Contents

Page
SECTION ONE; THE EAR -^ \ 3 \

Anatomy of the ear 1

Functions of the ear 11
Diseases of the auricle 13
Diseases of the external ear canal 17
Acute otitis media 27--^
Chronic non suppurative otitis media 32
Chronic suppurative otitis media 37
Complications of suppurative otitis media 46
Trauma to the middle ear 66
Otosclerosis 72
Tumors of the middle ear 76
Meniere's disease 80
Acoustic neuroma 83.
Facial nerve 88
Deafness 99
Otalgia 115
Otorrhea 117
Vertigo 118
Tinnitus 123---
Ear operations 124

SECTION TWO: THE NOSE (o 5

Anatomy of the nose and paranasal sinuses 131

History and physical examination 141
Congenital diseases 143
Traumatic conditions of the nose 144
^Inflammations of the nose 151
Diseases of the nasal septum 165
^ A c u t e sinusitis 171
^Chronic sinusitis 176
 Complications of sinusitis 181
^Allergic rhinitis 191
Fungal infections of the nose and sinuses 198
Tumors of the nose and paranasal sinuses 201
Symptoms and sign of nasal diseases 214
Nasal operations 230

SECTION THREE: THE LARYNX -> 7©

Anatomy of the larynx 236

Examination of the larynx 242
Congenital diseases 244
^Trauma to the larynx 248
^Inflammation of the larynx 255
Vocal cord paralysis 268
Tumors of the larynx 275
Stridor 292
Hoarseness of voice 294
Laryngeal operations 295

SECTION FOUR: THE PHARYNX ~y 75

Anatomy of the pharynx 305

Diseases of the nasopharynx 310
^Inflammatory conditions of the pharynx 326
Suppurations related to the pharynx 343
Tonsillectomy 352
Stomatitis and oropharyngeal ulceration 361
^^Plummer Vinson syndrome 366
^ Pharyngeal pouch 372
The occult primary 374
^^^noring and sleep apnea 376

SECTION FIVE: THE OESOPHAGUS 380

SECTION SIX: LASER IN E.N.T. 396
SECTION SEVEN: NECK SWELLINGS 400
 PREFACE
The aim of this manual is to provide the medical stu-
dent and the practitioner with an updated and concise knowl-
edge in the management of diseases that involve the ear,
nose, throat, pharynx, larynx, oesophagus as well as related
head and neck conditions.
The principles of operative procedures are stated but
details of the technique aren't considered to be within the lim-
its of this book.
During the last thirty-five years, new modalities for
treating old diseases have evolved. The introduction of func-
tional endoscopic sinus surgery and CT scanning have
changed the concepts in managing chronic sinusitis.
Laser surgery, particularly C02 laser paved the way to
a new era in endoscopic management of laryngeal diseases
namely benign and malignant lesions,
The recently developed chemotherapy protocols for
advanced laryngeal cancer provided the hope for organ
preservation.
The old dream of making a totally deaf patient hears
has become a reality the introduction of cochlear implants.
Several photographs were provided through this book,
they demonstrate a sample of a collection gathered by the
author over the last thirty-five years of work in Kasr El Aini
hospitals, Cairo University.
My cordial thanks and appreciation go to my young
colleague Dr.Mohamed Mosleh Ibrahim Khalil. His tremen-
dous effort and sincerity during preparation of the
manuscripts and the painstaking suffering in revising and
printing the drafts deserve special recognition.
I would also like to take this opportunity to thank my
teachers who gave me the skills to practice otolaryngology.
My special thanks to my colleagues, my students and
my patients from whom I learned a lot.

Editor
Prof. Maged El Shennawy
September, 1999
 THE EAR
Anatomy of the ear
The ear is the organ concerned with hearing and maintenance
of equilibrium. It is composed of three parts; the external middle,
and inner ear.

I. External ear
It consists of the auricle, external auditory canal, and the
tympanic membrane (drum).

A. Auricle
This is a cupped appendage, which is composed of skin
covering cartilage. It serves to collect sound waves and direct
them into the external auditory canal. Rudimentary muscles
attach the auricle to the skull. Although normal variations occur,
certain components are common to the auricle, and these are:
(Fig. 1)
a.Helix: rolled edge of the periphery.
b.Antihelix: "Y-shaped" .within confines of the helix.
c.concha: bowel-shaped depression in the center.
d.Meatus: entrance of the external auditory canal.
e.Tragus: Cartilagenous prominence anterior to the meatus.
f Lobule: Fleshy inferior Portion devoid of cartilage.

Tragus

Concha

Lobule
Fig.1. The auricle

B. External auditory canal (E.A.C.)

-It extends from the bottom of the concha to the tympanic
membrane. It measures about 2.5 cm in length. It is oval
in section.
-It is partly formed by cartilage and partly by bone.
 10

T.M. arc supplied by the auriculotemporal nene.

branch from the 3'^ division (Mandibular) oi' the
trigeminal nerve,
c. The posterior wall and floor of the E.A.C.,
postauricular groo\'e and the concha are supplied, by
the auricular branch of vagus (Arnold's nerve).
2. The middle ear is supplied by the tympanic branch of the
glossopharyngeal nerve (Jacobson's nerve).
3. The mastoid antrum and cells are supplied by meningeal
twigs of the Gasserian ganglion of the trigeminal neiTc.

B. Motor
1. Auricular muscles; supj)lied by the facial nerve.
2. Tensor lympani; is supplied by the mandibular division of
the trigeminal nerve.
3. Stapedius; is supplied by the facial nerve.
 11

Functions of the ear

A. Hearing
1. The external ear: The auricle acts as a collector of sound,
and the sound waves are transmitted to the T.M. through
the E.A.C. The external auditory canal because of its
shape and dimensions amplifies the sound, thus the T.M
is set into vibrations.
2. The middle ear: it has three functions:
a. Conduction of the sound waves from the T.M., to the
oval window via the ossicular chain.
b. Magnification of sound about 20 times, this is due to
• The T.M. has a surface area 17 times greater
than that of the oval window.
• The lever action of the ossicular chain which
procedures a gain of 1.2/1.
• So this process ser\'es as an impedance-
matching between air (in the E.A.C.) and fluid
(in the inner ear).
• Waves propagate through the inner ear fluiils
due to phase difference between the oval and
round windows (i.e. the oval window is
triggered in an early phase, compared to the
round window and not at the same time).

3. The inner ear

When the oval window is set into vibration, this produces a
movement in the inner ear fluids, causing a traveling wave to be
created along the basilar membrane and its organ of corti. This leads
to bending of the sterocilia with depolarization and stimulation of
the hair cells of the organ of corti, and here, the mechanical sound
waves are converted into electrical impulses that are transmitted
along the cochlear division of the eighth nerve.

N.B. The electrical event in the organ of corti is called the cochlear
microphonics, and that occurring in the nerve is called the action
potential.

The electrical nerve impulses are transmitted along the

auditoi7 nei"ve to the cochlear nuclei in the brain stem to the high
 12

cortical hearing center (auditory area and auditory association area),

in the superior temporal gyrus where it is perceived as a meaningful
sound.

B. Equilibrium
The receptors (hair cells) are located in the maculae of the
otolith organs (utricle and saccule), and on the cristae of the
semicircular canals. The otolith organs are stimulated by linear
acceleration and the semicircular canals are stimulated by rotation
(angular acceleration).
 13

Diseases of the auricle

I. Congenital anomalies of the auricle
They result from maldevelopment of the first and second
branchial arches and they include:

A. Auricular atresia (aplasia)

• It varies form mild malformation (microtia) to complete absence
of the auricle. It may be unilateral or bilateral.
• It is usually associated with anomalies in the external canal
(meatal atresia) and in the middle ear. Conductive hearing loss is
frequent.
• It may be due to chromosomal abnormality, or embryopathies as
rubella infection or drug intake as thalidomide during the first
trimester of pregnancy.
• Treatment: Plastic reconstructive surgery, before school age.

B. Preauricular cyst and fistula

• It is commonly found at the root of the helix. It may be unilateral
or bilateral.
• Repeated infections may occur in the fistula with purulent
discharge, pain, tenderness and swelling.
• Treatment: Surgical excision if repeatedly infected, taking care of
the frontal branch of the facial nerve.

C. Preauricular appendages (accessory auricle)

• Small skin covered tags in the preauricular area on a line drawn
from the tragus to the angle of the mouth.
• Treatment: Surgical treatment is not indicated unless cosmetically
undesirable.

D. Protruding ear (bat ear = lop-ear deformity)

• This is the commonest auricular deformity.
• Treatment: Plastic surgery if manifesting.

E. Macrotia: (abnormally large auricle)

 14

II. Trauma to the auricle

Because of its exposed location the auricle is accessible to
any sort of trauma.

A. Auricular haematoma
.Aetiology: It is due to blunt trauma, which is frequently seen in
boxers. This causes haemorrhage under the perichondrium due to
disruption of adherence between perichondrium and cartilage.

Clinical picture: It appears as a bluish, rounded, smooth, cystic

swelling, which may be painful, but not tender.

If left untreated it may lead to cartilage necrosis and infection

ending in deformity of the auricle "Cauliflower ear".

Treatment: The goal of treatment is to prevent deformity

1, Aspiration: Simple needle aspiration and application of local
pressure dressings.
2. Incision and evacuation; is indicated in
- Rcaccumulation after aspiration
- Organized haematoma (not cystic).
.V Svstemic antibiotics; to avoid infection.

B. Frost bite
fhe auricle appears white, slightly shiny, with loss of sensation of
the affected part. Bullae may be present.
Treatment
• Gradual rewarming, hot compresses and antibiotics.
• Surgical dcbridment if the above measures failed.

( . Lacerations
• They range from mild lacerations to complete avulsion of
the auricle
• Treatment
1. Surgical repair
2. Prophylactic antibiotics, to avoid infection and
subsequent defomiity.
 15

III. Perichondritis of the auricle

Inflammation of the cartilage of the auricle. The auricle is a
continuos sheet of cartilage so infection of one part spreads to
involve the whole auricular cartilage and perichondrium which may
end in cartilage necrosis and shrinkage of the whole auricle
(Cauliflower ear).

Aetiology
1. Trauma to the auricle: e.g. Infected haematoma.
2. Fumculosis of the external ear canal if inadequately treated.
3. Postoperative; following ear surgery.
4. Idiopathic.

Causative organism; usually streptococcus pyogenes.

Clinical picture
• The whole auricle including the lobule is swollen, red, hot and
tender.
• The periauricular soft tissues maybe involved.
• Defonnity and shrinkage of the auricle may occur due to cartilage
necrosis (Cauliflower ear).

