Calcium and magnesium salts are precipitated from the nasal secretions
on a foreign body, blood clot, stagnant pus or mucus.

- Clinical picture:
-Unilateral fetid purulent nasal discharge and obstruction.
-Foreign body is seen by anterior rhinoscopy or felt by a probe.

Treatment:
Removal by hooks or forceps or better done under general anaesthesia.

- Fracture Nasal Bones

- Causes:
Trauma as in blows, boxing and falls.(commonest fractured bone in body)

- Types:
- Type 1: Due to anterior trauma, leading to depressed fracture.

50
 - Type 2: Due to lateral trauma displacing nasal bone laterally (C shaped fracture).
- Type 3: Due to major trauma leading to marked deformity involving the ethmoids,
nasal septum and nasal bones.

- Clinical picture:
1- Deformity, crepitus and tenderness of nasal bones.
2- Surgical emphysema, edema and hematoma (black eye).
3- Epistaxis due to nasal mucosal tear.
4- Nasal obstruction due to deviated septum or hematoma.
X-ray: lateral view shows the fracture line.

- Treatment:
1- Immediate reduction by Walsham’s forceps within 6 hours before edema forms.
2- Delayed reduction after 7 days when edema subsides under anesthesia..
3- Permanent deformity: Rhinoplasty.

- Cerebrospinal Rhinorrhoea
(Leak of CSF from the nose)

- Origin: Cribriform plate of ethmoid, frontal or sphenoid sinuses.

- Causes:
1. Congenital dehiscence.
2. Traumatic: fracture skull base or during endoscopic sinus surgery.
3. Inflammatory: osteomylitis of frontal and ethmoid sinus.
4. Neoplastic: malignant tumours of frontal, ethmoid and sphenoid sinus.
5. Idiopathic: hypertension and obesity.

- Clinical picture:
1. Unilateral dripping of clear, tasteless, watery nasal discharge.
2. Dripping increases by coughing, straining or tilting head forward.
3. Dries soft on the handkerchief (no mucous or proteins content).

- Investigations:
- Analysis of discharge: high sugar content and contains B2 Transferrin.
- CT scan with intrathecal radioactive dye to detect the site of leakage.

Treatment:
1- Conservative: The defect may heal spontaneously
- Bed rest in semi-setting position.
- Antibiotics to prevent meningitis.
- Avoid straining, nose blowing, coughing and lower blood pressure.
3-Endoscopic repair: By septal or middle turbinate flaps with injection of Flourescin
intrathecally to detect the site of the defect during closure.

51
- Oro-Antral Fistula (Oro-Maxillary Fistula)
It is s fistula communicating the oral cavity with the maxillary sinus.

- Causes:
1. Trauma: -After extraction of the 2nd premolar or 1st molar tooth.
-After excision of dental and dentigerous cysts.
-After radical antrum operation, if the sublabial incision does not close.
2. Complicating: Osteomyelitis or cancer maxilla.

- Clinical picture
- Unilateral regurgitation of fluid through the nose.
- Unilateral fetid nasal discharge (sinusitis of dental origin).
- A probe can pass through the fistula to the sinus.

- Investigations: CT scan for PNS to show the site of fistula.

- Treatment:
Surgical: Closure of the fistula using sublabial or buccal mucosa after effective
drainage of the maxillary sinus.

ACUTE INFLAMMATIONS OF THE NOSE

- Furunculosis of The Vestibule
It is a staphylococcus infection of a hair follicle in the nasal vestibule.

- Clinical picture:
- Tender and painful swelling of the nasal vestibule.
- Recurrent in diabetic patient.

Complications:
Cavernous sinus thrombosis: due to extension of infection through the facial vein or
ophthalmic vein, especially if the furuncle is squeezed or incised.

Treatment:
1- Antibiotics.
2- Test for diabetes in recurrent cases.

- Acute Non Specific Rhinitis (Common cold)

It is a viral (rhinovirus) infection usually followed by secondary bacterial infection (strept,
staph and Haemophilus influenza).

- Predisposing factors:
Low resistance, bad hygiene and overcrowding.

- Stages and clinical picture:

1- Ischaemia: Dryness, sneezing and burning sensation.
2- Hyperaemia: Nasal obstruction, watery discharge and fever.
3- Secondary infection: Nasal obstruction, purulent discharge and fever.
4- Resolution: Occurs in 4-7 days.

52
 - Complications:
Sinusitis, acute otitis media, pharyngitis and bronchitis.

- Treatment:
Rest, antiallergics, analgesics and antibiotics.

Rhinovirus
Rhinoviruses are the most common viral infective agents in humans ,the causative agent
of the common cold. There are over 110 serologic virus types which explain repeated
infection of this disease.

Transmission and epidemiology:

a- Aerosols of respiratory droplets.
b- From contaminated surfaces.

Incubation period:1-2days. The patient is most infective during the early symptoms
of sneezing, coughing and runny nose.

Pathogenesis: The primary route of entry for rhinoviruses is the upper respiratory tract.
There is no viremia. Type specific immunity is by local Ig A.

Rhinoviruses rarely cause lower respiratory tract disease probably because they grow
poorly at 37°C.Secondary bacterial infection may cause otitis media, sinusitis,
bronchitis and bronchopneumonia especially in children.
Vaccine: There are no vaccines as there is no cross-protection between the 110
serotypes

CHRONIC INFLAMMATIONS OF THE NOSE

- CHRONIC NON-SPECIFIC RIIINITIS

- Hypertrophic Rhinitis
Hypertrophy of the nasal mucosa, commonly affecting the turbinates.
- Causes:
- Recurrent acute rhinitis, repeated sinusitis, adenoiditis, deviated nasal septum and
allergic rhinitis.
- Rhinitis medicamentoza: excessive usage of vasoconstrictor nose drops.
- Clinical picture
1- Nasal obstruction and nasal discharge.
2- Hypertrophy of the nasal mucosa especially of the inferior turbinates.
- Treatment:
To reduce the inferior turbinates size by: Partial turbinectomy, submucosal
diathermy, or laser turbinectomy.

53
 - Atrophic rhinitis
Chronic non specific inflammation characterized by atrophy of the nasal mucosa and
underlying bone.
- Etiology:
- Primary atrophic rhinitis: Unknown cause and could be due to;
1- Hormonal: Oestrogen deficiency in females at puberty.
2- Infection: By Klebsiella ozaena.
3- Autoimmune.
4- Vitamin A and iron deficiency.
5- Autonomic imbalance with sympathetic over-activity.
- Secondary atrophic rhinitis:
1- Deviated nasal septum in the wider side.
2-Traumatic: Excessive partial turbinectomy.
3-Inflammatory: Rhinoscleroma, syphilis and lupus.
4-Iatrogenic: Post irradiation for malignant disease.
- Pathology:
Peri-arterial fibrosis and endarteritis cause degeneration of the epithelial
ceromucinous glands leading to formation of thick crusts in the nose which become
secondary infected. The turbinates mucosa and bone are atrophied and the airway is
widened.
- Clinical picture: Wide nasal cavity (roomy nose) with:
1. Nasal obstruction due to crusts and atrophy of sensory nerves.
2. Crusts with foul smelling discharge due to secondary infection.
3. Anosmia due to atrophy of olfactory mucosa.
4. Epistaxis due to separation of crusts.
- Treatment:
Medical:
- Alkaline nasal lotion to remove crusts.
- Menthol paraffin nose drops: soften the crusts and overcome foul smell.
Surgical:
- Partial closure of one nostril for one year to prevent drying effect of air.
- Submucosal insertion of fat, cartilage or Teflon in septum and nasal floor to
reduce the caliber of the airway.

- Chronic specific rhinitis (Granulomas of the nose)

Rhinoscleroma
Chronic specific inflammation of the nose caused by Klebsiella rhinoscleromatous
(gram –ve Frisch bacilli). It is common in Egypt and is endemic in some governorates
(Sharkyia, Dakahlyia and Menophyia).
- Pathology: Submucosal infiltration by granulation tissue characterized by:
-Mikulicz cells: Large foamy cells containing the bacilli (diagnostic).
-Russel bodies: Plasma cells with hyaline degeneration.

54
 - Clinical picture: Three stages
A) Catarrhal (atrophic) stage: As it likes prolonged acute non specific rhinitis with symptoms
as nasal obstruction, discharge and crustations.
b) Granulomatous (active) stage: Bilateral reddish, non ulcerating nodules at the
mucocutaneous junction between the nasal cavity and the skin in the vestibule. They coalesce
to form a soft and red tumour like mass filling the nasal cavity and may cause external
deformity. The mass may extend to the pharynx, larynx and the lacrimal apparatus.
c) Fibrotic (sclerotic) stage: Extensive fibrosis and adhesions leading to nasal obstruction and
deformity.
- Investigations:
- Culture of the discharge: Frisch bacilli.
- Biopsy and histopathology: Mikulicz cells and Russel bodies.
- Treatment:
a) Medical:
- Streptomycin one gram daily for 6 weeks (ototoxic and nephrotoxic).
- Rifampicin 300 mg two times daily for 6 weeks.
b) Surgical: Debulking of the mass and reconstruction for nasal deformity.

55
Diseases of the paranasal sinuses
- Acute Sinusitis
An acute inflammation of the mucosal lining of the paranasal sinuses.
a) Nasal causes:
1. Acute rhinitis of influenza.
2. Foreign body.
3. Nasal pack.
4. Diving and swimming.
b) Dental causes:
Infection and extraction of the second premolar or first molar tooth causing oro-
maxillary fistula.
c) Traumatic causes:
1. Fractured maxilla.
2. Foreign body in the sinus.

- Predisposing factors:
a) General: Low resistance, bad hygiene, overcrowding.
b) Local: Nasal obstruction by deviated septum, polypi or adenoids in children
causing retention of secretions and infection.

- Pathology:
The inflammatory changes of the sinus mucosa include; hyperemia, edema, cellular
infiltration, increased mucous production, serous and purulent exudation.

- Clinical picture:
- General: Fever, headache, malaise and anorexia.
- Local: Nasal obstruction, mucopurulent discharge; fetid in dental cases.
Headache, affection of smell and pain over the affected sinus. It increases
with straining or coughing:
a) In maxillary sinusitis: Pain on the cheek and is referred to the teeth
or ear. Cacosmia (smell of bad odour) occurs
in sinusitis of dental origin.
b) In frontal sinusitis: Periodic pain over the forehead. It starts after
arising from bed and subsides two to three hours
later. It is a vacuum headache (negative
pressure) due to absorption of air caused by
obstruction of the fronto-nasal duct.
c) In ethmoidal sinusitis: Pain on the nasal bones between the eyes.
Orbital complications are common due to
thin lamina paparycea esp. in children.
d) In sphenoidal sinusitis: Pain is occipital and behind the eyes.
- When infection spread to all sinuses it is called pansinusitis.

56
 - Diagnosis:
1- X-ray sinus and CT scan shows thickened mucosa or fluid level.
2- Nasal endoscopy shows pus in the middle meatus.

- Treatment:
Medical: Antibiotics, antiallergics and analgesics.
Surgical: Is required in the acute stage if:
-The above treatment fails or complications appear.
-Functional endoscopic sinus surgery (FESS) to drain the affected sinus.

- Chronic Sinusitis
- Etiology:
Recurrent attacks of acute sinusitis due to inefficient treatment, inadequate drainage,
and low resistance of the patient or persistence of the cause of obstruction as deviated
septum, polypi or adenoids in children.

- Pathology: Hypertrophic, atrophic, allergic or mixed.

- Symptoms:
1- Symptoms of sinusitis:
a) Nasal obstruction.
b) Nasal discharge which is fetid in dental cases.
c) Headache which is increased by straining
d) Smell affection and coughing.
2- Symptoms of descending infections: Otitis media, laryngitis and pharyngitis.
3- Symptoms of septic focus: Headache, arthritis.... etc.

The sinus headache is deep and dull. It increases by straining or by movement of the
head. It appears over the affected sinus and is periodic in frontal sinusitis.

- Signs:
1- Tenderness over the affected sinus.
2- Congestion and pus in the middle meatus; seen by anterior rhinoscopy or nasal
endoscopy.

- Radiology:
Plain X-ray and CT scan for paranasal sinuses shows thickened mucosa of the sinuses
and the middle meatus (osteo-meatal complex).

- Treatment:
- Medical: As in acute sinusitis and it is of little value.
- Surgical: Functional endoscopic sinus surgery (FESS).

57
- Fungal sinusitis
Recently, there is increasing incidence of fungal sinusitis (7-10% of cases of sinusitis).

Causative organism: Aspergillus is the commonest.

A) Invasive fungal sinusitis: Occurs in immunocopromized patients (elderly, diabetic,
AIDS and patients receiving immunosuppressive
therapy).
- Clinical picture: (acute fulminating) rapidly extending to the orbit or
intracranially.
- Investigations: CT scan shows unilateral opacity in most of the sinuses
extending beyond the sinuses borders.
- Treatment: Surgical debulking of necrotic tissues and bone by endoscopic
sinus surgery and antifungal medication.
b) Noninvasive fungal sinusitis: Is either
1-Mycetoma (fungal ball): Accumulation of fungal hyphae within the sinus
with minimal mucosal reaction.
2-Allergic: Allergic reaction of sinus mucosa with specific fungus. It is
common in atopic patients, representing as unilateral nasal polypi.
- Investigations: CT scan shows bilateral sinus mass with focal hypodense
spots (calcifications).
- Treatment: Endoscopic removal with systemic and local steroids to prevent
recurrence.

Aspergillus are hyphae, when present in a mass it is called mycelia. The most common
species among paranasal sinus infections associated with aspergillosis is A.
fumigatus.

Pathogenesis:
Aspergillus can cause infection especially in immunocompromised individuals such
as diabetics .They may cause otomycosis, nasal sinusitis, and respiratory allergic
reactions. The infection occurs after inhalation of spores is generally called
aspergillosis, the most common forms of which are:
1- Aspergillosis of the ear canal (otomycosis) causes itching.
2- Invasive aspergillosis: develops mainly in immuno-compromised individuals,
affecting the deeper tissues.
3- Aflatoxin produced by Aspergillus flavus causing liver damage and cancer.

Laboratory diagnosis: Specimen: ear discharge, sputum, bronchial wash, and tissue
biopsies.

58
 COMPLICATIONS OF SUPPURATIVE SINUSITIS
I. Orbital cellulitis:
It is the commonest complication of sinusitis especially in children as a result of ethmoiditis.
Inflammatory oedema of lid: The upper lid is swollen in frontal, lower lid in maxillary, and
both upper and lower lids in ethmoid sinusitis.
Orbital cellulitis: When pus breaks through the periosteum, it spreads between the orbital fat,
extra-ocular muscles, vessels and nerves. Clinical features will include oedema of lids,
exophthalmos, chemosis of conjunctiva and restricted movements of the eye ball. Vision is
affected causing partial or total loss which is sometimes permanent. Orbital cellulitis is
potentially dangerous because of the risk of meningitis and cavernous sinus thrombosis.
Diagnosis:
CT scan for paranasal sinuses, coronal and axial cuts.
Treatment:
-Orbital cellulitis: Massive Antibiotics.
-Orbital abscess: surgical drainage of the orbit and the sinuses (FESS or external fronto-
ethmoidectomy operation).
II. Cranial complications:
Osteomylitis:
Osteomylitis of frontal bone (common) and maxillary bone as a result of frontal and maxillary
sinusitis.
-Frontal sinus: forehead fluctuant swelling subperiosteal abscess (Pott’s puffy tumour).
-Maxillary sinus: maxillary fluctuant swelling.
Diagnosis: CT scan for PNS.
Treatment:
-Medical: Massive antibiotics.
-Surgical: Endoscopic or external drainage of the infected sinus (FESS).
III. Intracranial complications:
Cavernous sinus thrombosis:
Clinical picture:
Ptosis , chemosis, proptosis, opthalmoplegia and papilloedema.
Treatment:
-Massive antibiotics, anticoagulants, cortisone and flagyl.
-Surgical drainage of the sinus infection.
IV. General complications: Symptoms of septic focus as arthritis and nephritis.

59
Nasal Allergy
Is an antigen-antibody IgE reaction in the nasal mucosa which releases histamine causing
vasodilatation, edema and exudation with eosinophilic infiltration.

- Types:
1. Seasonal: occurs in seasons e.g. hay fever in spring.
2. Perennial: non seasonal all over the year.

- Predisposing factors:
- Hereditary: Atopy is the inherited tendency for allergy.
- Physical changes of the humidity of inspired air.
- Infection may alter the permeability of nasal mucosa to antigens.

- Precipitating factors:
- Inhalants: Dust, pollens.
- Ingestants: Egg, fish or milk.
- Injectants: Penicillin or insulin.
- Infectants: Bacterial.
- Contactants: Powder, sprays.
- Physical: Cold or heat.

- Symptoms:
1- Intermittent watery nasal obstruction.
2- Itching.
3- Sneezing.
4- Headache.

- Signs:
1- Pale or blue edematous mucosa.
2- Polypi in the ethmoidal region may form.

- Investigations:
1- Skin tests for several antigens to detect the causative antigen.
2- Eosinophilia in blood and nasal secretions.

- Treatment:
a) Prophylaxis: Avoid the antigens (most important).
b) Medical: Antiallergics, steroids (local or systemic).
-Desensitization by injection of repeated doses of the antigen.
c) Surgical: To relieve nasal obstruction.
- FESS for polypectomy or partial turbinectomy

60
Vasomotor rhinitis
The term denotes combination of nasal obstruction, watery rhinorrhea and sneezing
without an allergic factor.

- Etiology: Is unknown but may be due to an imbalance between sympathetic and

parasympathetic supply of the nasal mucosa with predominance of the
parasympathetic activity.

- Predisposing factors: As in allergic rhinitis.

- Clinical picture and diagnosis:
- Same as in allergic rhinitis but without itching.
- Negative skin test, normal eosinophils in blood and nasal secretions and normal IgE
in blood and nasal secretions.

- Treatment:
a) Prophylaxis: Avoidance of predisposing factors.
b) Medical: Antihistaminics, steroids (local or systemic).
c) Surgical: To relieve nasal obstruction.
- FESS for polypectomy or partial turbinectomy.
- Endoscopic vidian neurectomy: Cutting the nerve leads to
vasoconstriction of the nose.

61
Diseases Of The Nasal Septum
- Deviated Septum
It is a significant deviation of the septum causing nasal obstruction.

- Causes:
1- Trauma to the nose (commonest).
2- Rapid development of the septum more than the surrounding bones.

- Types:
1- C or S-shaped deviation.
2- Deviation with spurs or crests at the junction of cartilage and bone.
3- Deviation with anterior dislocation from columella.

- Clinical picture:
- Unilateral nasal obstruction in C- shaped or bilateral in S-shaped.
- Nasal discharge: When it causes sinusitis.
- Vacuum headache: Due to obstruction of the fronto-nasal duct.
- Descending infection: Causing pharyngitis and laryngitis.
- Atrophic rhinitis or hypertrophy of turbinates in the wider side.

- Treatment: Submucous resection (SMR) of the septum or Septoplasty.

- Perforation of The Septum

- Anterior perforation in the cartilagenous part causes:
1- Trauma: After S.M.R (commonest) or cautery for epistaxis.
2- Inflammation: After septal haematoma and abscess.

- Posterior perforation in the bony part causes:

1. Syphilis.
2. Malignancy.

- Treatment:
1- Surgical closure with mucosal flaps is usually unsatisfactory.
2- Closure by a button like obturator.

- Haematoma of The Septum

Collection of blood beneath the mucoperichondrium and mucoperiostium of the septum.
Causes: Surgical after SMR or trauma to the nose.

- Clinical picture:
Bilateral nasal obstruction and swelling on both sides of the septum.

- Treatment:
1- Incision and evacuation.
2- Anterior nasal packing to prevent recollection.
3- Antibiotics.
62
- Abscess of The Septum
Collection of pus beneath the mucoperichondrium and mucoperiostium of the septum.
Usually it is secondary to septal haematoma due to infection.

- Clinical picture:
1- Nasal obstruction.
2- Throbbing pain and tenderness over the bridge of the nose.
3- Fever and headache.

- Complications:
1- Necrosis of cartilage and its perforation.
2- Depression of the cartilaginous dorsum in the supratip area.
3- Cavernous sinus thrombosis.

- Treatment:
1- Incision and drainage.
2- Antibiotics.

Nasal Polypi
Pedunculated, edematous mucosa of the nose or paranasal sinuses. It occurs in any sinus
but commonly in the ethmoidal region due to sagging of the mucosa by accumulated
allergic transudates in the lax submucosa.

- Types and causes:

1- Allergic rhinitis.
2- Vasomotor rhinitis.
3- Inflammatory: Ethmoidal polyposis, antrochoanal polyp.
4- Malignant: May accompany neoplasms of the nose and PNS. It is usually single,
friable and bleeds on touch.
5- Bleeding polyp of the septum: (angioma).

- Ethmoidal Polyp: The commonest type (allergic).

- Symptoms:
1- Nasal obstruction which is complete when the polypi fill the nose.
2- Watery discharge, sneezing and anosmia.

- Signs:
Multiple, bilateral glistening (as grapes) polypi arising from the ethmoidal sinuses and
appear in the nose towards the anterior nares.

- Radiology: CT scan for PNS

- Treatment:
Surgical: Endoscopic ethmoidectomy.
Medical: Antiallergics, steroids.

63
- Antro-Choanal Polyp
A single polyp arising from the maxillary sinus, then it passes through its ostium and
backwards through the posterior choana, to appear in the nasopharynx.

- Symptoms:
1- Unilateral nasal obstruction.
2- Unilateral nasal discharge.

- Signs:
Single unilateral polyp appearing in the nasopharynx and usually occurs at a young
age before 20.

- Radiology: CT scan for PNS.

- Treatment:
- Endoscopic polypectomy with widening of the maxillary ostium.
- Radical antrum operation may be done for recurrent cases.

- Mucocele
It is a cystic expansion of the sinus due to accumulation of mucous. Mucocele is due to
blockage of mucous gland duct or obstruction of the sinus ostium.
It commonly affects the frontal sinus, ethmoid or fronto-ethmoid.

- Clinical picture:
- Cystic swelling if enlarges causes egg-shell cracking sensation at orbital roof (frontal
mucocele) or at inner canthus (ethmoid mucocele).
- Proptosis: Downwards and laterally in frontal mucocele and laterally in ethmoid
mucocele.
- If infected it forms a pyocele with fistula formation.
- May invade orbit and brain.

- Radiology: CT scan for PNS.

- Treatment: Drainage of the sinus using nasal endoscopy.

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Tumours of The Nose And Sinuses
- Connective tissue tumours
- Osteoma:
- This is the most common tumour of the nose and PNS.
- A hard swelling usually arising from the frontal bone.
- Clinical picture: Headache and proptosis if large.
If small: it could be discovered accidentally in CT scan of PNS.
- Treatment: Endoscopic excision if causing obstructive symptoms.

- Angioma:
- May be capillary or cavernous. It is sessile and affects the septum causing bleeding
(bleeding polyp of the septum).
- Treatment: Cauterization or excision.

- Malignant Tumours
Squamous cell carcinoma is the commonest malignant tumour of the nose and sinuses
(80%). Adenocarcinoma arises from palate and maxillary sinus glands. It affects males
more above 50 years. Exposure to nickel may predispose to squamous cell carcinoma
while wood dust may predispose to adenocarcinoma. The maxillary sinus is commonly
affected (60%), then the nasal cavity (30%) and ethmoid sinus (10%).

- Cancer maxilla
- Spread and Clinical picture:
- Downwards: Perforates the palate, loosens the teeth.
- Upwards: Proptosis due to invasion of the orbit.
- Inwards: Nasal obstruction, epistaxis, and bleeding mass in the nose.
-Anteriorly: Swelling and parasthesia of the cheek (inferior orbital nerve).
-Posteriorly: TRISMUS (invasion of pterygoid muscles) and facial pain
(invasion of maxillary nerve).
- Enlarged deep cervical glands.
- Diagnosis: CT scan for PNS and biopsy.
- Treatment:
1- Surgical: Total maxillectomy (Weber Fergussen’s operation):
Removal of: i) Hard palate.
ii) Alveolar margin.
iii) Tumour and orbit if invaded.
- Dental prothesis to close the defect and artificial eye.
- Radical neck dissection for LNs.
2- Postoperative radiotherapy.
3- Chemotherapy for advanced cases.

65
Symptoms of Nasal Diseases
- Nasal Obstruction
- Bilateral Nasal Obstruction:
1. Congenital: Choanal atresia, Syphilis.
2. Trauma: Fracture nasal bones, septal haematoma.
3. Inflammation: Acute and chronic rhinitis and sinusitis.
4. Tumours: Malignant tumours of the nose.
5. Developmental: Deviated septum S shaped.
6. Allergic: Rhinitis, ethmoidal polypi.
7. Nasopharyngeal masses: Adenoids, benign and malignant tumours.

- Unilateral nasal obstruction:

1. Congenital: Unilateral choanal atresia.
2. Trauma: Foreign body, fracture nasal bones.
3. Inflammation: Unilateral sinusitis, antrochoanal polyp.
4. Tumours: Benign and malignant of the nose and paranasal sinuses.
5. Developmental: Deviated septum C shaped.

- Nasal Discharge
- Bilateral nasal discharge:
1. Mucopurulent or purulent: causes of bilateral nasal obstruction.
2. Blood: Epistaxis.
3. Watery: Allergic rhinitis. Early viral stage of influenza.
Excess lacrimation. Cerebrospinal rhinorrhoea.
4. Water and food: Regurgitation from mouth
1. Congenital: Cleft palate.
2. Inflammatory: Syphilitic perforation of hard palate.
3. Neurogenic: Palatal paralysis due to diphtheria or bulbar palsy.
4. Malignant: Erosion of the palate.

- Unilateral nasal discharge:

1. Mucopurulent or purulent: causes of unilateral nasal obstruction.
2. Blood: Epistaxis.
3. Watery: Cerebrospinal rhinorrhea, Oro-antral fistula.
4. Water and food. Same causes of bilateral discharge.
5. Serous: Cysts of maxillary sinus rupturing in the nose.

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- Epistaxis
Bleeding from the nose.

- Causes of epistaxis:
- Local causes
1. Idiopathic: 90% from Little's area.
2. Traumatic: FB, fractures nasal bones and skull base, after nose surgery.
3. Inflammatory: Acute and chronic rhinitis.
4. Neoplastic: Benign and malignant tumours of nose, sinuses and nasopharynx
(nasopharyngeal fibroma and carcinoma).
5. Deviated nasal septum: congestion from angulations.
- General causes:
1. Hypertension: commonest cause in elderly (anterior ethmoidal artery).
2. High venous pressure: cardiac and pulmonary diseases.
3. Blood diseases: Purpura, leukaemia, haemophilia.
4. Vitamin deficiency: vitamin C (scurvy) and vitamin K (liver diseases).
5. Drugs: Anticoagulants, salicylates.

- Site of bleeding:
1. Little's area: The site of 90% of cases of epistaxis.
2. Above the middle turbinate in cases of hypertension.

- Management of epistaxis:
1. First aid stop the bleeding:
- Place the patient in the sitting position (decrease venous congestion).
-Put a piece of cotton soaked in adrenaline or nasal vasoconstrictive drops in
the nose and compress the nose from outside.
-Cold compresses may be applied to cause reflex vasoconstriction.
2. Nasal packs:
-Anterior nasal pack: A50 cm Vaseline gauze is packed into the nose in layers
from below upwards and removed after 24-48 hours. Recently Merocel
packs are used because of its easy insertion in the nose.
-Posterior nasal pack: Indicated when, the anterior nasal pack fails or the
bleeding is coming from a posteriorly placed lesion.
3. Cautery of the bleeding vessel: by
- Electric cautery.
- Chemical cautary: 50% silver nitrate sticks or crystals of chromic acid.
4. Surgical treatment: When cautery or packs fail or epistaxis is severe.
a) Arterial ligation: of
-Endoscopic sphenopalatine artery ligation.
-Maxillary artery in pterygopalatine fossa through maxillary sinus.
-Ligation of the external carotid artery.
b) Submucous resection of severe deviated septum.

- General treatment:
-Control hypertension, give coagulants drugs and vitamin K.
-Blood transfusion in severe cases.

67
 - Investigations of epistaxis:
- Blood picture: for
a) Haemoglobin for anaemia.
b) White cell count for leukemias.
c) Platelets for purpura.
d) Bleeding coagulation and prothrombin times.
-Biopsy: For tumour masses.

Anterior nasal pack Posterior nasal pack

- Headache And Facial Pain

Pain in the upper half of the head from the orbit back to the suboccipital region.

- Pain sensitive structure in the head and neck:

- Intracranial structures:
- Dura of skull base.
- Arterial and venous sinuses.
- Cranial nerves 5th, 9th and 10th.
- Cranial structures: Periosteum of the skull.
- Extracranial structures:
- Arteries, muscles and fascia of the skull and neck.
- 1st, 2nd and 3rd cervical nerves.
- Nasal sinuses, teeth, eyes and ears.

- Causes of headache:
1. Raised intracranial pressure.
2. Migraine.
3. Traumatic: after head injury.
4. Inflammatory: meningitis and osteomylitis.
5. Neoplastic: intracranial and cranial tumours.
6. Vascular: hypertension, temporal arteritis.
7. Psychogenic: tension headache.
8. Referred pain: nose, sinuses, ears, eyes and cervical spines.
9. Idiopathic: Functional neuralgias.

68
- Smell Disorders
Smell is the process by which an odorous substance stimulates the olfactory mucosa. The
olfactory nerve transmits the odorous impulse from the olfactory mucosa to the olfactory
bulb in the brain.