Treatment
A. Prophylactic
1. Avoid incisions in an inflamed external ear canal.
2. Prophylactic antibiotics for risk cases e.g. haematoma.

B. Curative
1. Systemic antibiotics: I.V. antibiotics, better according to culture
and sensitivity.
2. Topical antibiotics.
3. Analgesics.
4. Incision and drainage
• Indication: evidence of pus collection under the perichondrium
(pitting oedema, pointing and fluctuation).
• All necrotic cartilage should be excised and drainage is
maintained.
 16

IV. Tumours of the auricle

These are rare, and the most common are:
1. Basal cell carcinoma (rodent ulcer)
Ulcer with rolled in beaded edges, indurated base.
Treatment: surgical excision with safety margin

2. Squamous cell carcinoma

• Ulcer with raised everted edges, rough necrotic haemorrhagic
floor and indurated base.
• There may be lymph node metastases (mastoid, parotid or upper
deep cervical nodes).

Treatment:
1. Surgical excision with safety margin ± postoperative
radiotherapy.
2. Enblock radical neck dissection if there are lymph node
metastases.

Diseases of the external auditory canal (E.A.C.)

I. Congenital atresia of the external canal

Congenital obstruction of the external auditory canal due to
dcfccli\c development of the first branchial arch.

Clinical picture
1. Commonly unilateral but may be bilateral. It varies from thin
membranous atresia to complete bony obstruction.
2. Conductive deafness is present. There may be sensorineural or
mixed deafness if there is associated inner ear anomaly.
3. Microtia may be associated.

Investigations
1. CT scan; to detect condition and areation of the middle ear,
condition of the inner ear, and the length of the atretic segment.
2. Audiological investigations; PTA, ABR.

Treatment
A. Hearing aid; for infants with bilateral atresia.
B. Surgical:
 " ^

17

• In unilateral cases surgery is elective and can be postponed, while

in bilateral cases at least one side should be done at the age of 5-6
ears.
• Operation: Canalomeatoplasty with plastic reconstruction of the
auricle if microtia is associated.

Otitis externa
Inflammation of the skin of the external auditory canal.
Classification
I. Infections
Bacterial
• Diffuse otitis externa.
• Furunculosis.
• Malignant otitis externa.
Fungal
Otomycosis.
Viral:
• Herpes Zoster.
• Herpes simplex.
• Bullous otitis externa.

II. Non infectious

May be a part of skin disease:
• Eczematoid otitis externa.
• Seborrhaeic otitis externa.
• Neurodermatitis.

Otitis externa may be:

• Acute
• Chronic
chronic
• Recurrent (especially in diabetics and immunocompromized).
 18

Furunculosis (acute localized otitis externa)

Acute staphylococcal infection of the pilosebaceous follicles

of the outer cartilagcnous portion of the external canal (as it is the
portion that carry hair follicles). It begins as folliculitis and then
extend to form a furuncle

Clinical picture
May be multiple and recun'ent especially in diabetics.
May be single or multiple furuncles.

Symptoms
1. Severe pain especially on moving the auricle and on mastication.
Pain is severe due to limited room for expanding oedema.
2. Scanty purulent, cheesy discharge when it ruptures.
.3. Conductive deafness due to obstruction of the canal by a large
furuncle.

Signs
1. Severe pain is elicited on moving the auricle, pressing on the
tragus or insertion of an car speculum.
2. localized reddish swelling (may be multiple) in the area of the
cartilaginous portion of the external canal with surrounding
cellulitis beyond it.
3. Possible regional adenopathy.

Investigation; blood suuar in bilateral and recuirent cases to

exclude diabetes.

Ircatment
1. Packing the external canal with a piece of gauze soaked with
• (jlycerin iethyol 10%. Glycerine is hygroscopic and icthyol is
counter initant). It stood the test of time.
• Steroids and antiseptic cream. The pack is changed after 48 hrs.
2. Repeated local cleaning (aural toilet).
.3. Avoid incision of a ruruncle as it may spread infectioti to the
cartilage leading to perichondritis. If it becomes fluctuant
incision and drainatie can be done.
 "TJ

19

Local heat is very important to relieve pain, oedema and

preauricular tenderness.
Systemic antibiotics.
Analgesics.

Acute diffuse otitis externa

Acute diffuse inflammation of the skin of the external canal.
Aetiology
Predisposing factors:
Environmental changes especially hot humid atmosphere.
Excessive moisture from swimming or bathing.
Mild trauma from scratching or self cleaning of the canal.
Seborrhaeic (waxy) skin and dandruff of the scalp.
Decreased immunity as in diabetics and immunocompromized.

Causative organisms;
Pseudomonas, proteus, staph,, strept.

Clinical picture
Symptoms
1. Severe pain increased on mastication. Itching may occur before
pain.
2. Mild conductive deafness may be present with plugged sensation
in the ear.
3. Scanty purulent discharge.

Signs
1. Pain elicited on auricular movement and Iragal pressure.
2. Diffuse oedema and reddness of the skin of the canal.
3. The external canal may be completely blocked by oedema or
desquamated debris obscuring the drum.
4. Possible regional adenopathy (postauricular).

Investigations
1. Blood sugar level especially in recurrent cases.
2. Culture and sensitivity of discharge in resistant cases.
a. The cartilagenous portion: (Outer 1/3).
- It is about 8 mm long.
-Cartilage is continuos with that of the auricle. Cartilage is
deficient in the upper and posterior parts being replaced b\
fibrous membrane.
-It is lined by skin containing haii, fat, sebaceous glands.
and ccruminous glands (wa.x producing).

b. fhe bony Portion: (medial 2/3).

- It is about 16 mm in length.
- It is lined by skin devoid of hair and glands.
'fhe medial end is marked by a narrow groove {t_\nipanic
sulcus), in which the tympanic membrane is lodged

The E.A.C. forms an s-shapcd curve, and is directed at llrst

medially, forwards and slightly upwards. It then passes mcdiall).
backwards and upwards, and lastly, it is carried medial 1\, forwards
and slightly downwards.
It presents two constrictions, one in the medial end of the
cartilaginous portion, and another 5 mm from the tsnipanic
membrane, and is called the isthmus.
Anteriorly, it is related to the parotid gland, and
temporomandibular joint. Posteriorly, lies the mastoid process.

('. The tympanic membrane (T.M.)

• I'his is an oval, concave
membrane situated at the medial
end of the E.A.C, lying in a
c o n e of I'g^il
groove of bone called the
tympanic sulcus. Which is
deficient above (notch of Rivinus)
(Fig. 2).
• It is composed of two parts:
a. Pars tensa: It is the lower greater portion and enclosed
within the tympanic sulcus
b. Pars flaccida (Shrapnell's membrane): It is the upper part
extending along the notch of Rivinus.
• Both parts arc separated by the anterior and posterior malleolar
folds.
 20

Treatment
1. Repeated local cleaning of the canal (aural toilet).
2. Avoid entry of water into the ear.
3. Topical steroid ear drops.
4. Packing the external canal with a piece of gauze Soaked with
aluminium acetate 8% (astringent). Then steroid drops are placed
over the pack 4 times/day and the pack is removed after 48 hrs.
5. Systemic antibiotics.
6. Analgesics.

Malignant otitis externa

(necrotizing external otitis)
This is a persistent severe infection that extends beyond the
confines of the external canal to involve bone and soft tissues of the
skull base (osteomyelitis of the skull base and other periaural soft
tissues). It occurs almost exclusively in elderly diabetics and may be
terminal.

Aetiology
Predisposing factors
1. Diabetes; as it causes microangiopathies and decreases the
phagocytic activity of leucocytes.
2. Immunocompromized (e.g. AIDS, chemotherapy, immuno-
suppressive drugs).

Pathology
• Microangiopathy.
• Ostcomyetitis of the skull base (temporal bone).

Clinical picture
Severe persistent otitis externa in an elderly diabetic patient
with;
1. Progressive or persistent severe pain which is deep seated or
boring, and worsnes by night.
2. Scanty purulent aural discharge.
3. Persistent granulations in the posteroinferior portion of the
external canal at the bony-cartilagenous junction. The bone may
be exposed.
 21

4. Manifestations of extension of infection across the skull base:

a. Mastoiditis.
b. Facial nerve paralysis (due to involvement of the
stylomastoid foramen).
c. Zygomatic swelling and extension to the temporomandibular
joint.
d. Involvement of the parotid gland.
e. Brain abscess.
f Extension to the Jugular foramen leads to paralysis of the last
four cranial nerves (IX, X, XI, XII), which are manifested as
follow:
• 9' nerve: loss of pharyngeal sensation
• 10 nerve: vocal cord paralysis.
• 11 nerve: weakness of stemomastoid and trapezius.
• 12' nerve: Paralysis of one half of the tongue.
G. V (tngemnal) cranial nerve paralysis (loss of sensation of one
half of the face) due to extension of infection to the petrous apex.

Investigations
1. Fasting blood sugar level.
2. Base line kidney function tests.
3. Pure tone audiogram (PTA).
4. Culture and sensitivity of discharge.
5. Erythrocyte sedimentation rate (ESR).
6. CT scan of temporal bone.
7. Bone scan (Gallium 67, and tecnecium).
8. Biopsy from granulations to exclude malignancy.

N.B. Any elderly diabeteic patient with persistent or progressive

otitis externa for more than two weeks despite the standard medical
treatment should be carefully evaluated for necrotizing external
otitis.

Treatment
1. Hospitalization.
2. Control diabetes.
3. Systemic antibiotics: (Antipseudomonal antibiotics).
a. Quinolones: e.g. Ciprofloxacin, Ofloxacin, given first l.V.
for 2 weeks, then continued orally.
 22

b. Aminoglycosides: e.g. Gentamycin 80 mg I.M. 8 hourly,

however, they are Ototoxic and nephrotoxic but strongly
effective as antipseudomonal weapon when combined with
semisynthetic penicillins e.g. carbinicillin, ticarcillin,
netilicin, etc....
c. Third generation cephalosporins.
Prolonged therapy (at least 6 weeks), and combination antibiotics is
recommended.
4. Local:
a. Daily aural toilet.
b. Topical antibiotic ear drops, e.g. polymixin, tobramycin.
5 Surgical treatment: is restricted to local debridement.
• Local debridment of granulations.
• Removal of sequestra.
• Drainage of the abscess.

Otomycosis
This is an inflammatory reaction secondai7 to fungal
infection of the external canal.
Causative fungi
• Aspergillus (niger and fumigatus).
• Candida albicans.