1. Anosmia:
Is bilateral complete loss of sense of smell. Hyposmia: is partial loss of smell.
Causes:
- Developmental: Severe septal deviation.
- Traumatic: Fracture skull base involving olfactory fibres.
- Neoplastic: Brain tumours.
- Allergic: Allergic rhinitis, polyposis, and hypertrophied turbinates.
- Vasomotor: Vasomotor rhinitis.
- Neurologic: Peripheral neuritis after influenza.
- Atrophic rhinitis.

2. Cacosmia:
Perception of bad odours.
- Maxillary sinusitis of dental origin.
- Foreign body.
- Fetid pus of CSOM.

3. Parosmia:
Perception of non-existing odours.
- Psychosis.
- Epilepsy.

4. Hyperosmia:
Increase sensitivity of smell which may occur with hysteria.

- Proptosis
Abnormal protrusion of the eyeball
Causes:
1-In the sinuses
a) Mucoceles especially fronto-ethmoidal.
b) Fungal sinusitis.
c) Neoplastic:
- Inverted papilloma, Fibrous dysplasia of maxilla, osteoma of frontal.
- Cancer maxilla and ethmoid.
2-In the nasopharynx:
Nasopharyngeal angiofibroma, cancer nasopharynx.
3-In the orbit:
a) Cellulitis, hematoma.
b) Orbital fracture.
c) Neoplastic: Glioma.
4- Cavernous sinus thrombosis.
5- Thyrotoxicosis.

69
- Operations of the nose and paranasal sinuses
-Submucous resection and Septoplasty
- Indications:
Deviated septum causing obstruction or its sequelae.
- Contraindications:
Submucous resection (SMR) in patients before 18 years as it disturbs the
growth of the face. Septoplasty could be done in children only dealing with the
cartilagenous part of the septum.
- Complications:
1. Haemorrhage: Treated with anterior nasal pack.
2. Septal haematoma: Less common in septoplasty.
3. Septal abscess: Evacuate and antibiotics.
4. Septal perforation: Less common in septoplasty.
5. Depressed tip or bridge due to excessive cartilage removal.
6. Adhesions: Cut and use repeated packs.

70
- Radical Antrum Operation (Caldwell-Luc)
- Indications: Recently FESS is done and this operation is not frequently performed
nowadays.
1. Chronic sinusitis.
2. Antrochoanal polyp.
3. Oro-antral fistula.
4. Foreign body or tooth in the sinus.
5. Blow out fracture of the orbit.
6. Cysts and tumours.
7. Maxillary artery ligation for epistaxis.

Radical antrum operation

- Complication:
1. Hematoma of the check: cold foments.
2. Loss of facial sensation on due to injury of infra-orbital nerve.

71
Functional endoscopic sinus surgery (FESS)
It is done for chronic sinusitis with a partially healthy mucosa, to ensure continuous drainage
and maintaining aeration of the sinuses at the osteomeatal complex. This removes the
diseased mucosa, polyps and granulations.
- Technique:
The operation is carried out using rigid nasal endoscopes with deferent angles which
provides excellent illumination and visualization. Hypotensive anesthesia is needed.
- Indications:
1. Chronic sinusitis (bacterial and fungal).
2. Nasal polypi.
3. Mucoceles of the sinus.
4. Choanal atresia.
5. Repair of CSF leaks.
6. Septum and turbinate surgery.
7. Inverted papilloma and nasopharyngeal fibroma.
8. Dacrocystorhinostomy.
9. Orbital decompression.
- Complications:
1. Orbital haematoma and optic nerve injury.
2. Skull base trauma leading to CSF leaks.
3. Failure due to residual disease.

- Rhinoplasty
It is an operation to modify the aesthetic appearance and functional properties of the nose
with operative manipulation of the skin, underlying cartilages and bones. It could be done
through open or closed approaches.

Indications:
- Post-traumatic nasal deformities.-Nasal tip modifications.
- Nasal hump removal. – Reduction of the nose size.

72
Anatomy of the The Pharynx
Definition: It is a musculomembranous tube which lies behind the nose, mouth and larynx.
Extent: It extends from the base of the skull down to the 6th cervical vertebra, opposite the
lower border of the cricoid cartilage. Here, it continues as esophagus.

Length and Dimensions:

- Length: 12 - 14 cm.
- Diameter: It is widest at its beginning (3.5 cm) and narrowest at its lower end at the
pharyngo-esophageal junction (1.5 cm).

Parts of the Pharynx:

- The unique feature of the pharynx is that its anterior wall is mostly absent, so that
the pharynx can communicate freely with 3 cavities, so it is divided into 3 parts:-
• With the nasal cavities through the choanae. It is the nasal part of pharynx or
nasopharynx.
• With the oral cavity through the oro-pharyngeal isthmus. It is the oral part of
pharynx or oropharynx.
• With the laryngeal cavity through the inlet of the larynx. It is the laryngeal part of
the pharynx or laryngopharynx.

Parts of the pharynx

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Structure of the Pharyngeal Wall:
From within outwards, the pharyngeal wall is composed of:
1. Mucous membrane: It is the interior of the pharynx.
2. Fibrous layer: called the pharyngo-basilar fascia.
3. Muscular coat.
4. Buccopharyngeal fascia: Covers the external aspect of the pharynx.

The Mucous Membrane or Interior of the Pharynx :

A. The Nasopharynx:
Extent: It extends from the base of the skull
down to the level of the soft palate.
• It is lined by respiratory
epithelium.
• The lamina propria contains
mucous and serous glands as
well as lymphoid tissue, the
nasopharyngeal tonsil.

Communications:
• Anteriorly: with the nasal cavities via the posterior nasal apertures (choanae).
• Inferiorly: with the oropharynx through the pharyngeal isthmus.
• Laterally: with the tympanic cavity (on each side) via the auditory tube.

Special Features:
- At the junction of its roof and the posterior wall, the mucosa contains the
nasopharyngeal tonsil. It is usually enlarged in children and is called adenoids
which may obstruct the nasopharynx with difficult nasal breathing. After 6 years
of age, it atrophies.
- On each lateral wall of the nasopharynx, there are:
• Pharyngeal opening of the auditory tube situated 1 cm behind the inferior
nasal concha.
• The pharyngeal opening is bounded above and behind by the tubal elevation,
produced by the cartilage of the auditory tube. Around the opening, the
mucosa contains a collection of lymphoid tissue called the tubal tonsil.
• The lower end of the tubal elevation is continuous with a vertical mucous fold
called the salpingeopharyngeal fold, produced by the salpingeopharyngeus
muscle. Behind the tubal elevation, there is the pharyngeal recess, related to
ICA outside the pharynx.

B. The Oropharynx:
Extent: It extends from the level of the soft palate down to the level of the upper end of
the epiglottis.

Communications:
• Above: with nasopharynx via the pharyngeal isthmus.

74
 • Anteriorly: with the mouth cavity via the oropharyngeal isthmus.
• Below: is continuous with the laryngopharynx.

Special Features:
• Anteriorly: oropharynx faces the posterior ⅓ of the tongue to which it is connected
by 3 folds: median glosso-epiglottic fold and the two lateral (Rt. and Lt.) glosso-
epiglottic folds. Between these three folds, there are two depressed areas called the
valleculae
• Its lateral wall presents the palatopharyngeal arch and tonsillar sinus which
contains the palatine tonsil.

Interior of nasopharynx

The Palatine Tonsil:

Definition: It is a mass of lymphoid tissue which lies in the tonsillar sinus in the
lateral wall of oropharynx between the palatoglossal and
palatopharyngeal arches.
Description and Relations:
1. Its medial surface: presents 10 - 15 orifices leading to deep recesses called
the tonsillar crypts. .
2. Its lateral surface: Is related to:
• Tonsillar hemicapsule: It is an extension from the pharyngeobasilar fascia
• Paratonsillar vein descends from the soft palate lateral to the tonsillar
hemicapsule.
• The superior pharyngeal constrictor (pierced by the tonsillar A.).

75
 3. Superiorly: the tonsil invades the soft palate.
4. Inferiorly: the tonsil invades the dorsum of the tongue.
Arterial Blood Supply:
• The tonsil is mainly supplied by the tonsillar A., a branch of the facial A.
• Additional blood supply is provided by ascending palatine, ascending
pharyngeal, greater palatine and dorsal lingual arteries.
Venous Drainage: By tonsillar veins which join the paratonsillar vein. The latter
pierces the superior pharyngeal constrictor muscle to join the
common facial V.
Lymph Drainage: Is mainly to the jugulo-digastric lymph nodes.
.

Waldeyer’ Ring of Lymphoid Tissue:

Definition: This ring of mucosa-associated lymphoid tissue surrounds the openings
into the digestive and respiratory tracts.
Components:
• Anteroinferiorly: The lingual tonsil.
• Laterally: The palatine and tubal tonsils.
• Posterosuperiorly: The nasopharyngeal tonsil.

Oropharyngeal isthmus and palatine tonsils

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 C. The Laryngeopharynx :
Extent: It extends from the upper end of the epiglottis down to the lower border of
the cricoid cartilage (C6 vertebra).
Communications:
* Anteroinferior: with the larynx via the laryngeal inlet.
* Inferiorly: is continuous with the esophagus.
Special Features :
- Anteriorly: The laryngopharynx is related to:
a. Inlet of the larynx.
b. Mucous membrane on the posterior surfaces of the arytenoid
and cricoid cartilages.
c. Piriform fossa: Which is a small recess on either side of the
laryngeal inlet beneath the mucous membrane
of the fossa are the branches of the internal
laryngeal N.

Interior of laryngopharynx

The Pharyngeobasilar Fascia :

- It is a thick fibrous layer which lies between the mucosa and muscular coat of the
upper part of the pharynx. It is thick in the nasopharynx where the muscle fibers
are absent.
Function: It provides a rigid wall for the nasopharynx, keeping it permanently opened.

77
The Muscular Coat of the Pharynx:
3 Circular (constrictor) and 3 longitudinal
A. The Three Constrictors :
(1) The Superior Constrictor:
(2) The Middle Constrictor:
(3) The Inferior Constrictor:
It has 2 functional parts (thyropharyngeus and cricopharyngeus)

Functions of the Pharyngeal Constrictors:

- The superior and middle constrictors and the thyropharyngeus part of the
inferior constrictor have a propulsive action during swallowing.
- The cricopharyngeus acts as a sphincter at the lower end of the pharynx. It is in a
continuous state of contraction to prevent suction of air into the esophagus. It
relaxes only at the end of the second stage of swallowing to allow passage of
food into the esophagus. If it fails to relax, the pharyngeal mucous membrane
herniates posterolaterally between the thyropharyngeus and cricopharyngeus
(through the dehiscence of Kilian) producing a pharyngeal pouch.

78
 B. The Three Longitudinal
Muscles :
(1) The stylopharyngeus muscle:
(2) The salpingeopharyngeus
(3) The palatopharyngeus muscle:
Actions: These 3 muscles elevate the larynx
and pharynx upwards (in the second stage of
swallowing) to close the laryngeal inlet.

The Buccopharyngeal Fascia :

This thin layer of fascia covers the
external surface of the constrictors
and passes forwards to cover the
buccinator.

Examination of The Pharynx

- Nasopharynx
-Posterior rhinoscopy (posterior nasal mirror).
-Endoscopic examination (rigid and flexible endoscopy).

- Oropharynx
-Inspection: of tonsil, posterior pharyngeal wall and movement of palate.

- Hypopharynx
-Moure’s sign: loss of laryngeal click: Friction of the cricoid cartilage to vertebrae showing
absent click in postcricoid carcinoma.
-Indirect laryngoscopy.
-Direct hypopharyngoscopy.
-Flexible fiberoptic endoscopy.

- Cervical lymph nodes examinations

- Radiology: CT scan: Demonstrates the pharynx, surrounding structure and cervical
lymph nodes.
- Throat swabs for culture and sensitivity
- Blood tests: CBC, ESR, etc
- Biopsy: For pathological examination of pharyngeal or tonsillar masses.

79
Diseases of The Nasopharynx
Adenoids
Hypertrophy of the lymphoid tissue of the nasopharynx sufficient to produce symptoms. It
is the commonest nasopharyngeal swelling. It occurs in children between 3 to 8 years due
to repeated upper respiratory tract infections. It has no capsule and is covered by
pseudostratified columnar ciliated epithelium.

- Clinical picture:
1-Symptoms of hypertrophy:
A) Bilateral nasal obstruction:
- Snoring and sleep apnea.
- Difficult suckling in infants.
- Nasal tone of voice.
- Anterior nasal discharge (Bilateral).
B) Eustachian tube obstruction:
- Conductive hearing loss due to secretory otitis media.
C) Adenoid facies: (idiot look)
- Narrow pinched nostrils. Inactive atrophied alae nasi
- The mouth is opened and the upper lip is short.
- Overcrowded protruding incisors.
- High arched palate.
- Receding mandible and enlarged lower lip.
2- Symptoms of recurrent infection:
- Rhinitis and sinusitis.
- Otitis media.
- Pharyngitis, laryngitis and bronchitis.
3- General symptoms:
- School retardation (due to deafness + interrupted sleep).
4- Reflex symptoms:
- Nocturnal enuresis.
- Laryngismus stridulus.
- Reflex cough.

- Investigations:
- Plain X-ray lateral view on nasopharynx shows soft tissue shadow leading to
narrowing of air column.
- Nasal endoscopy.

- Treatment:
Adenoidectomy (± tonsillectomy if indicated)

80
Tumours of the nasopharynx
- Benign tumours of the nasopharynx:
Fibroma, papilloma, adenoma and mixed salivary tumours

- Nasopharyngeal fibroma
(Juvenile Nasopharyngeal Angiofibroma)
It is a benign, highly vascular, locally aggressive tumour. It has a tendency to bleed
because there is no muscle coat in its vessels. It occurs in young males below the age of 18
years with spontaneous regression at sexual maturity.

- Behavior:
Either spontaneous regression (rare) at sexual maturity or extension to the surrounding
structures.

- Pathology:
- Origin: Superior margin of sphenopalatine foramen.
- Gross picture: Firm, lobulated, pinkish tumour, has no true capsule.
- Vascular supply: Most commonly from the internal maxillary artery.
Also: Internal carotid, external carotid, common carotid, ascending pharyngeal arteries.

- Microscopic picture:
-Angio = Vascular spaces without musculosa.
-Fibroma = Collagen bundles and fibroblasts.

- Clinical picture:
Nasal: Nasal obstruction, recurrent severe epistaxis.
Aural: Conductive deafness due to Eustachian obstruction.

- Signs:
-A smooth, lobulated, firm, easily bleeding mass.
a) Is seen in the nose.
b) Depresses the soft palate and appears behind it in nasopharynx.
-Extension of the tumour causes:
a) Widening of the nasal bones.
b) Proptosis and frog-face deformity.
c) Swelling of the cheek and zygoma.

- Differential diagnosis: of unilateral nasal mass.

N.B: A young boy with unilateral nasal obstruction and
epistaxis is diagnosed angiofibroma until proved
otherwise.

- Characteristic Presentation: Teenage or young adult male, recurrent epistaxis and

nasal obstruction.

- Investigations:
81
 1. C.T scan:
- Detects extension to orbit sphenoid sinus and pterygopalatine fossa.
- Bowing of posterior wall of maxilla (Holman-Miller Sign).
- Widening of sphenopalatine foramen.
2. Carotid angiography: to see feeding vessel, and to do preoperative embolization.
3. MRI: to detect intracranial extension.
4. Biopsy is contraindicated (bleeding), and not needed.

- Treatment:
1) Surgical: Surgical excision with preoperative emobilization.
a- Transnasal endoscopic removal.
b- Transpalatal: If the tumour is small localized to the nasopharynx.
c- Lateral rhinotomy: If it extends to the nasal cavity, sinuses or
pterygopalatine fossa.
d- Craniotomy may be needed if there is intracranial extension.
2) Hormonal: Combination of oestrogen and testosterone leads to maturation of
fibrous tissue and reduces vascularity.
3) Radiotherapy: Not done nowadays as it is carcinogenic except in recurrent cases or
if there is intracranial extension.

- Malignant tumours of the nasopharynx:

Squamous cell carcinoma is the most common. Lymphoepithelioma and sarcoma are rare.

- Nasopharyngeal carcinoma
- Incidence:
- More in males above 60 years than females.
- Chinese have a higher genetic susceptibility to nasopharyngeal cancer.
- Predisposing factors:
- Epstein Barr virus infection.
- Smoking of tobacco, smoke from burning wood.
- Irradiation.
- Gross picture:
-Shape: Ulcer, cauliflower mass or nodular or infiltrative.
-Site: The fossa of Rosenmuller is the commonest site.
-Metastatic cervical lymphadenopathy may be the presenting symptom.
- Spread:
-Direct: To the surrounding structures.
-Lymphatic spread: Retropharyngeal then to the upper deep cervical LNs.
-Nasopharynx is a midline structure, so bilateral nodal metastasis is common.
-Distant metastasis: Lung, liver, bone and brain.
- Prognosis:
- Bad as nasopharynx is a silent area, and in the midline.
- Clinical Picture:

82
 Aural manifestations:
- Unilateral secretory otitis media: due to obstruction of the Eustachian tube
could be the first presenting symptom.
- Referred pain in the ear through the 9th nerve.
Nasal manifestations:
- Nasal obstruction (unilateral or bilateral).
- Nasal discharge (unilateral or bilateral).
- Epistaxis.
Nodal manifestations:
Upper deep cervical LNs enlargement may appear before the primary is
detected.
Incidence of metastasis = 70%.
Neurological manifestations:
Cranial nerve palsies: In this order of frequency:
- 5th cranial nerve: Unilateral facial pain, numbness then loss of sensation.
- Ocular: 3rd, 4th, 6th nerves affection causing ptosis, proptosis and
ophthalmoplegia (paralysis of eye muscles).
- Lower four cranial nerves: 9th, 10th, 11th, 12th (compression by
retropharyngeal LNs at skull base):
th
- 10 nerve affection causing palatal and vocal fold paralysis.
- 11th nerve affection causing sternomastoid and trapezius paralysis.
- 12th nerve affection causing tongue paralysis.

Trotter's triad: (diagnostic for nasopharyngeal carcinoma)

1) Unilateral facial pain (trigeminal neuralgia).
2) Unilateral palatal immobility.
3) Unilateral conductive deafness.
- Investigations:
1. CT scan: To detect site, size and extensions of the tumour, and
retropharyngeal LNs enlargement (which is not clinically palpable).
2. MRI: To detect intracranial extension.
3. Biopsy by: Nasal endoscopy (local anesthesia).
4. Metastatic work up.
- Treatment:
1. Radiotherapy: to primary tumour in the nasopharynx and to neck (for LNs)
in both sides.
2. Surgery: has no place as a primary treatment, it is done only (radical neck
dissection) for persistent or recurrent LNs (after failure of radiotherapy).

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Diseases of the oropharynx
- Congenital anomalies
- Cleft palate:
It is due to failure of fusion of the different segments of the fetus palate. It will lead to
regurgitation from nose, nasal tone and Eustachian tube dysfunction. It is treated by
early repair to prevent complications. Submucosal cleft is defect in palatal muscles
only with intact mucosa and only a bifid uvula is present.

- InflammationS of the pharynx

- Acute pharyngitis:
- Acute non-specific pharyngitis: Simple pharyngitis.
- Acute specific pharyngitis: Diphtheria, vincent's angina and moniliasis.
- Acute pharyngitis due to blood diseases: Leukaemia, agranulocytosis and infectious
mononucleosis.
- Acute non-specific pharyngitis (simple pharyngitis):
It is caused by bacterial, viral or mixed infection of the mucosa and lymphoid
tissue of the pharynx.
- Causes: Low resistance, overcrowding, rhinitis, sinusitis.
- Symptoms: Fever, headache, sore throat and dysphagia.
- Signs: Congestion of the pharynx, cervical lymphadenitis.
- Treatment: Antibiotics and analgesics.

Orthomyxoviruses

Influenza:
True influenza is an acute infectious disease caused by influenza viruses a member of
family orthomyxovirus, Three types of influenza viruses are known: Types A, B and
C. All cause acute respiratory disease in human. Influenza A and C infect multiple
species, while influenza B almost only infects humans.

Influenza viruses:

Influenza virus
84
 Transmission: It is rapid by droplets and fomites with inhalation into the pharynx or
lower respiratory tract. Rapid spread leads to epidemics.

Incubation period is short: 1-3 days.

Infection may be very mild, even asymptomatic, moderate or very severe. Influenza is
characterised by fever, myalgia, headache and pharyngitis and cough. There is usually
not coryza (runny nose) which characterises common cold infections. Viremia is rare.

Laboratory diagnosis: Specimen : Respiratory secretions such as direct aspirate, gargle,

nasal wash.
A- Direct: Rapid examination of cells by immunofluorescence.
B- Viral isolation: Inoculation of cell cultures (or eggs).
C- Serology: by haemagglutination inhibition.

Influenza epidemiology : Localized epidemics of influenza occur every 2-3 years.

Vaccines give about 70% protection. Influenza A (H1N1),A (H3N2),and influenza B strains
are included in each year's influenza vaccine.

Coronaviruses –SARS and COVID-19

They infect humans and animals in which they cause respiratory and enteric disease.
They cause one third of "common colds" and the newly recognized severe acute
respiratory syndrome (SARS).

Coronaviruses

Pathogenesis:
Source: man

Transmission is by aerosols, contact with contaminated fomites or hands .In humans, the
major site of virus replication is the epithelial cells of the respiratory tract.
Some viruses infect the epithelial cells of gastrointestinal tract.

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Incubation period: 3-10 days.
The symptoms are similar to those of rhinovirus colds and diarrhea
can occur in some cases. In most cases the disease is asymptomatic
but there is shedding of infectious virus.

Complications: Middle ear infections, pneumonia in immuno-suppressed patients.

Epidemiology:
® Common cold is caused by coronaviruses in 30% of cases and Rhinovirus in 50%
of cases .Common cold occurs are more common in the winter.
® Reinfection by coronaviruses is common as there are many circulating serotypes of
the virus.
® No animal reservoirs exist.

Severe acute respiratory syndrome (SARS- CoV and COVID-19 )

In late 2002 and 2019, new syndromes were observed in China that spread rapidly to
North and South America and Europe. Unlike other corona-viruses SARS CoV and
COVID -19 causes infections with a significant morbidity and mortality. Respiratory
distress leads to death in 3-30% of cases.

Laboratory diagnosis:
A- Laboratory tests show a reduction in lymphocytes and a rise in aminotransferase
activity which indicates damage to the liver.
B- SARS-CoV and COVID -19 infections can be diagnosed by :
1- Direct detection: PCR
2- Viral Isolation: cultivation and identification of the virus.
3- Serology: Detection of rising antibody titer.

Infection control: Because of its high mortality and ease of spread, patients infected with
SARS-CoV and COVID -19 must be isolated in negative pressure
rooms, and health care providers must wear respirators.

Treatment: No specific antiviral drugs.

Vaccine: COVID -19 vaccines are available in many countries.

- Acute specific pharyngitis:

- Diphtheria:
An acute infectious disease caused by Corynebacterium diphtheriae. It is
transmitted by droplet infection. It is commonly affects children 2-6 years with
incubation period 2-5 days.
Symptoms: Insidious onset, severe toxaemia, mild fever: 38°C, sore throat.
Signs: 1. Membrane on the tonsil which is:
a) Grayish yellow, formed of sloughed mucosa, pus and thick fibrinous exudate.
b) Unilateral, exceeding the margins of the tonsil to the pharynx or larynx.

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 c) Adherent; when removed it leaves a raw bleeding area and recurs rapidly.
2. Rapid pulse, asynchronous with the temperature.
3. Enlarged cervical lymph glands.
Investigations: A swab is taken from the membrane for diphtheria bacilli
detection.
Differential Diagnosis: From other membranous or ulcerative conditions of
the tonsils.
Acute follicular tonsillitis, Vincent's angina,
Moniliasis, Blood diseases.
Complications:
Early in the first week
-Due to the effect of the membrane:
a) Laryngeal obstruction due to extension of the membrane.
b) Lung collapse due to inhalation of a piece of the membrane.
-Due to the powerful exotoxin produced by the organism.
a) On the heart: Toxic myocarditis.
b) On the Kidney: Acute nephritis.
Late in 2-3 weeks Due to peripheral neuritis
a) Palatal paralysis: Is the earliest paralysis:
i) Regurgitation of food and fluids through the nose.
ii) Deviation of the uvula to the normal side.
b) Eye muscles paralysis:
i) Diplopia due to 6th nerve paralysis.
ii) Loss of accommodation due to 3rd nerve paralysis.
c) Pharyngeal paralysis: Dysphagia.
d) Laryngeal paralysis:
i) Hoarseness.
ii) Ineffective cough.
e) Chest muscles paralysis (diaphragm and intercostals):
Suffocation.
f) Affection of the heart muscle: heart failure.
Treatment:
1. Rest for 3 weeks to prevent heart failure.
2. Isolation until 3 successive swabs is negative.
3. Anti-toxic serum is given as soon as the case is suspected.
4. Penicillin is given for 10 days.
5. Treatment of complications:
a) Dysphagia: Nasogastric tube.
b) Stridor: Tracheostomy.
c) Paralysis of chest muscles: mechanical ventilation.
- Prophylaxis:
Active immunization: Infants at 2, 4, 6, 18 months are immunized by D.P.T.
vaccine (diphtheria, pertussis and tetanus) given intramuscularly. Then a
booster dose is given at 6 years, i.e. at school age.
Passive immunization: Anti-toxic serum is given for contacts.

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 - Vincent's Angina
Is an acute ulcerative inflammation of the pharynx affecting tonsils and gums.
Causative organism : Spirochaeta denticola (tooth caries).
Symptoms: Mild fever, sore throat, fetor, severe pain.
Signs:
1. A unilateral ulcer on the tonsil covered by a grayish yellow membrane,
non adherent and easily removed.
Investigations:
Throat swab for the organisms.
Treatment:
Penicillin, Oxygen peroxide mouth wash.
- Fungal infections: Moniliasis (thrush):
It is a fungal infection of the pharynx by Candida albicans commonly in:
1- Debilitating conditions.
2- After broad spectrum antibiotics.
Symptoms and Signs:
- Sore throat and dysphagia but no fever
-Milky white raised membrane over the mucosa of the pharynx and cheek.
Treatment:
1- Mycostatin drops.
2- Gentian violet 1% paint.

Candida albicans
Is an endogenous organism. It is present as a commensal in the mouth, gut, and vagina
.It could be present as pathogenic organism when a patient has some alteration in
cellular immunity, normal flora or normal physiology.

Candidiasis is a commonly called yeast infection or thrush, caused by Candida species,

of which Candida albicans is the most common.

Predisposing factors for the overgrowth of Candida:

1- Extensive use of antibiotics.
2- External use of irritants.
3- Invasive procedures, such as surgery.
4- Hormonal or physiological disturbance as in pregnancy, the use of oral
contraceptives, hormone replacement therapy and infertility treatments
5- Diabetes mellitus and Immunosuppression.

Candidiasis can be:

1- Superficial, such as: Oral thrush
2- Systemic candidemia; are usually confined to severely immuno-compromised
persons, such as cancer, transplant, nutrient deficiency, steroids therapy and AIDS
patients, and are life-threatening diseases.

Diagnosis: Direct microscopic examination of throat swab and cultures.

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 - Acute pharyngitis of blood diseases:
- Infectious mononucleosis:
It is acute pharyngitis caused by Epstein Barr virus infection.
Clinical picture:
- Sore throat and dysphagia.
- Fever, headache and malaise (Febrile type).
- Pharyngeal ulcers surrounded by congested area and covered with whitish
membrane (anginose type).
- Generalized lymph node enlargement and splenomegaly (Glandular type).
- Jaundice: Hepatic type.
Investigations:
- Blood picture: Monocytosis and lymphocytosis.
- Paul-Bunnell test is positive: Serum of the patient agglutinates the sheep’s
RBCs due to abnormal antibodies.
Treatment:
Antibiotics, analgesic and antipyretics.

Epstein Barr Virus (IM)

Following primary infection, the virus persists in a latent form in the B lymphocytes
of the host. Periodic reactivation of the virus is associated with shedding of virus in
saliva. Clinical syndromes associated with EBV infection are:
A- Primary Syndromes:
1- Infectious Mononucleosis.
2- Chronic EBV infection.
B- Re-activation Syndromes:
1- Lympho-proliferative disorders in immuno-suppressed patients.
2- Burkitts Lymphoma, naso-pharyngeal carcinoma, T cell lymphoma and
Hodgkin's disease.

Pathogenesis and Clinical Features:

• Transmission: could be by close contact, especially kissing and mouthing of toys
by children. The virus is secreted intermittently in the saliva of asymptomatic
carriers and by blood transfusion. The primary infection is often asymptomatic but
the patient may shed infectious virus for many years.
• Incubation period: Some patients develop the disease after 1-2 months. The
disease is characterized by fever, generalized lympha-denopathy, sore throat,
splenomegaly, hepatomegaly, abnormal liver function tests and atypical
lymphocytosis in the peripheral blood. The disease is self limiting.

Laboratory Diagnosis:
A- Complete blood picture: Increase in total leucocytic count (above 25.000/cmm)
with predominance of monocytes and atypical lymphocytes.
B- Serological diagnosis:
1- Non specific serological tests: Paul-Bunnell test (Monospot test )
2- Specific serological tests: useful for confirming the diagnosis (IgM)
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Ulcers of The Oropharynx
1- Traumatic:
-Caused by foreign bodies, burns or ill-fitting dentures.

2- Inflammatory:
Acute
a) Viral:
- Herpes simplex and zoster, measles (Koplik’s spots).
- AIDS
b) Bacterial:
- Diphtheritic ulcer.
- Vincent’s ulcer.
c) Fungal: moniliasis.
Chronic:
- Syphilis: Deep punched-out edges.
- T.B: bluish undermined edges.