Clinical picture
Symptoms
1. Intractable itching felt deep in the ear canal. Pain occurs later if
secondary bacterial infection occurs.
2. Creamy or greyish white aural discharge.
3. Deafness if the fungal mass obstructs the canal.

Signs
1. Erythema of skin lining the external canal.
2. I'ungal mass: black, gray or white fungal debris resembling a
piece of wet newspaper is seen in the deep part of the canal.
 23

Treatment
1. Removal of the fungal mass by suction or ear wash.
2. Topical antifungal treatment: (Antifungal ear drops).
a. Nystatine eardrops.
b. Clotrimazol ear drops.
c. 2% salicylic acid (keratolytic) in 70% alcohol (antifungal).
d. 2% acetic acid solution.
3. Packing the external canal with a piece of gauze soaked with an
antifungal cream e.g. Canesten, over which topical antifungal
ear drops are placed 4 times/ day and pack is left for 48 hours.

Viral otitis externa

A. Herpes simplex
• Occurs with fever e.g. influenza and common cold.
• Appears in the form of vesicles filled with fluid in the external
canal, T.M., and nose. It ruptures and heals leaving no scar.

B. Herpes zoster
Caused by varicella zoster virus.
Clinical picture
• Unilateral retroauricular or infra-auricular pain, vesicular eruption
appear 3-7 days after pain. It affects the cymba concha, (the part
supplied by the 7th cranial nerve).
• Ramzy hunt syndrome: Consists of otalgia, facial nerve paralysis
(due to affection of geniculate ganglion), sensorineural hearing
loss and dizziness (due to affection of 8 ' nerve).
• May be multicranial nerves involvement.
Treatment
1. Rest, Fluids, Light diet, warm compresses.
2. Analgesics.
3. Topical debridement and topical acyclovir.
4. Systemic antiviral e.g. Acyclovir to be given \cry early in the
disease.
5. Steroids in severe cases v/ith facial paralysis.
 24

C Bullous otitis externa

• Sudden sever Otalgia which is followed by bloody or
serosanguinious discharge with relief of pain.
• Bluish red haemorrhagic bullae covering the skin of the bony
portion of the external canal. May be associated with bullous
myringitis.
Treatment
• Analgesics, steroids, topical antibiotic ear drops, systemic
antibiotics.
• Decompression of bullae by sterile needle if there is severe
pain.

Impacted ear wax

Wax (cerumen) is the normal brownish secretion of
cereuminous and sebaceous glands situated the skin of the outer
cartilaginous part of external canal. Normally, it is cleared off the
external canal, by epithelial migration, but excessive accumulation
and dryness of wax causes its impaction and this produces
symptoms.

Symptoms
1. Deafness (when the canal is completely obstructed by impacted
wax), noticed usually after bathing or swimming, as wa.\ imbibes
water and occludes the canal.
2. Tinnitus.

Signs
Dark brownish mass is seen occluding the canal (hard wax), it may
be yellowish (soft wax).

Treatment
1. Soft wax; is rcmo\cd by ear wash.
2. Hard wax; is softened by glycerine bicarbonate ear drops then
removed by ear wash after few days.
 25

Foreign body of the external canal

Occurs in children and mentally retarted adults.

Types
A. Animate F.B.: insects e.g. Flies, larvae.
B. Inanimate F.B.:
a. Vegetable: e.g. beans, seeds (swell by imbibing water).
b. Nonvegetable: e.g. Buttons, stones ...etc.

Clinical picture
1. History given by his relatives of F.B. put into the ear.
2. Severe irritation and noise in case of animate F.B.
3. Conductive deafness.
4. Otitis externa if left for a long period.
5. Rupture of the drum and bleeding per ear, and lacerations in the
external canal especially with sharp pointed F.B.

Treatment; Removal of the F.B. as Follows:

1. Animate F.B.: Killed first by applying oily drops, or glycerine
then removed by ear wash or suction.
2. Inanimate F.B.
a. Vegetable: Remove by a hook.
b. Nonvegetable: remove by ear wash or a hook.
3. If the patient is uncooperative or the F.B. is deeply impacted, it is
better removed under general anaesthesia using the microscope
to avoid injury of the external canal or the drum.

Ear wash
Indications
1. Impacted wax.
2. Foreign body.
3. Otomycosis (Fungal mass).
4. Caloric test.

Contraindications
1. Traumatic or dry pathological perforation of the T.M.
2. Vegetable and impacted foreign body.
 26

3. Chronic Suppurative otitis media.

4. Postoperative after car operations.

Techniques (Fig. 10)

The car syringe is filled with wami water (best at body
temperature), and the syringe is applied with its nozzle directed
towards the posterosupcrior meatal wall. After ear wash, the canal is
dried with alcohol.

Complications
1. Traumatic rupture of the tympanic membrane due to
maldirection of the water stream or vigorous wash. The patient
feels se\xrc pain, discomfort and vertigo, and there is blood
coming out of the car.
2. 1 rauma to the skin of the external canal by the nozzle of the
syringe.
3. Vertigo due to stimulation of the inner ear by too hot or too cold
water (Caloric stimulation).
4. F<.encx coughing or vasovagal attack due to stimulation of the
auricular branch of vagus.
5. Otitis externa if unstcrilized instruments are used.

Fig 10 ear wash

 27

Acute otitis media (A.O.M.)

This is an acute inflammation of the mucosal lining of the

middle ear cleft (middle ear, Eustachian tube, mastoid air cells).

Aetiology
A. Route of infection
1. Through the Eustachian tube: (commonest route).
a. Extension of infection from the nasopharynx, following upper
respiratory tract infections as in common cold, tonsillitis,
adenoiditis, sinusitis, and exanthemata (e.g., measles and
mumps).
b. Passage of infected materia! through the Eustachian tube as
vomitus, water in swimming and diving and cases with
nasogastric tube feeding.
2. Through the tympanic membrane (T.M.): rare,
• Either through a perforation in the T.M., or through ventilation
tubes as grommet's tube.
3. Haematogenous spread:' very rare.

B. Causative organisms
The majority of upper respiratory tract infections arc
triggered by viral agents and most acute otitis media arc caused by
pyogenic secondary infection, and they include;
• Streptococcus pneumoniae.
• Group A- beta haemolytic streptococci.
• Haemophilus influenza.
• Pneumococci.
• Branhamella catarrhalis.

Pathology: The condition passes through the following stages:

1. Stage of Eustachian tube obstruction (Tubal catarrh): Tubal
obstruction due to oedema and congestion, later air is absorbed
from the middle ear.
2. Stage of hyperaemia and congestion: There is oedema and
congestion of the middle ear mucosa with accumulation of serous
lluid exudate.
 28

3. Stage of suppuration: Before perforation of the T.M. the serous

exudate becomes infected (mucopurulent) and pus accumulates
under tension.
4. Stage of perforation and discharge: Necrosis of a part of the T.M.
occurs because its blood supply is end arteries (like skin), with
passage of the mucopurulent discharge through the perforation.
.'i. Resolution: The T.M. heals and the fluid becomes thin and
serous. This can occur at any stage depending on the vimlence of
the organism, host resistance and the efficacy of treatment.

Clinical picture
The disease passes through several clinical stages
corresponding to the pathological stages, and the process may be
unilateral or bilateral.

A. Stage of tubal catarrh

Symptoms
1. Sensation of fullness and obstruction in .the ear.
2. Mild deafness.
3. Tinnitus may be present.

Signs
1. Otoscopy shows retracted T.M., which is detected as:
• Prominent lateral process of malleus.
• Shortened handle of malleus.
• Exaggerated anterior and posterior malleolar folds.
• Disturbed cone of light.
• Pneumatic siegalization shows limited mobility of T.M.
2. Tuning fork tests: show conductive hearing loss.

\i. Stage of congestion

Symptoms
1. Starting general manifestations: Fever, headache, malaise, and
anorexia.
2. Pain.
3. Deafness.
4. Tinnitus.
 29

Signs
1. Otoscopy: The colour of the T.M. varies according to the degree
of congestion, first lustreless, later on, congested with prominent
vascularity along the periphery of the T.M., and handle of malleus.
• Lost cone of light.
2. Tunning fork tests: Show conductive hearing loss.

C. Stage of suppuration
Symptoms
l.The severity of constitutional manifestations increase (fever,
headache, malaise), and are more marked in children than in
adults.
2. Pain becomes more severe and throbbing.
3. Deafness increases.
4. Tinnitus.

Signs
1. Otoscopy: Marked diffuse congestion of the T.M., which
• is bulging either in a part or as a whole.
• lost cone of light.
2. Tunning fork tests: Show conductive hearing loss.

D. Stage of perforation
Symptoms
1. The general constitutional manifestations start to subside.
2. Appearance of aural discharge.
3. Deafness may improve or persist.
4. Pain starts to subside.

Signs
1. Aural discharge: mucopurulent, purulent or serosanginuious, and
is pulsating.
2. Perforated T.M., and if the perforation is large the middle car
mucosa appears oedematous and congested, 'fhe site of
perforation is anteroinferior (near the mouth of the Eustachian
tube).
3. Tunning fork tests: show conductive hearing loss.
 • The T.M. is formed of 3 layers:
1. Outer squamous layer (Skin) which is continues with that
oftheE.A.C.
2. Middle fibrous layer which is composed of two layers of
fibrous tissue one with concentric and the other with
radial orientation. The handle of malleus is embedded in
this layer. This layer is deficient in the pars flaccida.
3. Inner mucosal layer continuous with the lining of the
middle ear.
The T.M. is 0.1 mm thick in adults. It is thicker in infants
and young children. It is set obliquely at an angle 55° with the floor
of the E.A.C., so that the anteroinferior portion is deeper, and the
light directed onto the T.M. appears coned anteroinferiorly.

semicircular canals

facial nerve

cochlear nerve

cochlea

vestibule

Anatomy of the ear

II. MIDDLE EAR

The middle ear cleft is an air-filled space and it consists of
1. Middle car cavity (tympanic cavity).
2. Eustachian tube (E.T.),
3. Mastoid air cells.
 ~m

30

Investigations
1. Culture and sensitivity of discharge.
2. Audiogram (Pure tone audiogram PTA): shows conductive
heariim loss.