3- Dyspeptic:
Aphthous ulcers: recurrent yellowish, painful ulcers. It may be associated with GIT
troubles.

4- Neoplastic:
Have everted edges and an indurated wide base.

5- Blood diseases:
Infectious mononucleosis.

6- Skin diseases:
-Pemphigus and Lichen planus.
-Behcet’s syndrome: iritis with oropharyngeal and genital ulcers.

- Acute Tonsillitis
It is acute inflammation of lymphoid tonsillar tissues.

- Causes: Low general resistance and upper respiratory tract infections.

- Causative organism: Starts by viral infection then secondary bacterial infection. The
commonest organism is Beta-hemolytic streptococci.

- Pathology:
1. Acute catarrhal tonsillitis: Edema and congestion of mucosa of tonsils.
2. Acute follicular tonsillitis: Pus within the crypts appears as yellowish spots on the
surface.
3. Acute parenchymatous tonsillitis: Hugely enlarged tonsils.

- Symptoms:
1. Fever, headache and malaise.

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 2. Soreness, dysphagia, salivation and referred otalgia (9th cranial nerve).
3. Cervical adenitis: enlarged glands, specially the jugulo-digastric.

- Differential diagnosis:
Other causes of membrane on the tonsil: diphtheria, Vincent’s angina, glandular fever
and fungal infection(moniliasis).

- Complications:
A. General: 1- Rheumatic fever.
2- Arthritis.
3- Acute glomerulo-nephritis.
B. Local: 1- Peritonsillar and retropharyngeal abscesses.
2- Acute otitis media.
C. Descending infections: Laryngitis, bronchitis.

- Treatment: Bed rest, antibiotics and analgesics.

- Chronic Tonsillitis
- Causes:
-Repeated attacks and inefficient treatment of acute tonsillitis.
-Usually associated with adenoids and cervical lymphadenopathy.

- Local symptoms:
1- Recurrent acute attacks.
2- Snoring (sleep apnea) and dysphagia.
3- Bad odour and taste.

- General symptoms:
Symptoms of a septic focus: Chronic bacteraemia or toxemia caused by chronic
inflammations.
1- General ill-health, fatigue and anorexia.
2- Headache, arthritis and myositis.
3- Low grade fever.

- Local signs:
1- The crypts are irregular and ooze pus on pressure by a tongue depressor.
2- Irregularity of the shape and size of the tonsils.
3- Congestion of the anterior pillars.
4- Enlarged jugulodigastric glands draining the tonsils.

- Investigations: Elevated Erythrocyte sedimentation rate (ESR) and Antistreptolycin

titre (ASOT) (normal up to 200 tods unite).

- Treatment: Tonsillectomy

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Streptococcus
Gram positive cocci arranged in pairs or chains.
Streptococcus pyogenes and streptococcal Disease: .
Rheumatic fever: Occurs two weeks after a Streptococcus pyogenes infection,
usually pharyngitis. Rheumatic fever is characterized by
migratory polyarthritis, carditis and uncontrolled movements
of limbs or chorea and nodules under the skin. M protein
cross reacts with epitopes on heart, myosin and sarcolemma,
joint and brain tissue. There are many rheumatogenic strains
of group A S.pyogenes, for this reason repeated recurrences
of rheumatic fever can occur and lead to more damage to
heart valve. Long -term prophylaxis by antibiotics e.g
penicillins are recommended to prevent repeated attacks.

Laboratory diagnosis:
Specimen taken could be throat.
1. Direct examination:
a. Gram positive cocci arranged in pairs or chains .
b. Latex agglutination test. It is a rapid test which detects S. pyogenes
antigens extracted from throat swab.
2. Direct culture on blood agar, the culture shows small, beta-hemolytic
colonies.

C-Serological tests:
1-Specific test:
a- Anti-streptolysin O titers (ASO) above 200 units are found in acute
rheumatic fever.
b- Anti-streptokinase above 80 units is diagnostic for rheumatic fever.
c- Anti-hyaluronidase titers above 128 units is diagnostic for rheumatic
fever
2-Non-specific test include mainly: Elevated sedimentation rate, positive
C-reactive protein test and elevated
white blood count.

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- Suppurations of Spaces Related To The Pharynx
1. Peritonsillar abscess (Quinsy).
2. Parapharyngeal abscess.
3. Retropharyngeal abscess.
4. Ludwig's Angina.

- Peritonsillar Abscess (Quinsy)

It is collection of pus outside the tonsil, between its capsule and the superior constrictor
muscle. It is usually superior but may be posterior or lateral to the tonsil. The infection
passes out mainly through crypta magna in the course of acute tonsillitis to the peritonsillar
space.

- Clinical picture:
- Fever, headache, malaise and anorexia.
- Dysphagia: Severe, dribbling of saliva.
- Pain: Throbbing and referred to the ear (9th cranial nerve).
- Trismus: Inability to open the mouth (irritation of the medial pterygoid).
- Torticollis: Stiff neck associated with muscle spasm on the diseased side.
- Swelling above and lateral to the tonsil pushing the tonsil downwards and medially
and pushing the uvula to the opposite side.
- Enlarged, tender jugulodigastric L.N.

- Complications:
-Laryngeal edema.
-Parapharyngeal abscess.

- Differential Diagnosis:
-Tumours: No acute symptoms,
-Aneurysm: no pulsations.

- Treatment:
- Before suppuration: I.V antibiotics, antipyretics and analgesics.

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 - After suppuration: Incision and drainage when pus forms: as indicated by throbbing
pain, hectic fever, trismus or pus on aspiration. Incision is done at
the most prominent pointing point or through the crypta magna.
This is followed by I.V antibiotics, antipyretics and analgesics.
-Tonsillectomy should be done after one month to avoid recurrence.

- Parapharyngeal Abscess
Collection of pus in the parapharyngeal space.

- The parapharyngeal space: It is present on either side of the pharynx extends from
skull base to the hyoid bone (inverted pyramid).
- Laterally: Ramus of mandible and parotid gland.
- Anteromedially: Buccopharyngeal fascia.
- Posteromedially: Prevertebral fascia.

Contents of the parapharyngeal space:

- Carotid sheath and its contents.
- Deep cervical LNs along internal jugular vein.
- Sympathetic chain.
- Last four cranial nerves.

- Causes:
1- Tonsillitis.
2- Quinsy.
3- After tonsillectomy.

- Clinical picture:
- Fever, headache, malaise and anorexia.
- Beck's triad = Parapharyngeal abscess

1- Internal swelling pushing tonsil medially.

2- External swelling below angle of mandible.
3- Trismus.

- Investigations: CT scan is diagnostic.

- Complications:
- Laryngeal edema.
- Thrombosis of the internal jugular vein.
- Rupture of the carotid artery.
- Pyaemia and septicemia.

- Differential diagnosis: From other parapharyngeal swellings.

- Treatment:
- Hospitalization
-Parenteral antibiotics, analgesic, antipyretics.
- Incision and drainage along the anterior border of the sternomastoid muscle.

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- Retropharyngeal Abscess
The retropharyngeal space is the space lying between the posterior pharyngeal wall,
covered by buccopharyngeal fascia and cervical vertebrae covered by prevertebral muscles
and fascia. It contains a pair of lymph nodes of Henle on either side of the midline. They
receive afferents from the pharynx.

1. Acute Retropharyngeal Abscess

- Suppuration of the retropharyngeal glands of Henle.
- Age: Only below 5 years, later the glands atrophy.
- Causes: Tonsillitis, Adenoiditis.
- Symptoms:
- Fever, malaise.
- Dysphagia
- Laryngeal obstruction: Collection of pus behind hypopharynx.
- Signs:
- Internal swelling: in the posterior pharyngeal wall to one side of the midline
limited by the median raphe.
- External swelling: Enlarged, firm, tender deep cervical LNs.
- Investigations:
- C.T scan: widening of prevertebral space with normal vertebrae. Treatment:
- Antibiotics.
- Incision and drainage is done from inside, with head down.

2. Chronic Retropharyngeal Abscess

It is a tuberculosis infection with collection of caseous material behind the prevertebral
fascia. It is also called cold abscess or Pott's disease of the spine in adults.
- Clinical picture:
General:
T.B toxaemia: (Loss of weight, Loss of appetite, Night fever, Night
sweating).
Local:
- Pulmonary T.B: Cough and hemoptysis.
- Dysphagia with dripping of saliva.
- Internal swelling: in the mid-line of posterior pharyngeal wall.
- External tenderness and rigidity: over the cervical spines.
- Investigations:
-CT scan: Widening of the prevertebral space with destruction.
-Investigations for T.B: As chest X-ray and sputum analysis.
- Treatment:
-Incision and drainage along the posterior border of the sternomastoid muscle.
-Anti-tuberculous treatment.

- Ludwig’s Angina
Collection of pus in the submandibular space.
The submandibular space is the space extending from the floor of the mouth above, to the
deep fascia of the submandibular region below.

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 - Causes:
1- Dental infection: in most cases.
2- Submandibular sialadenitis.

- Clinical picture:
- Fever, headache, malaise and anorexia.
- Dysphagia with dripping of saliva, Dyspnea later stridor.
- Internal swelling: In the floor of the mouth pushing the tongue above and backwards.
- External swelling: In the submandibular region. First: It is indurated (hard). Later on,
it becomes fluctuant (pus
formation).

- Treatment:
1- Antibiotics.
2- Tracheostomy if stridor occurs.
2- External incision in the submandibular region and drainage of the pus.

Malignant Tumors of the oropharynx

The commonest site is the tonsil and the base of the tongue. It affects males more above 50
years. Squamous cell carcinoma constitutes 75% while lymphomas 25% of malignant
tumours of oropharynx.

- Predisposing factors: smoking, alcohol and irradiation.

- Clinical picture:
- Dysphagia.
- Pain in oropharynx referred to the ipsilateral ear.
- Ulcer (in carcinoma), mass (in lymphoma), or nodular infiltrative.
- Neck swelling: lymph node metastasis.

- Investigations:
- CT scan: Demonstrate site, size and extension and L Ns metastasis.
- Biopsy: Tonsillectomy of the affected tonsil.
- Metastatic work up.

- Treatment:
- Radiotherapy: for the tumor and neck LNs.
- Surgery: Commando operation in failed radiotherapy (Combined neck dissection,
Mandibulectomy and Oropharyngeal resection)

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- Velopharyngeal Incompetence (VPI)
It is a malfunction of the velopharyngeal sphincter leading to air escape through the nose
during speech (Rhinolalia aperta) and fluids during swallowing (Nasal regurgitation).
Rhinolalia aperta (Hypernasality): Increased nasal tone of voice.
Rhinolalia clausa (Hyponasality): Decreased nasal tone of voice as in bilateral nasal
obstruction.

- Muscles of velopharyngeal sphincter:

Tensor and levator palati muscles, palatopharyngeus and palatoglossus muscles,
superior constrictor muscle and uvular muscles.

- Causes of VPI:
1- Congenital:
- Cleft palate and submucous cleft.
- Cervical spine or skull base deformity.
2- Acquired:
- Penetrating injuries as gun shot.
-Post surgical: as after tonsillectomy, adenoidectomy, maxillectomy, erosion
by tumour and palatal fistula.
- Neuromuscular due to paralysis of palate and pharynx: as Diphtheria, bulbar
palsy, meningitis and skull base lesions.
3- Inflammatory: erosion of palate (Syphilis).
4- Psychogenic.

- Treatment of VPI:
1- Treatment of the cause: repair of cleft palate.
2- Speech therapy for minimal VPI, and post operative.
3- Lengthening of soft palate by palatoplasty.
4- Pharyngoplasty or pharyngeal flap to narrow velopharyngeal sphincter.

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Diseases of The Hypopharynx
- Plummer Vinson Syndrome
Chronic inflammation of the mucous membrane of the hypopharynx and upper oesophagus
which leads to submucosal fibrosis forming a web.

- Causes: May be iron and vitamin deficiency in females (40 years).

- Clinical picture:
1. Dysphagia: chronic pharyngo-oesophagitis + web.
2. Angular stomatitis and glossitis.
3. Achlorhydria: atrophy of gastric mucosa.
4. Pallor: due to anemia.
5. Koilonychia (Spoon shaped nails).
6. Splenomegaly.

- Prognosis:
1- Stenosis.
2- Precancerous (postcricoid carcinoma).

- Treatment:
1- Correction of anemia: iron and vitamins.
2- Repeated dilatation.
3- Regular follow up (as the condition is precancerous).

- Pharyngeal pouch (Zenker’s diverticulum)

Herniation of the pharyngeal mucosa between the oblique and transverse fibres of the
inferior constrictor muscle (Killian’s space). It usually occurs in elderly males.

- Causes:
High intrapharyngeal pressure due to:
- Spasm of the cricopharyngeal sphincter.
- Failure of relaxation of the cricopharyngeal sphincter.

- Clinical picture:
- Small pouches are asymptomatic.
- Dysphagia in long standing pouches.
- Regurgitation of undigested food.
- Cough: aspiration of food into the larynx.
- Neck: Swelling under the left anterior border of the sternomastoid which is:
Cystic, compressible and increases with coughing and straining.
- Indirect laryngoscopy shows froth in pyriform fossa.

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 - Investigations:
- X-ray with barium swallows: Retort-shaped appearance.
- Hypopharyngoscopy: The opening of the pouch is seen.

- Complications:
0.5 -1% develops squamous cell carcinoma in the pouch.

- Treatment:
- Endoscopic treatment:
- Repeated dilatation of the cricopharyngeal sphincter.
- Endoscopic diathermy or Laser of the septum between the pouch and the
oesophagus.
- Surgical treatment:
- Cricopharyngeal myotomy.
- Excision of the pouch (diverticuiectomy): With cricopharyngeal myotomy to
prevent recurrence.

- Malignant tumours of the hypopharynx

It is usually a squamous cell carcinoma affecting old age above 50 years, more in males.
The hypopharynx consists of 3 parts
a) Pyriform Fossa: Inverted pyramid bounded by:
- Laterally: Thyroid cartilage and thyrohyoid membrane.
- Medially: Cricoid cartilage and aryepiglottic fold.
b) Postcricoid area: Extends from the arytenoid cartilage to the lower border
of cricoid cartilage below.
c) Posterior pharyngeal wall.

- Predisposing factors:
1- Plummer-Vinson syndrome: Leads to postcricoid carcinoma.
2- Smoking, irradiation, alcohol.

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- Sites: - Pyriform fossa (50%).
- Post-cricoid (40%).
- Posterior pharyngeal wall (10%).

- Spread:
1. Lymphatic spread:
- Pyriform fossa is one of the silent areas in head and neck, so lymphatic
spread to the upper and lower deep cervical lymph nodes could be the
presenting symptom in more than 70% of cases.
- Postcricoid is a midline structure which gives bilateral nodal metastasis.
- Postcricoid also gives to the superior mediastinal LNs (bad prognosis).
2. Direct spread: to the surrounding structures eg. larynx.
3- Early distant metastasis.

- Prognosis: Bad, 5 years survival rate in 30% of patients.

- Clinical Picture:
- Dysphagia; first to solids, then to solids and fluids.
- Pain referred to the ipsilateral ear (9th cranial nerve).
- Hoarseness of voice, later stridor (extension to larynx).
- Cough and may be hemoptysis.
- Underweight (Cachexia).
- Neck swelling: LNs. Enlargement

Hypopharyngoscopy:
- Ulcer, Cauliflower mass or nodular infiltrative.
- Froth collection in pyriform fossa or postcricoid area.

Examination of the neck:

- Moure's sign: friction of the cricoid cartilage to vertebrae showing absent click in
postcricoid carcinoma.
- Upper and lower deep cervical lymph nodes enlargement.

- Investigations:
- Barium swallow: to see lower limit of the tumour.
- C.T scan for neck shows:
* Widening of the prevertebral space in postcricoid carcinoma.
* Site, size, and extension of the tumor and if there is LNs enlargement.
- Direct hypopharyngoscopy and biopsy.
- Metastatic work up.

- Treatment:
- Curative treatment: - Total pharyngolaryngectomy and stomach pull up.
- Radical neck dissection for LNs involvement.
- Postoperative radiotherapy.
- Palliative treatment: For extensive tumours fixed to vertebral column and/or with
distant metastasis: Radiotherapy and chemotherapy.
- Surgery as tracheostomy for respiration and gastrostomy for
feeding.
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Snoring and Sleep apnea
Snoring is an undesirable sound that occurs during sleep. Muscles of the pharynx are relaxed
during sleep and causes partial obstruction. Breathing against obstruction causes vibration of
soft palate, tonsillar pillars and base of the tongue, producing the sound of snoring.
Sleep apnea is cessation of air flow at the mouth and nostrils lasting at least 10 seconds. The
syndrome of sleep apnea is diagnosed if there are at least 30 apnoeic episodes during 7 hours
of sleep.

- Types of sleep apnea:

Obstructive sleep apnea: due to obstruction of the upper air way during sleep.
Causes of obstructive sleep apnea:
1. Nasal: Deviated nasal septum, nasal polypi, hypertrophied nasal turbinates.
2. Nasopharyngeal: Adenoids, nasopharyngeal tumours.
3. Oropharyngeal: Enlarged tonsils, redundant soft palate, uvula and anterior pillars.
4. Hypopharyngeal: Macroglossia (huge tongue base), micrognathia (receding lower jaw)
and hypopharyngeal tumours.
5. General: Obesity, short neck, acromegaly and myxoedema.

- Clinical picture:
- Loud snoring interrupted with sleep apnea, restless sleep and nightmares.
- Day time somnolence, lack of concentration, drowsiness.

- Complications: Due to hypoxia and accumulation of CO2

Cardiac arrhythmias, pulmonary hypertension and congestive heart
failure.

- Investigations:
- ENT examinations : Fibreoptic nasopharyngoscopy.
- Polysomnography: In sleep laboratory to diagnose apnea.

- Treatment:
1. Weight reduction, avoidance of night sedation and alcohol.
2. Medical: In central causes, protriptyline works to reduce rapid eye movements in
which most of apnoeas occur.
3. Surgical:
- For Nasal obstruction: adenoidectomy, septoplasty, turbinectomy or polypectomy.
- Uvulopalatopharyngoplasty (UPPP): For oropharyngeal obstruction, including removal of
tonsils, uvula, redundant part of the soft palate, posterior pillars of the tonsils leading to
widening of the oropharyngeal orifice. The operation could be done with conventional
instruments or CO2 laser surgery (Laser assisted uvulopalatoplasty).
- Tracheostomy may be considered for patients who failed all above measures.
- Continuous positive airway pressure (CPAP): Air is supplied to patient under pressure
during sleep.

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Operations of the pharynx
- ADENOIDECTOMY
- Indications: enlarged adenoid causing symptoms.
- Operation:
- Anesthesia: General with an endotracheal tube.
- The adenoid is shaved with adenoid curette.
- A pack is put in the nasopharynx for few minutes until bleeding stops.
- Adenoidectomy may be done in young age without removal of the tonsils.
- Contraindication: Cleft palate to avoid velopharyngeal incompetence.

- Complications:
1- Hemorrhage:
a) Primary hemorrhage during the operation is due to: blood diseases, injury of
mucosa and muscles, aberrant vessels and incomplete removal.
b) Reactionary hemorrhage within the first 24 hours after the operation.
c) Secondary hemorrhage due to secondary infection.
It is treated by cautary for bleeding, posterior nasal pack and antibiotics.
2-Injury of:
a) Eustachian tube: causes otitis media and deafness.
b) Palate: causes regurgitation and nasal tone (VPI).
3- Recurrence: due to incomplete removal.

Adenoidectomy

- Tonsillectomy

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- Indications of tonsillectomy:
1. Recurrent acute attacks, more than 5 per year.
2. One attack of peritonsillar abscess (Quinsy).
3. Marked enlargement of the tonsils, interfering with respiration and deglutition.
4. Chronic tonsillitis:
- If the tonsils act as a septic focus.
- Local signs of chronic tonsillitis:
a) Irregular crypts that ooze pus on pressure by a tongue depressor.
b) Irregularity of the shape and size of the tonsils.
c) Congestion of the anterior pillars.
d) Enlarged jugulo-digastric lymph gland draining the tonsils.
5. Tumours of tonsils.
6. F.B in the tonsil.

- Contraindications:
- Absolute: Blood diseases: as haemophilia, purpura or leukaemia.
- Relative:
1. During acute attack of acute tonsillitis.
2. Recent attack and upper respiratory infections (wait 3 weeks).
3. During rheumatic activity with high sedimentation rate.
4. During epidemics, specially of poliomyelitis.
5. During an active general disease as diabetes or hypertension.
6. Pregnancy and menstruation.
- Septic focus:
A focus of infection which causes a state of toxaemia and bacteraemia due to
absorption of toxic material. Chronic tonsillitis causes rheumatic manifestations,
endocarditis, nephritis, arthritis, prostatitis, iritis or optic neuritis.
Sites of septic focus: Tonsils, teeth, sinuses, appendix, gall bladder, prostate and
fallopian tubes.
- Pre-operative management:
- History: To exclude any contraindications, e.g. bleeding tendency.
- Clinical examination: General: Temp., pulse, chest and heart.
Local: No acute attack.
- Laboratory investigations:
1- CBC: for anemia, leukaemia, purpra.
2- ESR: 5-10 mm./lst hour, 10-15 mm./ 2nd hour.
3- Coagulation profile:
a) Bleeding time: Normal 1-3 mm.
b) Coagulation time: Normal 3-6 min
c) Prothrombin time (12 seconds) and concentration (100%).
4- Urine should be free of albumin and sugar.

- Complications of tonsillectomy:

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Post tonsillectomy hemorrhage:
A) Primary hemorrhage: Bleeding during the operation.
- Cause: Operating on a patient with a contraindication.
- Treatment: 1- Ligate the vessels.
2- Give blood transfusion when needed.
B) Reactionary hemorrhage: Bleeding within 24 hours after the operation.
- Causes: Increased blood pressure, slipped ligature or dislodged clot.
- Treatment: Ligate the bleeding points under general anesthesia.
C) Secondary hemorrhage: Bleeding after the 6th to the 10th day.
- Causes: Sepsis leading to sloughing of vessels and tissues.
- Treatment:
1. Pack the bed of the tonsils with gauze and suture the pillars over it,
as tissues are too friable to be ligated.
2- Sedation.
3- Antibiotics.
4. If not stopped, consider external carotid artery ligation.

Tonsillectomy

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Diseases of the oesophagus
- Trauma of oesophagus
- Foreign bodies:
1- Coins in children (commonest).
2- Meat, bones, pins and dentures in adults.

- Sites of impaction
At the cricopharyngeal sphincter or constrictions (congenital or acquired).

- Clinical picture
Pain, dysphagia, regurgitation, excessive salivation.

- Dignosis:
Plain X-ray and barium swallow.

- Complications:
Oesophagitis, ulcerations and perforation, mediastanitis, tracheo-oesophageal fistula or
aorta (fatal hemorrhage).

- Treatment:
Removal by oesophagoscopy.

- Corrosive oesophagitis:
The condition is usually accidental in children and suicidal in adults.
Corrosives may by alkaline (potash) or acids.

- Acute phase:
- Severe pain and dysphagia from burn and ulceration.
- Stridor from laryngeal edema.
- Regurgitation of saliva and food.
- Treatment:
- Immediate neutralization by weak acid like vinegar or lemon juice.
- Milk and egg as demulcent.
- Antibiotics, IV fluids, steroids (prevent fibrosis).

- Chronic phase: Oesophageal stricture:

- Develops after 4-6 weeks due to fibrosis.
- Dysphagia , regurgitation, loss of weight.
- Investigations:
Barium swallow and oesophagoscopy.
- Treatment:
- Repeated dilatation for mild cases.
- Colon bypass in severe cases.

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- Inflammation of the oesophagus:
Inflammation of oesophageal mucosa (oesophagitis).

- Causes:
1. Trauma: foreign body, instrumentation and corrosives.
2. Gastric reflux as in hiatus hernia and recurrent vomiting .
3. Stasis as in achalasia and diverticlum of the oesophagus.

- Complications: Perforation of the oesophagus or stricture formation.

- Achalasia of the cardia (Cardiospasm):

Dilatation of the 1ower two-thirds of the oesophagus with retention of food and secretions.
It is due to neuromuscular disorder.

- Etiology:
Failure of relaxation (achalasia) of the lower end of the oesophagus due to
degeneration of Auerbach’s plexus.

- Clinical picture:
- Dysphagia: Intermittent and more to fluids than to solids.
- Regurgitation of undigested food.

- Investigations:
1- X-ray with barium: Marked dilatation of the lower 2/3 of the oesophagus with a
smooth tapering lower end (parrot-peak appearance and fluid
level).
2- Oesophagoscopy: shows pin point cardia.

- Treatment:
- Medical:
Antispasmodics: Amyl nitrite inhalation.
- Surgical:
1- Early: repeated dilatation.
2- Late: Heller’s operation (cardiomyotomy): the circular muscle fibres of the
cardia are incised down to the mucosa.
3- Cardioplasty: The cardiac sphincter is incised by a longitudinal incision and
sutured transversely.
4- Anastomosis between stomach and oesophagus in advanced kinked cases.

- Globus hystericus
Sensation of lump in the throat during swallowing of food and saliva with no organic
causes.

- Etiology: unknown, may be from cancer phobia.

- Investigations: Barium swallow and endoscopy are normal.
- Treatment: Psychological reassurance.
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Tumours of The Oesophagus
- Benign: Rare, liomyoma and papilloma at the upper part.
Treated by endoscopic removal.

- Malignant: More common, squamous cell carcinoma.

- Incidence: It is a common cause of dysghagia in old age affecting males more than
females. The lower ⅓ of oesophagus is more affected.

- Predisposing factors:
- Chronic oesophagitis, peptic ulcer.
- Achalasia of the cardia.
- Plummer Vinson syndrome (upper third in females).

- Gross picture:
1. Annular stricture 2- Ulcer. 3- Cauliflower mass.

- Clinical picture:
1- Dysphagia: Progressive, first to solids then to fluids.
2- Regurgitation.
3- Haematemesis.
4. Pain.
5- Loss of weight.
6- Hoarseness of voice due to recurrent laryngeal nerve affection.

- Investigations:
1- X-ray with barium: irregular filling defect (rat-tail appearance).
2. CT scan: for the extent of the tumour.
2- Oesophagoscopy: to visualize the tumour and take a biopsy.

- Treatment:
Oesophagectomy and anastomosis between upper end of oesophagus and the stomach.

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Dysphagia
Dysphagia is the medical term for the symptom of difficulty in swallowing. Dysphagia is
distinguished from other symptoms including odynophagia, which is defined
as painful swallowing, and Globus hystericus, which is the sensation of a lump
in the throat. A psychogenic dysphagia is known as phagophobia.

Causes of Dysphagia
a) Oral causes:
1. Congenital: Cleft palate.
2. Traumatic: Corrosives and wounds.
3. Inflammatory: Stomatitis, glossitis and ulcers.
4. Neuromuscular: Paralysis of the tongue, palate and cheek muscles.
5. Neoplastic: Cancer tongue.

b) Pharyngeal causes:
1. Traumatic: Corrosives and lacerations.
2. Inflammatory: Tonsillitis, pharyngitis, peritonsillar abscess, parapharyngeal
abscess and Plummer Vinson syndrome.
3. Neuromuscular: Pharyngeal pouch.
4. Neoplastic: Cancer pharynx.

c) Oesophageal causes:.
1. Trauma: Foreign body, corrosives and endoscopy.
2. Inflammatory: Oesophagitis and Plummer-Vinson syndrome.
3. Neuromuscular: Achalasia and bulbar paralysis, paralysis of diphtheria and
myasthenia gravis.
4. Neoplastic: Cancer oesophagus.

d) Extra-oesophageal causes:
1. In the neck: Malignant thyroid glands and pharyngeal pouch.
2. In the chest: Retrosternal goitre, enlarged glands, carcinoma, dilated left atrium,
aortic aneurysm and hiatus hernia.
3. In the abdomen: Enlarged left lobe of the liver.

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Gastro-Esophageal Reflux Disease (GERD)
Frequent spontaneous transient relaxation of the lower oesophageal sphincter (cardia)
leading to retrograde flow of gastric contents to oesophagus, pharynx and larynx.

- Etiology:
- Decreased lower oesophageal sphincter pressure due to hiatus hernia, smoking,
alcohol, dietary fat, chocolate and milk.
- Gastric hypertension due to stress, smoking, alcohol, caffeine, spicy food and citrus
fruits.

- Complications:
- Oesophagitis, ulcer, and stricture. -Chronic pharyngitis and laryngitis.
- Cancer oesophagus and larynx. -Secretory otitis media.

- Symptoms:
- Oesophageal: retrosternal burning may be diagnostic.
- Pharyngeal symptoms: sensation of throat irritation.
- Laryngitis symptoms: Hoarseness of voice and irritative cough due to chronic
laryngitis.
- Laryngismus stridulus in infants due to nocturnal laryngeal irritation.

- Signs:
-Flexible oesophagoscopy: oesophagitis, oesophageal ulcer and stricture.

- Investigations:
-Twenty four hours double probe pH monitoring.

- Treatment:
- General: weight reduction, elevation of head during sleep, avoidance of eating before
bed time, low fat diet and reduction of caffeine and spicy food.
- Medical: anti acids, H2 blockers to increase lower sphincter pressure, reduce juice
production and promote gastric empting.
- Surgical: if medical treatment fails, Fundoplication operation.