Treatiiu'iif
[. II the patient presents before perforation of the r..M.
A. Medical treatment: (for 10-14 days).
L Rest, light diet, fluids.
2. Systemic antibiotics:
• 'fhe most commonly used are amoxycillins, or anio.wciUin
combined with elavulanic acid, and oral cephalosporins.
• In severe cases they are given parenteral (LV. or L.M.).
4. Analgesics, antihistaminics (decongestant).
.S. Local decongestant nasal drops to enhance areation and dramage
through the Eustachian tube.
(). Local warm glycerin phenol ear drops to decrease oedema ami
pain, and to improve local blood supply.
B. Surgical treatment: Myringotomy and drainage.
Indications
1. Failed medical treatment for more than 48 hours (persistent pain
and fever).
2. Bulging T.M. as the myringotomy incision heals better than the
pathologically perforated drum due to necrosis and suppuration in
the latter. Remember not to expect bulging of T.M. in infants and
young children as the drum is thick.
3. Development of complications e.g. facial paralysis (due to
dehiescent fallopian canal.
4. Immunosupprcssed patients, infants and neonates for fear of
complications.
Procedure
• It is done under local anaesthesia in
adults, and general anaesthesia in
infants and children.
• Using the myringotomy knife, the
myringotomy incision is done from
below upwards (due to obliquity of
thcT.M.). (Fig. 11) Fig.11. myringotomy i
 31

• It is done in the posteroinferior quadrant of the T.M., with great

care not to injure the ossicles. The obtained discharge is sent for
culture and sensitivity.

After myringotomy, medical treatment is continued for at

least two weeks, with the following additions:
• Antibiotics are given according to culture and sensitivity.
• Topical antibiotic ear drops, but avoid ototoxic drugs. The safest
is chloramphenicol.
• Avoid entry of water into the ear.
• Aural toilet to remove discharge (suction or dry mopping).

II. If the patient comes with the T.M. already perforated with
discharging ear
A. Medical treatment
1. Antibiotics according to culture and sensitivity.
2. Topical antibiotic ear drops (avoid ototoxic ones).
3. Aural toilet (repeated suction or dry mopping) to remove
discharge frequently.

B. Myringotomy is done in small or high perforation to provide

liberal wide drainage

Acute otitis media in infancy

and early childhood
A.O.M. is more common among infants and young children
due to the following predisposing factors which may also lead to
recurrence.
1. The Eustachian tube is wider, shorter, and more horizontal than in
adults with easier ascent of infection.
2. Upper respiratory tract infections are more common.
3. Exanthemata e.g. measles and mumps are more common.
4. Adenoiditis and tonsillitis are more frequent.
5. Immunity system is not well developed.
6. Feeding problems: A.O.M. is more common in bottle fed than
breast fed infants due to feeding the baby flat and not semisitting
as in breast feeding. In addition bottle milk may become
 32

contaminated during processing, while breast milk is sterile and

contains immunoglobulines.

Cliaical picture
Similar to A.O.M. of adults with the following points to be taken in
consideration:
1. The general constitutional manifestations are more severe than in
adults with high fever and may be rigors.
2. Vomiting and diarrhea may occur.
^. i*"requcnt pulling of the car or head shaking.
4. Restlessness, and frequent crying.
.s. Diffuse hyperacmia and congestion of the T.M. Bulging and
perforation are less common as the drum is thick.

The liability of A.O.M. to produce complication is more common in

infants and young children due to
• Lowered resistance and immunity.
• T.M. resists perforation with accumulation of pus.

Treatment
As mentioned before in A.O.M. but remember that the T.M.
is thick and do not wait for its bulging. The decision is to incise the
drum (Myringotomy) if there is persistent pain and fever for more
than 48 hours despite giving medical treatment.

Chronic non-suppurative otitis media

This is a form of chronic non-suppurative otitis media

characterized by accumulation of serous, mucinous or seromucinous
Ouid in the middle ear clefl behind an intact T.M. It is the most
common cause of hearing loss in school-age children.
 33

It is either:
a. Serous otitis media: Transudation of plasma from blood vessels
due to hydrostatic pressure difference.
b. Mucoid Otitis media: active secretion by glands and cysts in the
lining of the middle ear cleft due to long standing irritation.

Aetiology
1 Incomplete resolution of acute suppurative otitis media due to
inadequate treatment especially inadequate antibiotic therapy.
2 Eustachian tube obstruction: due to
• Eustachian tube dysfunction.
• Hypertrophied adenoids.
• Nasopharyngeal tumours e.g. carcinoma and angiofibroma.
Palatal cleft e.g. cleft palate due to improper action of levator
palati.
• Sinusitis, rhinitis and nasal allergy.
3 Allergy of middle ear mucosa.
4 Viral inflammation.
5 Otitic barotrauma.
6 Radiation therapy to the head and neck.
7 Immunologic and metabolic deficiencies.

Clinical picture
• It is either unilateral or bilateral especially in cases due to
adenoids.
"There may be a history of recurrent attacks of A.O.M. inbetwcen
which the ear never returns to normal.

Symptoms
1. Deafness:
• This is the main and may be the only symptom.
• Noticed in children as inattention at school or diminished,
response to sounds, while adults complain more of ear
obstruction.
2. Occasional feeling of bubbling in the ear.
3. Tinnitus.
 34

Signs
1. The T.M. {better viewed by otoscopy) is: (Fig. 12)
• Intact, slightly congested and
usually retracted.
• When retracted there is
foreshortened handle of malleus,
prominent lateral process of
malleus and exaggerated anterior
and posterior malleolar folds,
disturbed or absent cone of light,
and reduction or absence of the Fig.12. secretory otitis media
T.M. mobility on pneumatic
sicgelization.
• The colour of the T.M. is characteristic, it varies from amber
yellow (serous effusion) to dull gray (Mucoid effusion).
• There may be a fluid level (hair line) appearing as a biconcave
line upwards (the line is concave due to surface tension of the
(luid). There may be air bubbles, appearing through the
semitranslucent T.M.

2. Tunning fork tests: show conductive hearing loss.

Investigations
1. Audiogram (PTA): mild to moderate conductive hearing loss with
air-bone gap.
2. Tympanogram: to measure the middle ear pressure, show s flat
curve (Type B).
3. X-ray nasopharynx lateral view: To detect adenoid hypertrophy.
4. Nasopharyngoscopy: may reveal a nasopharyngeal cause e.g.
tumour or adenoids.

N.B.: Any elderly patient with unilateral secretory otitis media

should be carefully evaluated by nasopharyngeal examination,
nasopharyhgoscopy, nasopharyngeal biopsy and CT scan of the
nasopharynx to rule out the possibility of nasopharyngeal carcinoma.
 35

Treatment
I. Conservative
1. Proper treatment of predisposing factors e.g. control of upper
respiratory tract infections as sinusitis, adenoidectomy, repair of
cleft palate.
2. Systemic antibiotics.
3. Corticosteroids: Systemic (anti-inflammatory) and Topical nasal
spray.
4. Decongestant nasal drops.
5. Mucolytics.
6. Eustachian tube ventilation exercises by autoinflation (Valsalva's
manouevre).
7. Avoid antihistamines as it render secretions more viscid
(Atropine like effect).

The conservative treatment is tried up to 3 months and in a

large percentage of cases the middle ear effusion resolves.

II. Surgical
• Myringotomy and insertion of
tympanostomy ventilation
tubes. (Fig. 13)
• The ventilation tube allows
normalizing middle ear
pressure, and drainage of
Fig. 13. grommet
fluid. It is followed by
immediate improvement of
hearing and decreases the
tendency to recurrent effusion.
• Indications
1. Chronic middle ear effusion lasting more than 3 months
despite medical treatment.
2. Marked conductive hearing loss.
3. Nasopharyngeal tumour and prior to radiotherapy.
• Myringotomy incision is done in the anterosuperior portion of the
T.M. (least migrating epithelium, so as not to allow early
extrusion.
• Tympanostomy tubes in use are either spontaneously extruded
after 3-6 months e.g. Grommet's tubes or permanent as T-tubes.
 36

Atelectatic otitis media

There is retraction of the T.M. onto the promontory and the

ossicls with partial or complete obliteration of the middle ear space.

Aetiology
1. Long standing Eustachian tube dysfunction.
2. Chronic middle ear effusion,
3. Recurrent A.O.M. (thinning and weakness of T.M.).

Clinical picture
Symptoms
1. Deafness.
2. linnitus.

Signs
1. The T.M. is retracted onto the promontory and ossicles but is not
adherent to the medial wall of the middle ear. There is limited or
absent mobility of the T.M. on pneumatic sieglization.
2. Tunning fork tests: conductive hearing loss.

Investigations
1. Audiogram: conductive hearing loss.
2. Tympanogram: Eustachian tube dysfunction (type C).
3. X-ray mastoid: poorly pneumatized.

Treatment
1. Proper treatment of A.O.M., and middle ear effusion to avoid
atelectasis.
2. Surgery: Insertion of ventilation tubes (T-tube), and the condition
is reversible.

Adhesive otitis media

There is retraction and adhesion of the T.M. onto the medial

wall of the middle ear with complete obliteration of the middle ear
cavity and fonnation of fibrous adhesions
 37

Aetiology: Long standing and recurrent improperly treated A.O.M.,

or secretory Otitis media.

Clinical picture
Symptoms
1. Deafness.
2. Tinnitus.

Signs
1. The T.M. is retracted and adherent to the promontory and ossicles
(plastered). It is dull opaque, and thinned (Atrophic). There is
limited or absent mobility on pneumatic siegelization.
2. Tunning fork tests: conductive tearing loss.

Investigations
As in atelectatic O.M.
Treatment
1, Early: ventilation tubes (T-tube) to allow areation of the middle
ear.
2. Late: cartilage tympanoplasty, using a thin slice of tragal cartilage
to support the atelectatic epithelium.

Chronic suppurative otitis media (C.S.O.M.)

This is a chronic inflammation of the mucosal lining of the

middle ear cleft by pyogenic organisms and is characterized by
irreversible pathological changes, intermittent or persistent aural
discharge and a perforation in the T.M.

Types
A.Tubotympanic (safe) type; the pathology affects the mucosa of
the middle ear cleft. It is less liable to produce complications if it
is limited to the mucosa.
B. Atticoantral (unsafe) type; the pathology affects mainly the attic,
the antrum and the mastoid. The lining changes into flat
squamous epithelium and is frequently associated with formation
of polypi and granulations. It is more liable to produce
complications because the disease is not limited to the mucosa,
with increased frequency of bone erosion.
 38

Tubotympanic CSOM
Aetiology
It occurs usually secondary to A.S.O.M. due to:
1. Inadequate treatment: inadequate antibiotic therapy, or inadequate
drainage of discharge (small or high perforation).
2. High virulence of the organism.
3. Repeated middle ear infection through the Eustachian lube or
through a persistent T.M. perforation.
4. Low resistance of the patient.
.'^. Persistent predisposing factor e.g. E.T. dysfunction.

( linical picture
SMiiptoms
1. Persistent or mtemiittent aural discharge.
2. Deafness.
3. I'innitus.

Signs
1 Aural discharge: It is mucopurulent or mucoid, usually odourless.
and profuse in amount due to mastoid reservoir. It may be
pulsating in cases of acute exacerbations.
2 r.M. perforation; The perforation is usually central in the pars
lensa. It may attain any size or shape and there is a rim of the
T.M. all around the perforation (i.e. the perforation never reaches
the bony annulus). (Fig. 14)
3 Middle ear mucosa: if visible through the perforation may look:
• Ocdcmatous, congested and velvety pink during active
infection.
• Thin pale during the inactive phase.
• Granulations are common, these are sessile reddish
projections and bleed easily on touch. They arc due to
chronic irritation of the mucosa.
• Aural polyp: It is pedunculated oedematous mucosa passing
through the T.M. perforation and appearing in the external
canal.
4 Tunning fork tests: Variable degree of conductive hearing loss,
due to:
• T.M. perforation.
 39

• Impaired ossicular chain mobility due to discharge and

granulations.
N.B. The ossicular chain is usually intact, but it may be eroded and
the commonest is the long process of incus.

Figi4,
a: central perforation
b: large central perforation

Investigation
1. Audiogram (PTA): Variable degrees of conductive hearing loss.
2. Plain X-ray of mastoid; to detect the state of the mastoid and the
position of the lateral sinus and dural plates.
3. Culture and sensitivity of the discharge to detect the infecting
organism and select the best antibiotic.
Treatment
A. Conservative treatment
The aim of conservative treatment is to obtain a safe dry ear
to allow spontaneous healing of the perforation or as a preparation
before surgery.
1 Systemic antibiotics:
• Best according to culture and sensitivity.
• Avoid ototoxic drugs e.g. aminoglycosides.
• They may not be effective as fibrosis doesn't allow
antibiotics to reach tissues in a proper concentration.
2 Topical application of antibiotic ear drops but avoid ototoxic ones
(e.g. polymixin and neomycin). The safest are tetracyclines and
chloramphenicol. They are better combined with steroids.
3 Aural toilet: Repeated local cleaning and removal of discharge
either by;
• Suction with a sterile fine cannula.
• Or dry mopping by sterile cotton tipped probe especially in
children.
Then disinfection after aural toilet by hydrogen peroxide or
alcohol 70% with a cotton tipped probe.
A. The middle ear cavity (Tympanic cavity)
It is an air-filled space similar to a rectangular box (i.e. six-
walled). It is wedge shaped with the posterior wall wider than the
anterior wall. It is rather narrower from side to side (15 mm) than
antcroposteriorly (2-6 mm).

The cavity is divided into three part:

1. Epitympanum (Attic): This is the superior portion located
above the level of the T.M. It is connected with the
mastoid antrum through the aditus ad antrum. So, it's outer
wall is bony (part of squamous temporal bone) and not the
pars flaccida as sometimes misunderstood.
2. Mcsotympanum: This lies opposite the T.M.
3. Hypotympanum: This is the most inferior portion below
the level of the T.M.
Walls of the middle ear
1. Roof; it is formed by a thin plate of bone which separates the
attic from the dura of the middle cranial fossa. It is called the
tegmen tympani and it is continuous with the roof of the
antrum.
2. Floor; it is formed by a thin plate of bone separating the
middle ear from the superior bulb of the internal jugular vein
(Beginning of the jugular vein). Sometimes, this wall is
deficient with direct relation of the bulb to the middle ear
cavity.
3. Anterior wall; from above downwards it shows the following:
a. Opening of the canal for tensor tympanic muscle.
b. Opening of the Eustachian tube.
c. Bony plate separating the middle ear from the internal
carotid artery.
4. Posterior wall; from above downwards it shows:
a. Aditus ad antrum connecting the attic with the mastoid
antrum.
b. The pyramid, which is a hollow bony pyramidal process,
containing the stapedius muscle.
c. Vertical (mastoid) portion of the bony canal (Fallopian
canal) of the facial nerve.
5. Medial wall; it shows: (Fig. 4, 5)
a. The promontory: This is an elevation corresponding to
first (Basal) turn of the cochlea. It is the most prominent
 40

4. Avoidance of reinfection:
• Avoid forcible blowing of the nose during rhinitis.
• Avoid wetting the ear during washing the head or bathing.
• Control upper respiratory tract infection e.g. sinusitis, tonsillitis.
• Adenoidectomy in cases of enlarged adenoids.

5. Aural polypectomy:
Excision of an aural polyp from the external auditor)' canal if
present to improve drainage of discharge, facilitate aural toilet and to
facilitate application of topical ear drops. Don't pull on the polyp
(avulsion is forbidden) as it may be attached to ossicles especially
the stapes, labryinthin fistula or to an exposed facial ner\'e.

B. Surgical treatment
• Tympanoplasty with or without cortical mastoidectomy.
• Aim:
1. Eradication of irreversible changes in the middle ear mucosa
and to clear it from infection.
2. Reconstruction of the conductive hearing mechanism
(ossicular reconstruction).
• Cortical mastoidectomy is combined with tympanic membrane
grafting, if there is persistent aural discharge (mastoid reservoir)
to eradicate the mostoid pathology.
• The grafting material commonly used to repair the defect in the
T.M. is temporalis fascia.

Cholesteatoma (atticoantral disease)

Definition: The presence within the middle ear cleft of a squamous
epithelial pocket or sac filled with keratin debris (i.e. skin in an
abnormal site).
Cholesteatoma is a misnomer because it is neither a tumour,
nor it necessarily contains cholesterol crystals.

Pathology
A cholesteatoma is a sac lined by keratinizing stratified
squamous epithelium (matrix) and is filled with concentric sheets of
white-yellow keratin flakes in which the cholesterol crystals may be
embedded. It has an onion like appearance on cut section.
 41

Types
A. Congenital cholesteatoma.
B. Acquired cholesteatoma:
1. Primary acquired cholesteatoma.
2. Secondary acquired cholesteatoma.

A. Congenital cholesteatoma (Rare)

• This is a cholesteatoma (epithelial cyst) which develops from
embryonic extradermal cell rests. It may occur in any cranial
bone, but the commonest is in the temporal bone in the following
sites.
• Cerebellopontine angle.
• Jugular foramen.
• Petrous apex.
• Middle ear.

It is sterile so long as it is not connected with the external

canal (i.e. cholesteatoma behind an intact T.M.), and becomes
infected when it finds its way outside.

B. Acquired Cholesteatoma
Migration of keratinizing stratified squamous epithelium
from the surface of the T.M. and adjoining part of EAC into the
middle ear due to:
1 Primary acquired cholesteatoma (No previous history of O.M.)
• Retraction pocket theory (Attic retraction): Most accepted,
prolonged intratympanic negative pressure (due to prolonged
E.T., obstruction or intratympanic adhesions) causes
invagination of part of T.M. into the middle ear with
fonnation of retracdon pocket which becomes filled with
keratin and debris and subsequent formation of cholesteatoma.
Retraction pocket occurs in two sites:
Pars flaccida (lacks middle fibrous layer i.e. weak).
Posterosuperior quadrant of pars tensa. Here fibrous
annulus is deficient.

• Migration theoi7; the direction of migration of canal

epithelium is reversed being inwards instead of being
outwards.
 42

• Metaplasia theory; metaplasia of flat squamous epithelium of

the artic into keratinizing stratified squamous epithelium.

2. Secondary acquired cholesteatoma (previous history of O.M)

a. Migration therapy: Direct migration of stratified squamous
epithelium from surface of T.M. into the middle ear through a
marginal perforation.
b. Metaplasia theory: due to chronic irritation of the middle ear
mucosa by chronic infection.

Sequelae of cholesteatoma
Kxpansion (due to)
a. Repeated infection and accumulation of keratin.
b. iioiie erosion (rarifying osteitis = osteoporosis).

Hone erosion is due to:

1. Oslcolytic en/ymes and coUagenascs secreted b\'subepithelial
IM.
2. Secondary bacterial infection, so, the cholesteatoma becomes
acti\'atcd to secrete deminiralizing and osteolytic enzymes.
^. Osteoclastic activity.
4. Pressure necrosis by the cholesteatoma sac leading to bone
resorption due to pressure ischaemia (doubtful).

Active expansion of cholesteatoma is accompanied by:

1. Mastoid sclerosis: bone osteoporosis of mastoid is accompanied
by deposition of new sclerotic bone limiting space available for
expansion of cholesteatoma.
2. Destruction of the ossicular chain especially, long process of
incus, then whole incus, then head of malleus and may be the
whole ossicular chain.
}. If the disease is allowed to run its course, the whole mastoid and
middle ear become replaced by cholesteatoma " natural radical
cavity.
4. Complications: see later.
 43

Clinical picture
Symptoms
1. Deafness.
2. Aural discharge and may be bleeding per ear due to accompanied
granulations except in the congenital type where the drum is
intact.
3. Tinnitus.
4. Lower motor neuron facial paralysis may be the early presenting
symptom in the congenital type.
5. Symptoms of complications if they arise.

Signs
1. Aural discharge: occurs due to secondary infection of the
cholesteatoma. It is purulent (never mucoid or mucopurulent),
and may be serosanguinous due to formed granulations and
polypi. It is scanty and has a foul odour (characteristic) which is
due to bone necrosis (osteitis) and anerobic infection. It may
contain cheesy white epithelial flakes (debris).
2. T.M. Perforation: It is.a marginal
perforation (destruction of the
* *- attic erosion
bony annulus), in the postero-
superior quadrant of pars tensa or
attic perforation.
3. A retraction pocket may be seen
posterosuperiorly without
perforation in the T.M. Fig, 15. cholesteatoma
4. Cholesteatoma itself may be seen
as pearly white sheets or cheesy
white masses of keratin. (Fig. 15)
as sessile, fleshy red
5. Granulations are frequent and appear
projections that bleed easily on touch.
6. Signs of complications when they arise.
7. Tunning fork tests:
• Variable degrees of conductive hearing loss, but may be mixed
conductive and sensorineural hearing loss if the inner ear is
invaded.
• Sometimes, there is normal or mild conductive hearing loss,
and this occurs with early retraction pocket or when the
cholesteatoma itself" Bridges" the gap in the ossicular chain.
 44

In\cstigation
1 Audiogram (PTA): Variable degrees of conductive or mixed
hearing loss.
2 Plain X-ray mastoid:
• The cholesteatoma appears as an irregular area surrounded by
sclerosed bone.
• Bone erosion.
• Level of the dural and lateral sinus plates.
3 CT scan of petrous bone: to detect the cholesteatoma mass, bone
erosion and condition of the ossicular chain. It should always be
done if complication is suspected.
4 Culture and sensitivity of discharge.