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 Anatomy of The Larynx
The Cartilages of the Larynx: (3 single and 3 paired)
The single cartilages The paired cartilages
• Thyroid cartilage. • 2 arytenoids.
• Cricoid cartilage. • 2 corniculates.
• Epiglottis. • 2 cuneiforms

(1) The Thyroid Cartilage:

• It has 2 laminae which are fused anteriorly in their inferior 2/3 forming the laryngeal
prominence (Adam’s apple).

(2) The Cricoid Cartilage:

• It has the shape of a ring, formed of an anterior narrow arch and a posterior broad
lamina.

(3) The Epiglottis:

• It is a leaf-like sheet of elastic fibrocartilage which projects upwards behind the tongue
and hyoid bone.

(4) The Two Arytenoid Cartilages:

• They are placed on the sloping shoulders of the upper border of the cricoid lamina.
• -Each is a three-sided pyramid, has an apex, base, 3 surfaces.

(5) Corniculate and (6) Cuneiform Cartilages:

• Are small nodules in the posterior part of the ary-epiglottic fold. They stiffen it.
Functions of the Laryngeal Cartilages: They prevent collapse of the air passages and
give attachment to a series of muscles.

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Cartilages of the larynx, Anterior view

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Interior of the Larynx :
The cavity of the larynx
-Extends from the laryngeal entrance to the lower border of the cricoid cartilage.
1. The glottis:
Is the space between the two vocal folds.
2- Supraglottic region: Consists of
a) Ventricular bands (false folds).
b) Ventricles: between the false and true folds; are covered with columnar ciliated epithelium.
c) Vestibule of larynx: epiglottis and aryepiglottic folds; are covered with stratified squamous
epithelium.

3- Subglottic region: between the vocal folds and cricoid cartilage

Interior of the larynx

Coronal section

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Intrinsic Muscles of the Larynx
@ Key facts:
1. All are confined to the larynx, connecting the different laryngeal cartilages.
2. All are supplied by the recurrent laryngeal N. except the cricothyroid muscle which
is supplied by the external laryngeal N.
(1) Cricothyroid Muscle (Tensor): It elongates and tenses the vocal ligaments.

(2) Posterior Crico-arytenoid (Abductor): It abducts the vocal cords and widens
the rima glottidis by rotating the arytenoid cartilages laterally. It is the only
abductor of the vocal cords and the only opener of the rima glottidis.

(3) Lateral Crico-arytenoid Muscle (Adductor): It adducts the vocal cords and
narrows the rima glottidis by rotating the arytenoid cartilages medially.

(4) Transverse Arytenoid Muscle (Adductor): It adducts the vocal cords by

approximating the arytenoid cartilages.
(5) Oblique Arytenoid Muscle (Adductor): It adducts the vocal cords.
(6) Thyro-arytenoid muscle: form the body of the vocal folds.
It shorten the vocal folds by pulling the arytenoid (back) end of the vocal folds toward the
thyroid (front) end thus lowering the pitch of voice. The thyroarytenoid muscles also have a
force to strengthen glottic closure.
The deep part is termed the vocalis muscle, and lies parallel with the vocal ligament.

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Blood Supply, Lymph Drainage, Sensory Nerve Supply:
Above the vocal cords
Arteries : Superior laryngeal A, a branch of
the superior thyroid A.
Veins : Superior laryngeal V. ® superior
thyroid V.
Lymphatics : Lymphatics pierce the
thyrohyoid membrane ® upper
deep cervical lymph nodes.
Sensory nerve Internal laryngeal N. of superior
supply to the laryngeal N. of vagus.
mucosa
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Below the vocal cords
Inferior laryngeal A, a branch
of the inferior thyroid A.
Inferior laryngeal V. ®
inferior thyroid V.
Lymphatics pierce the crico-
vocal ligament ®
prelaryngeal, pretracheal and
the lower deep cervical lymph
nodes.
Recurrent laryngeal N. of
vagus.
Rima glottides in different conditions

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 Histology of the Larynx
• It is lined by respiratory epithelium [except true vocal cord]
• Underlying CT. contains cartilages which support
the wall of larynx
• Laryngeal cartilages are 2 types:
o Large hyaline cartilages (thyroid, cricoid, and
lower part of arytenoids) and
o Small elastic cartilages
(Epiglottis, corniculate, and tips of arytenoids).
• Vocal cords are 2 pairs of folds
• Upper false &lower true vocal cords.
• False vocal cord(vestibular fold)
• They are covered by respiratory epithelium.
• True vocal cords:
• Covered by nonkeratinized stratified squamous epithelium.
Inferior to the vocal cords, the lining epithelium changes to respiratory epithelium.

Ciliated columnar cells

ccolumnared columnar

Goblet cell

Basal
cells

Examination of The Larynx

- History: Of
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 1- Hoarseness: A low pitched weak voice due to incomplete adduction of the vocal
folds.
2- Stridor: A difficult noisy breathing due to partial obstruction of the larynx.
3- Cough: If it is dry or with secretions.
4-Pain: If it is local or referred to the ear.
5- Dysphagia: Onset and is it for solids or liquids or both.
6- Haemoptysis: Is the expectoration of blood or blood-stained sputum.

- External examinations:
1- Inspection: For swellings, position, movements and suprasternal notch.
2- Palpation: For a) Tenderness. b) Broadening of the laryngeal contour.
c) Laryngeal click (Moure’s sign): It is a normal click due to sliding of
the laryngeal cartilages over the
vertebral column. It is absent in
postcricoid carcinoma.
d) Cervical and prelaryngeal lymph nodes.

- Indirect laryngoscopy:
Done by laryngeal mirror. It shows mobility and any
pathology of the vocal folds.

- Direct laryngoscopy:
Done under general anesthesia.
Indications
1- Diagnostic
a) To see the larynx in difficult cases as children or
those who have sagging epiglottis or exaggerated
gag reflex.
b) To take biopsy from a laryngeal mass.
2- Therapeutic
To remove a foreign body, polyp, nodule or small benign tumour.

- Endoscopic examination: Either by flexible nasopharyngoscope or rigid endoscopy

- Investigations:
1- Direct laryngoscopy and biopsy.
2- CT scan of larynx: tumours, trauma, stenosis.

Diseases of The Larynx

- Congenital Anomalies of The Larynx
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 1. Congenital laryngeal stridor (laryngomalacia).
2. Congenital glottic web.
3. Congenital vocal fold paralysis.
4. Congenital subglottic stenosis.

1. Congenital laryngeal stridor (Laryngomalacia):

It is the commonest cause of congenital stridor in infants
- The larynx shows:
-Folded, long epiglottis (Omega shaped).
-Short aryepiglottic folds.
-Soft laryngeal cartilages.
-Weak posterior cricoarytenoid muscle (abductor).
- Symptoms: Inspiratory stridor without hoarseness soon after birth.
- Laryngoscopy: Reduced laryngeal inlet due to folded supraglottic structures during
inspiration.
- Treatment:
- Self-limiting and in most of cases no treatment is required.
- Tracheostomy is rarely indicated.

2. Congenital laryngeal web (Glottic web):

It is a fibrous band between the two vocal folds anteriorly due to arrest of canalization
of the larynx.
- Symptoms:
- Weak hoarse cry.
- Dyspnea and stridor in severe cases
- Signs:
Laryngoscopy:
- The web is pink or white in colour with a curved edge.
- Small web = no symptoms.
- Medium sized web = hoarseness of voice.
- Large web = stridor and death.
- Treatment: Excision of the web by:
- Microlaryngosurgery.
- Laser surgery.
- Tracheostomy in severe cases with stridor.

3. Congenital vocal fold paralysis:

25% of all cases of congenital stridor in infants.
- Unilateral vocal fold paralysis:
- Causes: Birth trauma, congenital cardiovascular lesions.

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 - Clinical picture: Weak cry and stridor on exertion.
- Treatment: 50% recover spontaneously.
- Bilateral vocal fold paralysis:
- Causes: Hydrocephalus.
- Clinical picture: Severe stridor, feeding problems, aspiration and recurrent
chest infections.
- Treatment: tracheostomy, arytenoidectomy in late childhood.

4. Congenital subglottic stenosis:

- Abnormal thick cricoid cartilage.
- Usually discovered during intubation of the child.
- Treatment: Endoscopic submucosal resection in late childhood.

- Trauma of The Larynx

The cartilagenous framework and the lateral mobility of the larynx provide protection from
injury.

1-External trauma:
a) Closed: Strangulation.
b) Open: Cut throat and bullets.

2-Internal trauma:
a) Chemical: Corrosives.
b) Physical: Steam and irritant gases.

3- Operative trauma:
a) Clumsy laryngoscopy.
b) High tracheostomy.
c) Intubation granuloma.
- Symptoms:
1- Dyspnea. 2- Stridor. 3- Hoarseness.
- Signs:
1- Laryngeal edema.
2- Penetrating injury may result in
a) Skin Injury. b) Surgical emphysema.
c) Fracture laryngeal cartilage (crepitus and tenderness).
d) Hematoma and lacerations of the mucosa.
e) Bleeding.
- Treatment
Urgent tracheostomy followed by surgical repair and control of bleeding.

- Inhaled Foreign Body:

The airway is protected by the laryngeal sphincter (aryepiglottic folds, and vocal folds).
Also, the cough reflex aids in airway protection. A child inhales a foreign body during
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sleep, laughing or when frightened.

- Types of foreign bodies:

1- Vegetable foreign bodies such as seeds and beans.
2- Non-vegetable foreign bodies such as pins and beads.

- Clinical picture:
1- Laryngeal spasm, chocking, stridor and cyanosis. Then, the foreign body is either
coughed outside or inhaled inside.
2- It usually passes in the trachea to the right bronchus because it is wider and in line
with the trachea causing either partial or complete obstruction.
a) Complete obstruction of the bronchus leads to: atelectasis; there is dullness
and mediastinal shift to the same side.
b) Partial obstruction of the bronchus leads to: emphysema; there is resonance
and mediastinal shift to the other side.
3- Bronchitis occurs later and is due to obstruction, retention and infection.

- Diagnosis: X-ray for neck and chest:

-To show foreign body if it is radio-opaque.
-To show complications (collapse, emphysema, pneumonia).

- Treatment:
-First aid: Turn the child upside down and slap his back.
-Removal of the foreign body by direct laryngoscopy or bronchoscopy.

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Inflammations of The Larynx
I. Acute Non-Specific Laryngitis
It is an acute inflammation of the mucous membrane of the larynx.

- Causes:
- Secondary to upper respiratory tract infection.
- Secondary to lower respiratory tract infection.
- Voice abuse, smoking, irritant fumes, clumsy instrumentation.

- Symptoms:
1. Hoarseness in adults, cough and fever.
2. Stridor in children (croup), because in children (infantile larynx):
a) Larynx is small.
b) Lumen is narrow (funnel shaped with narrow point at cricoid cartilage).
c) Cartilages are soft.
d) Position is high under the tongue.
e) Submucosa is loose leading to more edema (edematous laryngitis).
f) Instability of neuromuscular mechanism (cannot expel mucous easily).

- Signs:
1. Congestion of folds in adults.
2. Subglottic edema in children.

- Treatment:
- Antibiotics, antiallergics and steroids.
- In children oxygen inhalation and tracheostomy if indicated.
- In adults: Vocal rest, Tincture benzoin Co inhalation.

II. Acute Specific Laryngitis

- Diphtheritic laryngitis
It is usually secondary to tonsillar diphtheria.

- Clinical picture:
- Hoarseness of voice, cough and fever.
- Stridor following extension of diphtheric pseudomembrane to larynx.

- Treatment:
- Rest, isolation, anti-toxic serum and penicillin.
- Tracheostomy if needed before heart failure takes place.

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- Acute epiglottitis
It is usually affects children (2-6 years) due to Haemophilus influenza.

- Clinical picture
- High fever, drooling, inspiratory stridor.
- Laryngoscopy: inflammation and oedema of supraglottic structures.

-Treatment:
- I.V antibiotics, antipyretics analgesics and steroids.
- Tracheostomy may be indicated.

I. Chronic Non-Specific Laryngitis

- Chronic Hypertrophic
A. Chronic Diffuse Hypertrophic Laryngitis
- Causes:
- Recurrent acute laryngitis.
- Chronic upper respiratory tract infection (URTI).
- Chronic irritation by dust and smoking.
- Voice abuse.
- Gastroesophageal reflux disease (GERD).
- Clinical picture:
Hoarseness of voice, dry irritating cough and sore throat.
- Laryngoscopy:
- Bilateral, symmetrical hypertrophy of the laryngeal mucosa.
- Reinke's edema: bilateral vocal folds edema (sac-like appearance).
- Treatment:
- Avoid predisposing causes as smoking and recurrent URTIs.
- Voice rest and treatment of GERD.
- Stripping of the thickened mucosa by microlaryngosurgery.
B. Chronic Localized Hypertrophic Laryngitis
1- Vocal folds nodules (Singer’s nodes)
It is an organized hematoma in submucosal hemorrhage due to over use or
faulty use of voice by singers and teachers (voice abuse). It commonly affects
the two vocal folds. It may affect children (screamer nodules).
- Clinical picture:
- Hoarseness of voice.
-Laryngoscopy: Bilateral smooth, raised, nodule at the junction of the anterior
⅓ and posterior ⅔ of the vocal folds (maximum contact).
- Treatment:
- Rest of voice.
- Speech therapy for small nodules.
- Removal by direct laryngoscopy and microlaryngosurgery.
2- Vocal fold polyp
A sessile or pedunculated edematous polyp arises commonly from one vocal fold
which may turn into a fibrous or vascular polyp. It is caused by voice abuse.

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 - Clinical picture:
- Hoarseness of voice.
-Laryngoscopy: Smooth, localized, white or red polyp on the vocal fold.
- Treatment:
-Removal by direct laryngoscopy and microlaryngosurgery.
3- Leucoplakia
It is a change of the non keratinizing squamous epithelium of vocal folds into
keratinized type with intact basement membrane due to chronic irritation as
smoking. It is precancerous.
- Clinical picture:
- Hoarseness of voice.
- Laryngoscopy: white raised patches on the vocal folds.
- Treatment:
- Stripping by direct laryngoscopy and microlaryngosurgery.
- Regular observation to detect early malignant changes.

II. Chronic Specific Laryngitis (Granulomas of the larynx)

Laryngoscleroma
It is usually secondary to rhinoscleroma. It affects the subglottic area by submucosal
infiltration which produces swellings under the vocal folds. Later, fibrosis occur
leading to formation of subglottic stenosis. It is the commonest laryngeal granuloma in
Egypt.
- Clinical picture:
-Dyspnea and biphasic stridor later with stenosis, no much effect on voice
-Laryngoscopy: Bilateral, symmetrical, subglottic masses or web.
-Usually the disease previously affects the nose.
- Investigations:
- Direct laryngoscopy and biopsy: Russel bodies and Mikulicz cells.
- CT scan: to determine the degree and length of the stenosis.
- Treatment:
- Medical:
- Streptomycin I.M one gm daily for 40 days (ototoxic and nephrotoxic).
- Rimactan 300 mg 2 times daily for 6 weeks (hepatotoxic).
- Surgical:
- Tracheostomy when stridor occurs.
- Laryngoscopy and CO2 laser excision in short stenosis.
Tuberculosis of the Larynx
It is usually secondary to pulmonary tuberculosis. The posterior half of the larynx is
commonly affected due to stagnation of the infected sputum in the interarytenoid area.
Treatment:
- Antituberculous drugs. - Tracheostomy if there is laryngeal obstruction.
Syphilis of Larynx It affects the anterior part of the vocal folds and epiglottis.