Treatment (Surgical)
The main line of treatment is surgery. Two techniques are
used to eradicate the cholesteatoma.
A. Open (canal wall down) technique
This entails removal of all or apart of the posterosuperior
bony meatal wall and includes:
1. Atticotomy; in limited attic cholesteatoma.
2. Modified radical mastoidectomy (Bondy operation): in limited
cholesteatoma with good hearing.
3. Radical mastoidectomy; this is the most common procedure
performed.
Indications of radical mastoidectomy
a. extensive cholesteatoma.
b. Severe sensorineural hearing loss.
c. Presence of complication.
• It entails lowering of the facial ridge down to the level of lat.
S.C.C. and removal of the malleus and incus.
• Mcatoplasty (widening of the external ear canal) should be done
after radical mastoidectomy for adequate drainage of discharge.
• Closure of the tympanic opening of the Eustachian tube is rarely
done nowadays as it interferes with reconstruction later on.
• Problems of a radical cavity.
a. Persistent otorrhea due to failure of the cavity to heal.
b. The labyrinth is exposed and is susceptible to caloric stimulation
(vertigo).
c. Wax and epithelial debris should be removed frequently.
 45

B. Closed (Canal wall up) technique

• Combined approach tympanoplasty is the operation done. It
retains the normal anatomical contours as the posterior bony
meatal wall and the annulus, while the facial recess is opened and
removal of the cholesteatoma is managed through it.
• It is done in selected cases with localized atticoantral disease and
in children.
• A second look operation is mandatory after 6 months for
detection of residual or recurrent cholesteatoma.

Reconstruction of the radical cavity: may be needed including

reconstruction of hearing after being sure of complete eradication of
the cholesteatoma for a year or more later on.

Uses of endoscopy in the treatment of cholesteatoma

A 1.9 mm endoscope is recently introduced in the treatment
of cholesteatoma. It is used to detect residual or recurrent disease 6
months after performing the closed technique. It is introduced in the
cavity through a small postauricular incision under local anesthesia
and can be done in an outpatient clinic.
 46

Complications of suppurative otitis media

This is extension of infection beyond the mucoperiosteal

linint; of the middle ear cleft.

Causes
1. .-Xcute suppuratn'C otitis media (A.S.O.M.) especially infants and
children.
2. Chronic suppurative otitis media (C.S.O.M.) especially
cholesteatoma which is the commonest cause.
3. Acute exacerbation on top of C.S.O.M.

The incidence is uncommon nowadays due to advances of

antibiotics. Before the era of antibiotics they were mostly following
,'\.S.().M., nowadays, they are more common with long standing
C'.S.O.M. especially cholesteatoma. They may occur as a single
complication or more than one complication in the same patient.

Classification
I. Cranial (within the temporal bone)
1. Mastoiditis and mastoid abscess.
2. Ikv.old's abscess secondary to mastoiditis and it presents in the
neck.
,1 Cilteli's abscess which presents in the retropharyngeal space.
4. l^nrosilis.
5. Labyrinthitis and labyrinthine fistula.
(i lower motor neuron facial nerve paralysis.

II. Intracranial
1, I'xtradural abscess.
2. Subtlural abscess,
-v fiiain abscess.
4. Lateral sinus thrombophlebitis.
5. Meningitis.
6. Otitic hydrocephalus.
7. .lugular vein thrombosis secondary to lateral sinus
thrombophlebitis.

III. Extracranial
Otitis cxtcnia.
 47

Acut mastoiditis
Definition
Acute inflammation of the mucous membrane lining the
bony walls of the mastoid air cells and the mastoid antrum with
destruction of its bony partitions.

Pathology
• It occurs in a cellular mastoid bone. It is commoner following
A.S.O.M.
• The mastoid air cells coalesce together into larger cavities filled
with pus and granulations. This is due to:
a. Osteoporosis of the bony walls.
b. Progressive ischaemic necrosis of the bony walls due to
accumulation of pus.
• Extension of infection outside the mastoid leads to:
A. Subperiosteal abscess formation
Pus escapes through bone causing:
1. Sagging of the poslerosuperior meatal wall; due to forward
trickling of pus through the mastoid antrum.
2. Postauricular (mastoid) abscess: due to lateral trickling of pus
from the outer surface of the mastoid process.
3. Zygomatic abscess: due to lateral trickling of pus from infected
air cells at the root of zygoma.
4. Bezold's abscess: due to downward trickling of pus from the
lateral side of the tip of mastoid process into the sheath of
stemomastoid muscle.
5.Citteli"s abscess: due to trickling of pus through the peritubal
(around Eustachian tube) air cells. It presents in the lateral
phalangeal space.

B. Mastoid (Postauricular) fistula

It is due to inadequate drainage of mastoid air cells, pus
bursts through the periosteum, soft tissues and skin, leading to
persistent chronic mastoid fistula.
 48

Clinical picture
- It occurs more in children and young as the mastoid cortex is thin.
- It is more common after A.S.O.M., and acute exacerbation of
C.S.O.M.
Symptoms Symptoms of A.S.O.M. which becomes more severe in
2-3 weeks.
1. General; fever, headache, malaise and anorexia.
2. Aural discharge increases and becomes profuse and offensive.
3. Pain; increasing otalgia, which becomes dull aching. It is felt
rctroauricular and radiates downwards to the neck and backwards
to the occiput. It becomes throbbing with formation of the
abscess. Pain increases in the recumbent position.
4. Deafness increases.
5. Tinnitus may be present.
6. External swelling may occur in relation to the subperiosteal
abscess.

Signs.
XJj£asisL..
• high fever (38-39°C) may be higher in children. Fever is
hectic with abscess formation.
• Tachycardia and toxic facies.
2.-MastQid tenderness (diagnostic): This is detected by deep
pressure over the mastoid antrum (cymba conchae), pressure on
the auricle immediately posterior to the root of the helix, over the
mastoid tip (dependent and most superficial air cells), and later it
is detected all over the mastoid process. It is better to compare
both sides.
3. Oedema over the mastoid process with blurring ofthenomial
irregularities on its outer surface.
4. External swelling^ due to subperiosteal abscess fonnation, which
appears as a tender fluctuant swelling in the following sites:
iiPosUiuriculax; lies over the mastoid process pushing the
auricle downwards and forwards with presci-vation of the
rctroauricular sulcus.
b.ZygoiiTiitic _abscess; swelling lies above and in front of the
auricle \vith oedema of the eye lids.
c.Bczold's abscess; lies in the upper part of the neck, in the
posterior triangle below and medial to the tip of the mastoid.
 49

5• Ear examination:
a. Aural discharge; purulent or mucopurulent, thick, offensive,
it may be pulsating (indicates acute infection). It is profuse
and recollects rapidly after removal (reservoir sign),
b.Sagging of the posterosuperior wall of the external canal
(Diagnostic).
c.T.M. is usually perforated.
6. Tunning fork_t_ests_: show conductive hearing loss.

InyesligatLQns.
1. Audiogram (PTA): conductive hearing loss similar to A.S.O.M.
2. Culture and sensitivity of discharge.
3. Plain x-ray mastoid: clouding of the mastoid air cells with
blurring of their outlines due to destruction of the bony septae.
4. CT scan of petrous bone and mastoid; to exclude other cranial or
intracranial complications.

Differential diagnosis
1. Furuncle:
Furuncle Acute mastoiditis
Preceeding history No A.O.M. A.OTM:
Pain On mastication and Not related to
moving the auricle mastication
Deafness Conductive, if large Conductive, and always
furuncle occluding the present
_ - -- canal
Tenderness on moving the auricle over the mastoid
and pressure on the i
tragus.
T,M. ^___ Normal usually perforated { 1
Discharge scanty and purulent profuse and ' 1
mucopurulent :
X ray mastoid Normal air cells clouding of mastoid air
cells. i
1

2. Postauricular \y mphadenitis.
3. swellings overt :e mastoid e.g. Lipoma, hae matoma.
feature of the medial wall. The tympanic nerve (Branch
from the glossopharyngeal nerve) runs vertically across it.
Round window: It lies below and behind the promontory,
and is closed by the 2ry tympanic membrane.
Oval Window: It lies above and behind the promontory,
and is closed by the footplate of the stapes.
Sinus tympani. This is a triangular depression between the
round and oval windows.
Processes cochleariformis: a pully-like projection at the
superomedial part of the medial wall, around which the
tendon of tensor tympani hooks 90° to get inserted into
the neck of malleus.
Horizontal (tympanic) portion of the facial nerve running
from medial to lateral above the promontory and the oval
window.

Mn>ui.W«u

Promirifnct c/bt. Mincn-cond

Irorwtocf of Tociv WW
Aditui ID onirum hmM of n u ^ wirtdiyw
Pyfofliidol emiiwnce
Ap*ftur? for chorjo fymp.'
FoCH^ •>crv«,

IATIIUL W M I

ANT.WWL

IrHrtiofl tfttn%
^ymp,m(JJ,
Chordo ^ytnp.
Tymp.mfmb.

Fig.5- Anatomy of the medial wall of the ear

 50

Treatment
A. Medical
1. Systemic antibiotics according to culture and sensiti\itv.
2. Analgesics, anti-inflammatory.
3. Treatment as in A.S.O.M. (see before).

B. Surgical
1. Cortical mastoidectomy
Indications:
-Failure of medical treatment with persistent fever and pain for
more than 48 hours.
- Subperiosteal abscess fomiation (hectic fever, pitting oedema,
lluctuation).
- Presence of other complication.
2. Radical mastoidectomy: in mastoiditis with cholesteatoma.

Petrositis

- Inflammation of the air cells of the petrous apex of the temporal

bone, and it is usually associated with mastoiditis. OnK- 30% of
total population have a cellular petrous apex.
It usually occurs in diabetic patients.

( liiiical picture
Gradenigo's triad which consists of:
1. Pulsating aural discharge.
2. Diplopia and coincrgent squint due to affection of the abducent
(6th n.) at the petrous apex (Dorello's sign).
3. Facial pain due to affection of the trigeminal Gasserian ganglion
in the MeckcPs ca\c on the upper surface of the petrous apex.

Investigations
1. Audiogram.
2. Culture and sensitivity of discluirge.
3. C'T scan of petrous bone and brain.