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Tumours of The Larynx
A- BENIGN TUMOURS
- Epithelial: Papilloma, adenoma.
- Connective tissue: Fibroma, angioma and chondroma.

- Squamous cell papilloma: Commonest benign tumour of the larynx.

It is single in adults and multiple in children.

Single papilloma of adults Multiple papilloma of children

-Adult male (30-50 year).
- True neoplasm.
- Hoarseness rarely stridor.
- Site: anterior ½ of vocal fold.
- No recurrence after removal
- Removal by direct laryngoscopy
and if big through laryngofissure.
- No tracheostomy is needed.
- No medical treatment.
- May turn malignant.
-Children (5-15 years).
- Viral (HPV) or hormonal.
- Hoarseness and stridor.
- Site: any part of the larynx.
- Recurs rapidly till puberty.
- Repeated removal by direct
laryngoscopy, microsurgery and
laser surgery.
- Tracheostomy, closed after removal
each time (larynx grows normal).
- Estrogen, Interferon
- Does not turn malignant.

Human Papillomaviruses ( HPV) (Wart viruses)

Transmission:
• Contact
• During birth in the case of juvenile laryngeal papillomas.

The major groups of HPVs are:

1- Cutaneous warts: The viruses cause warts (benign tumours) of keratinised
squamous epithelium (skin).In most people skin warts regress spontaneously
.Malignancies are most likely to develop in sun-exposed and traumatised area.
2- Mucosal HPV lesions: The virus infects the genital tract, oral cavity, and
respiratory tract. Infections are latent with no visible lesions. HPVs are also the
most common sexually transmitted viruses.
3- Laryngeal papillomas: They are rare and found in both adults and children.

Laboratory diagnosis:
Direct examination:
1- Immuno-cytochemistry: To detect group specific capsid protein.
2- DNA detection by PCR.

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B - MALIGNANT TUMOURS
- Squamous cell carcinoma is the commonest.
- Adenocarinoma , verrucous carcinoma, sarcoma.

- Predisposing factors:
- Leukoplakia, chronic irritation (smoking and alcohol), irradiation, papilloma in
adults and gartro-esophageal reflux disease.

- Incidence:
- Age: Over 40 years.
- Sex: Males are more affected than females.

- Sites:
- Glottic (on the vocal folds) 70%.
- Supraglottic 20%.
- Subglottic 10%.

- Symptoms:
1- Hoarseness appears early in glottic carcinoma, late in other types.
2- Stridor.
3- Dysphagia.
4- Haemoptysis.
5- Late pain, may be referred pain to the ear.

- Signs:
1- An ulcer, nodule or a papillomatous mass.
2- Fixation of the vocal fold due to infiltration of the intrinsic muscles.
3- Enlarged cervical lymph glands.

- Prognosis:
- Glottic: Early symptoms, early diagnosis, late metastasis, good prognosis.
- Supraglottic and subglottic: Late and vague symptoms, late diagnosis, early
metastasis and bad prognosis.

- Diagnosis:
- CT scan of larynx: shows the tumour and its extension.
- Direct laryngoscopy: for biopsy and definitive diagnosis.

- Treatment:
A) Surgical:
- Partial laryngectomy with safety margin for tumours limited to the vocal folds
without fixation and without cervical glands affection.
- Laser excision for glottic carcinoma limited to vocal fold.
- Total laryngectomy: If the vocal folds are fixed or if there is extension to:
anterior commissure, arytenoids, subglottic, supraglottic
areas or for recurrence after radiation or partial
laryngectomy.
- Block neck dissection if the cervical lymph glands are palpable.

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 B) Radiotherapy:
- Alternative to cordectomy in glottic carcinoma limited to vocal fold.
- Postoperative.

C) Palliative treatment:
For inoperable cases: Extensive infiltration to the surrounding sutrcures or distant metastasis:
- Radiotherapy, cytotoxic drugs, sedative as morphine.
- Tracheostomy for stridor, Gastrostomy for feeding.

Rehabilitation of voice after total laryngectomy:

- Development of oesophageal speech.
- Use of artificial larynx.
- Tracheo-oesophageal shunt (Provox).

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Paralysis of The Larynx
- Causes of laryngeal paralysis:
1- Intracranial:
Vascular as hemorrhage or thrombosis, tumours and multiple sclesosis.
It is usually accompanied with symptoms of the original disease.
2- Cranial: Affecting the vagus nerve at the skull base.
- Fracture base.
- Nasopharyngeal malignant tumours, glomus jugulare
3- Extracranial:
In the neck:
- Thyroidectomy (commonest cause of bilateral abductor paralysis).
- Malignant tumours of the Thyroid gland.
- Malignant cervical lymphadenopathy.
In the chest: Affect the left vocal fold only because the right recurrent
laryngeal nerve loops around the subclavian artery and does not
enter the chest.
Causes: Aortic aneurysm and bronchogenic carcinoma.
4- Idiopathic:
More than 30% of cases, no cause could be found and the paralysis may be due
to peripheral neuritis from viral infection like influenza.
5-Functional paralysis:
- Absence of voice with no organic cause.
- The condition is treated by psychotherapy and speech therapy.

- Investigations of a case of vocal fold paralysis:

If the cause could not be detected from history and clinical examinations:
- CT scan for chest, neck and skull base.
- Endoscopy of larynx and nasopharynx and biopsy from any lesion.
- Sputum analysis and Tuberculin test.

- Recurrent laryngeal nerve (RLN) paralysis

1- Unilateral RLN paralysis:
- There is no affection of respiration.
- Hoarseness of voice may disappear after 6 months to one year due to
compensation of the healthy vocal fold which crosses the midline to meet the
paralyzed fold.
Treatment:
- Spontaneous recovery.
- Speech therapy
- Medialization of the affected fold is done after 6 months if no
compensation from the healthy side occurs by thyroplasty or fat injection.

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 2-Bilateral RLN paralysis (Bilateral abductor paralysis):
Surgical trauma (Thyroidectomy) is the most important causes. The condition
is often acute.
As all the intrinsic muscles of larynx are paralysed, the vocal folds lie in
median or paramedian position due to unopposed action of cricothyroid
muscles. The airway is inadequate causing dyspnoea and stridor but the voice
is good. Dyspnoea and stridor become worse on exertion or during an attack of
acute laryngitis.

- Treatment:
- Tracheostomy as an emergency procedure if stridor occurs.
In long-standing cases, the choice is between a permanent tracheostomy with a
speaking valve or a surgical procedure to lateralise the vocal fold. The former
relieves stridor, preserves good voice but has the disadvantage of a tracheostomy
hole in the neck. The latter relieves airway obstruction but at the expense of a good
voice; however there is no tracheostomy hole in the neck.
- Lateralisation of the vocal fold:
Aim is to move and fix the vocal fold in a lateral position to improve the
airway
- Cordectomy: excision of one fold done by CO2 laser surgery.
- Cordopexy: endoscopic ligation and fixation of one fold laterally.
- Woodman’s operation: arytenoidectomy and cordopexy, i.e. suturing the fold
laterally to the thyroid cartilage through a laryngofissure approach.

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Symptoms of Laryngeal Diseases
- Hoarseness of Voice
It is a rough, low pitched voice due to incomplete adduction of the vocal folds.

Production of voice by the larynx is done with:

- Full adduction of the vocal folds.
- Tensing the vocal folds.
- Vibration of the vocal folds.
Lesions preventing full adduction, tension and vibration of the vocal folds will lead to
hoarseness of voice.
1- Congenital: Congenital web
2- Traumatic: Voice abuse, clumsy endoscopy.
3- Inflammatory: Acute and chronic laryngitis.
4- Neoplastic: Benign and malignant tumours affecting vocal folds.
5- Allergic: Laryngeal edema.
6- Neuromuscular: Unilateral RLN paralysis, myasthenia gravis.
7- Others: arthritis of crico-arytenoid joint, hysterical, smoking.

- Stridor
It is difficult noisy breathing due to partial obstruction of the airway (larynx, trachea or
bronchi).

- Dyspnea: Difficulty in breathing, often associated with lung or heart disease and
resulting in shortness of breath.

- Stertor: A heavy snoring sound in respiration. It occurs in common with mouth

breathing due to chronic nasal obstruction. It is important to distinguish
stertor from stridor.

- Types of stridor:
- Inspiratory stridor: indicates obstruction at the level of the larynx (glottic and
supraglottic area), it is high pitched.
- Expiratory stridor: indicates bronchial obstruction as in bronchial asthma or foreign
body in a bronchus.
- Biphasic stridor (inspiratory and expiratory): indicates subglottic or tracheal
obstruction: malignant thyroid, lymphadenopathy, mediastinal tumours.

- Causes of laryngeal obstruction (Stridor):

1. Congenital: Laryngomalacia, glottic web.
2. Traumatic: Foreign body, chemical, operative.
3. Inflammatory:
a) Acute laryngitis in children, acute epiglottis and diphtheria.
b) Chronic specific laryngitis: scleroma, syphilis and T.B.
4. Neoplastic: Multiple papilloma in children, Malignancy in adults.
5 - Neuromuscular: Bilateral abductor paralysis.

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 - Causes of stridor in infancy and childhood:
1. Congenital: Laryngomalacia,, glottic web and vocal folds paralysis.
2- Inflammatory: Acute non specific laryngitis in children.
Acute epiglottitis and diphtheria.
3- Traumatic: F.B. inhalation
4- Neoplastic: Multiple papilloma.
5- Laryngismus stridulus: It is apyrexial laryngeal spasm causing stridor in children at
night. The child is free by the day. It is common in ill health
and malnourished children. Treatment: good diet, vitamins
and minerals (vitamin D and calcium).

- Subglottic stenosis:
Subglottic stenosis is a narrowing of the subglottic airway.

- Causes:
- Congenital: not common.
- Traumatic: Traffic accidents, prolonged cuffed intubation (commonest).
- Inflammatory: Laryngoscleroma (common in Egypt).
- Neoplastic: Subglottic tumours.

- Clinical picture:
- Biphasic stridor.
- Hoarseness of voice if vocal folds are affected.

- Investigations:
- Laryngoscopy and CT scan to show the stenosis and its grade.

- Treatment:
- Tracheostomy if needed.
- Laser excision in short small stenosis.
- Laryngofissure and excision of stenotic area with skin graft closure.
- Resection of the stenotic area with end to end anastomoses .

- Symptoms of laryngeal obstruction:

1. Dyspnea is at first present on exertion then at rest.
2. Stridor is at first inspiratory and on exertion. Later it becomes inspiratory and expiratory.
3. Tachypnea (rapid breathing).
4. Nervousness and irritability.

- Signs of laryngeal obstruction:

1. Cyanosis and congestion of the neck veins.
2. Recession of the suprasternal, supraclavicular and intercostal spaces.
3. Tachycardia (rapid pulse).
4. Contraction of the accessory muscles of respiration.

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The trachea
- Tracheostomy
It is a surgical opening in the anterior wall of the cervical trachea.

Indications of tracheostomy:
1. Upper respiratory tract obstruction: All causes of stridor.
2. Lower respiratory tract obstruction (lower trachea, lungs and bronchi):
Wet lung syndrome: This occurs in conditions inhibiting the cough reflex, causing
retained secretions inside the alveoli and impairment of the
exchange of gases leading to hypoxia and hypercapnea. The
patient will be drowned in his own secretions.
Causes of wet lung syndrome:
Prolonged coma due to:
a) Cerebral: vascular, thrombosis and tumours.
b) Toxic: exogenous as in barbiturate poisoning or endogenous as in uremia
and diabetes.
c) Traumatic: fracture base and head injuries.
Peripheral causes:
a) Paralysis of respiratory muscles: Poliomyelitis and diphtheria.
b) Myopathies: Myasthenia gravis.
c) Multiple fractured ribs causing severe pain preventing coughing.
3. Pre-operative:
Before tumour surgery for the nasopharynx, maxilla and tongue to prevent
inhalation of blood during the operation.

- Value of tracheostomy:
1- To bypass obstruction of the upper airway.
2- To aspirate the accumulated secretions as in wet lung syndrome.
3- To maintain artificial respiration in cases of central respiratory failure.
4- To reduce the dead space by about 75 to 90 cc (above the tracheostomy).

- Types of tracheostomy: According to level of tracheostome.

1. High tracheostomy: In the 1st and 2nd tracheal rings above the isthmus of the
thyroid. It is done in emergency cases, later it may lead to
subglottic stenosis due to perichondritis of the cricoid
cartilage.
2. Mid tracheostomy: In the 3rd and 4th tracheal rings behind the isthmus (operation
of choice).
3. Low tracheostomy: In the 5th and 6th rings below the isthmus. It is usually done in
subglottic cancer or thyroid cancer.

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 - Time of tracheostomy:
- Urgent: If there is respiratory obstruction.
- Elective: If respiratory obstruction is anticipated e.g. preoperative.

- Complications of tracheostomy:
1- Shock: Anaphylactic shock from local anaesthesia.
2. Haemorrhage:
a) Primary: Anterior jugular vein, thyroid isthmus or innominate vein in
children.
b) Reactionary (during the first 24 hours): The wound should be reopened and
the bleeding vessels are ligated.
c) Secondary haemorrhage. After one week due to infection.
3. Injury of:
a) Blood vessels e.g innomonate vein.
b) Pleura, especially in low tracheostomy leading to pneumothorax.
c) Oesophagus: Causing tracheo-oesophageal fistula.
d) Cricoid cartilage: High tracheostomy causes perichondritis of the cricoid
cartilage and later subglottic stenosis.

4. Pulmonary complications:
a) Apnea: Arrest of respiration due to sudden wash of CO2 which was acting
as stimulus for the respiration due to long standing obstruction.
Treatment: Close the opening for a short time to allow
accumulation of CO2.
b) Pulmonary edema: Due to sudden release of pressure inside the lungs and
exudation from the capillaries. It causes noisy respiration, and
cyanosis.
Treatment: Respiratory and cardiac stimulants.
c) Pneumothorax: Due to injury of the apex of the pleura especially in
children and low tracheostomy..
Treatment: Chest tube attached to an under water seal.
d) Surgical emphysema: Of the neck due to air leakage around a small tube,
wide tracheal opening or tight skin sutures during inspiration. It
may extend to the mediastinum.
Treatment: Re-open to allow air out and change tube with a larger
one.
6. Tube problems:
a) Slipped, blocked tube may cause respiratory obstruction.
b) Long curved tube causes injury of the oesophagus (fistula).
c) Subglottic stenosis after high tracheostomy.

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