[ rcatment
1. Massive systemic antibiotics, better according to culture and
sensitivity.
 51

2. Treatment of the underlying ear disease e.g. radical

mastoidectomy.
3. Drainage of infected petrous air cells cither through:
- Transmastoid approach to drain the supralabyrintliinc air cells, or.
supralabyrinthine.
- Middle cranial fossa approach to drain the tip cells.
- Infracochlear approach to drain petrous apex cells.

Facial paralysis (complicating suppurative O.M.)

It occurs in:
1. A.S.O.M.: due to dehiscence in the bony facial (Fallopian) canal.
2. C.S.O.M.: due to erosion of the bony facial canal by
, cholesteatoma or granulations.

Clinical picture: Lower motor neurone facial paralysis (see later):

1. In A.S.O.M., it is seen in infants and children, with a sudden
onset.
2. In C.S.O.M., it has a gradual onset and progressive course.

Investigations
1. Audiogram.
2. Culture and sensitivity of discharge.
3. CT scan of petrous bone and brain.
4. Tests for leveling the facial palsy (see later).

Treatment
A. In A.S.O.M.:
~ Urgent myringotomy.
- Systemic antibiotics.
- Steroids.
B. In N4astoiditis:
- Cortical mastoidectomy.
- Systemic antibiotics.
- Steroids.
C. In cholesteatoma:
- Urgent exploration and radical mastoidectomy, 'fhc nerve is
decompressed (but without slitting its sheath to avoid spread of
infection to the nerve fibers).
 52

Systemic antibiotics.
Steroids.

Labryinthitis (complicating suppurative O.M.)

This is an inflammation of the inner ear as a complication of
middle ear suppuration.

Aetiology
1. A.S.O.M.
2. C.S.O.M. espccialh' cholesteatoma (much more common).

Pathology
A. Labyrinthine fistula (localized or circumscribed
labyrinthitis)
There is a localized bone erosion of a part of the bony
labyrinth down to and exposing its endosteal lining and stops short
of it, and thus the membranous labryinth' is exposed. It can occur in
any part of the bony labyrinth but the commonest is the dome of the
lateral semicircular canal. This occurs more common with
cholesteatoma.

B. Serous labyrinthitis
There is exudation of serous fluid in the perilymphatic and
endolymphatic spaces, but, there is still no pus, or cellular exudation.

C. Suppurative labyrinthitis
If infection is not controlled there will be formation and
accumulation of pus, with degeneration of the sensory element of the
membranous labryinth, and the end result will be either:
- Healing by fibrous tissue with complete loss of function (no
hearing or vestibular sensations).
- Intracranial extension of infection along the internal auditory
meatus (1AM), cochlear and vestibular aqueducts.

Clinical picture
- Manifestations of suppurative O.M.
- The clinical picture depends on the pathological stage.
 53

A. Labyrinthine fistula
I.May be silent and asymptomatic being discovered accidentally
during surgery, so it should be expected in any case of extensive
cholesteatoma.
Vertigm recurrent mild transient vertigo, which may be induced
by sudden head.mov^rnent, tragal pressure or exposure to loud
sound (Tulio phenomenon). No nausea or vomiting.
3. Nystagmus with its rapid phase towards the diseased ear
(irritative), may occur during attacks of vertigo.
4. Positive fistula test (diagnostic): it is a clinical test to detect the
presence of labyrinthine fistula. It consists of brief attacks of
vertigo with or without nystagmus on:
a.Applying positive pressure in the EAC by a pneumatic
Siegle's otoscope,
b.Pressure on the tragus,
c. Manipulation of an aural polyp, if present.
Results
a. Positive test: occurrence of vertigo and may be nystagmus.
b. false negative test: (Fistula is present but the test is negative). This
may occur in case of:
OFistula in a non functioning labyrinth (dead ear).
OVery small Fistula.
©Inadequate sealing during sieglisation.
OMass of cholesteatoma preventing transmission of waves.

B. Serous labyrinthitis
1. Sudden severe spontaneous vertigo which may be continuous.
2. Nausea and vomiting are present and severe.
3. Spontaneous nystagmus with its rapid phase towards the diseased
ear.
4. Sensorineural hearing loss is present, but it is reversible in this
stage.

C. Suppurative labyrinthitis
- Manifestations are similar to those of serous labyrinthitis but
more severe.
a. Vertigo, nausea and vomiting are severe.
b. Nystagmus with its rapid phase towards the normal side.
 54

c. Increasing sensorineural hearing loss and it is irreversible in this

stage (dead labyrinth).
d. There is no or minimal constitutional manifestations, and if
present, look for other complications as meningitis.
- The distinction between serous and suppurative labyrinthitis is
made on a retrospective bases, if the patient reco\'ers hearing then
il was serous labr\'inthitis. but if becomes dead ear then it was
suppurative t\'pc.

i. Audiogram.
2. culture and sensitivity of discharge.
3. CT scan of petrous bone and brain.

Treatment
A. Medical treatment: (always start medical treatment first)
i. Hospitalization, bed rest, adequate fluids.
2. Systemic massive antibiotics; given according to culture and
sensitivity. Antibiotics that cross the blood brain bamer e.g.
sulpha, chloramphenicol, are recommended.
3. Sedatives.
4. AntivcrtiginoLis drugs e.g. Dramamine.
5. .Adequate treatment of middle ear infection.

B. Surgical treatment
1. In labryinthin fistula, operation should be done immediately for
fear of progression to diffuse serous or suppurative labyrinthitis.
- Radical mastoidectomy is done for eradication of cholesteatoma.
~ The fistula is exposed by careful peeling of cholesteatoma matrix.
The fistula itself should not be disturbed to avoid perilymph leak.
Then, it is covered by a graft e.g. temporalis fascia.
2. Drainage and destruction of the membranous labryinth by surgical
labrinthcctomy in suppurative labryinthitis with persistent disabling
manifestations e.g. profound deafness and residual dizziness.
 55

Lateral sinus thrombophlebitis

- Infection and thrombosis of the lateral venous jiiuis (sigmoid

sinus).
- It occurs more commonly with cholesteatoma.

Pathology
1. Periphlebitis: There is an extradural (perisinus) abscess with
localized inflammation of the outer dural wall of the sinus.
2. Endophlebitis: infection spreads to the inner dural wall of the
sinus, which becomes rough, and this will lead to the formation of
a mural thrombus, which occludes the sinus lumen.
3. Infection an progression:
a.Extension of thrombosis proximally and dislally
(propagating thrombus),
b.Infection and suppuration of the thrombus (inlrasinus
abscess),
c.Breakdown of the infected thrombus with subsequent septic
emboli and systemic pyaemia.

Clinical picture
It may be asymptomatic and discovered accidentally during
ear surgery being masked by the use of antibiotics (sterile
thrombus).
1. Intermittent fever: It consists of attacks of sudden rise of
temperature to 39''C - 40°C accompanied by rigors of short
duration and this is due to escape of septic emboli. This followed
by a rapid fall of temperature and profuse sweating. Attacks occur
at irregular intervals and in between, the patient seems well and
there is mild pyrexia. Some cases present with continuous fever
associated with nausea and vomiting.
2. Anaemia, pallor, anorexia, malaise and toxic facies.
3. Severe occipital headache.
4. Manifestations of increased intracranial tension (ICT). Severe
generalized headache, projectile vomiting, blumng of vision and
papilloedema. Increased I.C.T. is due to interference with cerebral
circulation as a result of occlusion of the dominant sinus (usualls
the right side) or extension of the thrombus to the confluence of
sinuses.
 56

5. Manifestations of thrombus extension:

a.To the iatfimaLtJUgukiLyein: neck pain limiting rotation (not
flexion as occurs in meningitis) and torticollis. The vein is
felt as a tender cord like structure along the side of the neck.
b Jx!_Lh.c_maslQid..-£iiiissary___teku oedema and tenderness over
the posterior border of the mastoid process (Griesinger sign).
cXo^tlie superior petrosal sinus and then to the cavernous
sinus: this will lead to cavernous sinus thrombosis
(proptosis, chemosis, total opthalmoplegia, ptosis and
papillocdema).
d.To the superior sagittal sinus: this will lead to otitic
hydrocephalus in the form of headache, vomiting, blurring of
vision, papilledema, and 6 nerve (abducent) paralysis
(convergent squint due to paralysis of lateral rectus and
diplopia).

Investigations
1. Blood picture:
- Leucocytosis more than 20.000 cm .
- Anaemia.
- Increased sedimentation rate.
2. Blood culture: It should be done during an attack of fever.
Positive culture indicates bacteraemia, while negative one doesn't
exclude it.
3. Lumbar puncture: It should be done in the recumbent position to
avoid hcmiation ofthemedullathroughtheforamenmagnum.lt
shows normal CSF pressure.
4. Positive Queckenstedt's (Tobey- Ayer's) test: while measuring
CSF pressure by a water manometer connected to a lumbar
puncture needle, pressure on thejugular vein in theneck on the
normal side causes brisk rise of CSF pressure, while pressure on
the vein on the diseased side (i.e. occluded by the thrombus)
produces no change.
5. Fundus examination: papillocdema (oedema of the optic disc) and
engorged retinal veins due to increased I.C.T. or cavernous sinus
thrombosis.
6. CT scan of petrous bone and brain: may show thrombosed lateral
sinus, and to exclude associated complications.
7. MR angiography (best investigation if available)
 57

8. Audiogram.
9. Culture and sensitivity of aural discharge.

Differential diagnosis
l,J4alaria: attacks of fever occur in a periodic rhythmic manner,
inbetween which the patient is free, leucopenia, and blood film
shows the parasite.
^•JIy-Rtifi.id-JSX?rj, Characteristic continuous step ladder fever,
leucopenia, enlarged spleen, and positive Widal test.
3-.Qtb£Il^,intl3iyi|nial_^^mpJicaUoi^ e.g. Meningitis and brain
abscess.

Treatment
Urgent surgical exploration

A. Medical treatment
To control infection only while preparing for surgery.
1. Massive antibiotics parenterally.
2. Antipyretics.
3. Anticoagulants only in cavernous sinus thrombosis.
4. Blood transfusion to correct anaemia.

B. Surgical treatment
1. Exposure and exploration of lateral sinus: a mastoidectomy is
performed and the lateral sinus is exposed and examined
intraoperatively to detect thrombosis.
- A .thrombosed j i n u s j s dull greyjshjfiiTOi pulsating, covered by
granulations, and aspiration with a needle can obtain blood or
brings pus.
In such case, the whole sigmoid sinus is exposed and granulations
removed until healthy dura appears in all directions. Then, the
sinus is incised and the thrombus is evacuated until free flow is
obtained proximally and distally.
- Ligation of the internal jugular vein in tiie neck may be
perfonncd if no free flow of blood could be obtained distally, lo
prevent showers of septic emboli to go into the circulation.
 58

2. Control of middle ear disease: A radical mastoidectomy is done

in case of cholesteatoma. It should be done before incising the sinus
as bleeding makes the operation difficult.

Extradural abscess

This is collection of pus between the dura mater and adjacent

diiral plate of bone, either that of the middle or posterior cranial
fossae.
It occurs more commonly after C.S.O.M. especially
cholesteatoma.

Site
a. middle cranial fossa in relation to the tegmen tympani.
b. posterior cranial fossa in relation to the lateral sinus (pcrisinus
abscess).

Clinical picture
1. Many cases are asymptomatic and are discovered during surgery.
2. Persistent ipsilatcral boring or throbbing temporal headache.
3. Low grade fever, anorexia, malaise.
4. Manifestations of C.S.O.M.: the discharge may be pulsating, and
there is deep seated earache.

Invcstigiitipns
I.C'I scan of brain and petrous bone: to show the abscess and to
exclude other complications.
2. Blood picture: shows leueocytosis.
3. Audiogram.
4. Culture and scnsiliNity ofilischarge.

I rcatment: urgent surgical exploration.

1. Medical
Systemic antibiotics according to culture and sensitivity
while preparing for surgery.

U. Surgery:
- Drainage of the abscess is done during surgei^ for the ear disease.
a. Cortical mastoidectomy in mastoiditis.
 59

b. Radical mastoidectomy in cholesteatoma.

- During surgery the dura! and sinus bony plates are removed until
healthy dura is exposed in all directions around the granulations.
Granulations on the dura should not be removed Ibr fear of CSI-~
leakage and meningitis.

Otogenic brain abscess

This is accumulation of pus in a localized area within the

brain substance. It occurs in young and middle ages (10-30 years),
and carries a great risk of mortality (10-50%). The commonest cause
is cholesteatoma.

Sites
a. Temporal lobe abscess (more common)
b. Cerebellar abscess (less common but more dangerous).

Aetiology
Routes^of spread of infection
1. Direct spread: from the middle ear through a defect in the bone as
in congenital dehiscence, or previous surgery.
2. Retrograde thrombophlebitis: secondary to thrombophlebitis of
the lateral sinus or superior petrosal sinus.
3. Infection of the Perivascular space of Virchow Robin as a result
of meningitis. This space is the pia- arachnoid sheath around the
cortical vessels.
4. Blood spread (metastatic brain abscess): rare, multiple and equal
sized.

Causative organisms
- Commonly anaerobic streptococci, staphylococci, and
pneumococci.
- Less commonly gram -ve bacilli as Pseudomonas and Proteus.

Pathology
Tt'passes'in the following stages:
1. Encephalitis: localized area of encephalitis with surrounding
oedema.
Contents of the middle ear
1. Air.
2. Three ossicles: Malleus, incus, stapes. (Fig. 6)
^. I'wo muscles:
• Tensor t>'mpani (Supplied by 5" nerve)
• Stapedius (Supplied by 7 ' nerve).
4. Nerves:
• Chorda tympani.
• Tympanic plexus on the promontory.
.S. Small blood vessels.

The middle car is lined by stratified columnar epithelium uith

goblet cells and scromucinous glands and is continuos \\ith the
lining ofthe E.T.

B. The Eustachian tube (E.T.)

It is a tube connecting the middle ear caxity with the
nasopharynx. It measures about 36 mm in length, and is directed
downwards and fbnvards
The lateral third is bony and opens in the anterior wall of the
nuddle ear, while the medial two thirds are cartilaginous and
opens in the superolateral wall of the nasopharynx, abut 1 cm
behind the posterior end ofthe inferior turbinate.
It is lined by respiratory mucosa continuous with that ofthe
middle car and nasopharynx.
•fhc tube is normally closed at rest and opens during yawning
and swallowing by the action of levator palati and to a lesser
extent the tensor palati.
fhc main functions ofthe E.T. is to equalize the air pressure on
both sides ofthe tympanic membrane (Protective), and to allow
ilrainagc of secretions of middle ear.
In infants and young children, the tube is wider, shorter and
more horizontal allowing easier spread of infection to the middle
ear.

C. I'he mastoid process (Fig. 7, 8)

» It is a three sided pyramidal bone with its apex directed caudallw
and it is a part ofthe temporal bone.
 60

2. Locali/ation: breakdown and suppuration in the area of

enccphahtis with fomiation of an abscess cavity. It becomes
surrounded by a glial capsule in two weeks with decrease in
manifestations.
3. Itnlargcmcnl: The abscess cavity enlarges on the expense of its
wall, with increase in the severity of manifestations.
4. lerminal stage: If not treated, the abscess may rupture into the
ventricular system with fatal meningitis, and the fonnation of
multiple satellite abscesses.
a. Temporal lobe abscess ruptures into the lateral ventricle.
b. Cerebellar abscess ruptures into the 4' ventricle.

Clinical picture
I. Stage of initial encephalitis
There is increased intracranial tension (I.C.I):
1. Severe generalized headache.
2. high fever, tachycardia and rigors.
3. Anorexia, nausea, and vomiting.
4. Irritability, drowsiness, may be stupor and coma.

These manifestations vary in severity according to the

masking by the more striking features of other concomitant
complications e.g. meningitis or lateral sinus thrombophlebitis.

II. Stage oflocalization (latent stage)

The manifestations decrease with encapsulation of the
abscess, and its duration is variable.
1. General constitutional manifestations decrease in severity.
2. Mild pyrexia.
3. Headache.
4. No focal neurologic manifestation.

III. Manifest stage (Due to enlargement of the abscess)

A) Manifestations of increased I.C.I, (space occupying lesion)
1. severe persistent generalized headache.
2. Projectile vomiting not related to meals.
3. Blurring of vision.
4. Papilloedema (oedema of the optic disc with engorged retinal
veins).
5. Subnormal temperature due to affection of heat regulation center.
 61

6. Slow pulse rate.

7. Slow respiration rate.
8. Abducent (6' nerve) palsy due to stretching of the nerve. It
manifests as diplopia and convergent squint due to paralysis of
lateral rectus. It is a false localizing sign.
9. Photophobia.
10.Slow cerebration, mental apathy, drowsiness and finally stupor
and coma.

B) Toxemia
- Anorexia, malaise, toxic facies.
- May be increased temperature.
- Breath has a foetid odour.

C) Focal neurologic manifestations

They vary according to the site of the abscess. They appear
in a late stage, but earlier in cerebellar than temporal lobe abscess,
due to limited space in the subtentorial area.
1. Temporal lobe abscess
- Nominal aphasia (inability to name objects) due to affection of
speech center.
- Contralateral upper motor neuron facial paralysis.
- Contralateral hemiplegia (affection of motor area).
- Contralateral hemianaesthesia (affection of sensory area).
- Homonymous hemianopia: This is loss of half of the field of
vision due to affection of the optic radiation.
2. Cerebellar abscess
-Ipsilateral hypotonia (muscle weakness).
- Cerebellar nystagmus: spontaneous, slow, coarse and pendular
with no rapid and slow phase.
- jVlu_sc_le incoordination:
• Ataxia and abnormal gait.
• Stacatto (explosive) speech.
• Intention tremors.
• Asymetria, Dysmetria, and past pointing in finger to nose
test.
• Dysdiadokokinesia: inability to repeat rapid movements.
• Positive rebound phenomenon.
 62

IV. Terminal stage (due to rupture of the abscess)

[bradycardia, chvne- stokes breathing.
Coma, dilated fixed pupils and death.

hnestigations
l.CT scan of brain with contrast: This is the best diagnostic
method. The abscess appears as a hypodense central area with
peripheral enhancement. It may cause compression of the
ventricular system leading to increased ICT.
Vahie of CT scan:- Differentiates between encephalitis and
encapsulated abscess.
- Locate site of abscess
- Follo\\' up during and after treatment.
2, MRl brain if available.
^. lAimbar puncture: to exclude meningitis. It should be done in the
recumbent position and should not be done in severely elevated
I.C.T.

Freatmcnt
To give large doses of antibiotics together with surgical
approach to drain the abscess through a clear field. Treatment of the
car disease (i.c, Cholesteatoma) should take a second place after 10-
14 days.
.A) Medical
1- Systemic antibiotics:
- Large doses of antibiotics are given parenterally (I.V) and better
those crossing blood brain bamer.
e.g. 1- Cephalosporins third generation
2- Sulphonamides
3- Chloramphenicol
4- Flagyl (Mctronida/ol) against anaerobes.
- They can be given according to culture and sensitivity after
aspiration of the abscess.
- In the stage of encephalitis antibiotics may resolve the condition.
2- Supportive measures:
a. Adequate fluid and electrolyte balance
b. Adequate nutrition, Ryle feeding is used if there is severe
anorexia.
c. Lowering I.C.T.: - Dexamethazone 4 mg/6 hours
 63

- Mannitol I.V. drip 20% 3 mg/ kg

d. Care of the comatosed: (if the patient is comatosed)
- Care of the back: massage of the back, with alcohol and
powder to avoid bed sores
- Care of respiration: suction.
- Adequate nutrition through nasogastric tube.
B) Surgical
Done when the abscess is formed as detected by CT scan (i.e.
in the manifest stage). This is done either by:
1- Tapping (Aspiration) of the abscess.
a. Through a craniotomy (burr holes):
- In temporal lobe abscess carionotomy is done in the
squamous temporal bone above the ear.
- In cerebellar abscess craniotomy is done midway between
the mastoid and the external occipital protuberance.
b. Through a transmastoid approach: If the decision is made
to treat the ear disease and to drain the abscess simultaneously.
- In temporal lobe abscess: the aspiration needle is
introduced through the tegmen tympani.
- In cerebellar abscess: it is aspirated through the Trautman's
triangle bounded by the sigmoid sinus posteriorly, posterior
semicircular canal anteriorly and the petrosal sinus
superiorly).
N.B.: Repeated tapping of the abscess may be necessary as
recollection may occur.
2- Surgical treatment of ear disease:
Radical mastoidectomy is performed in cases of
cholesteatoma when the condition allows and the abscess shows
complete resolution as detected by CT scan. It is usually done after
10-14 days.

Meningitis (Leptomeningitis}

--This is diffuse inflammation of the pia and arachnoid maicr, ami

the subaraclinoid cerebrospinal fluid space of the brain and spinal
cord.
It may complicate both A.S.O.M. and C.S.O.M.
 64

Pathology
1. MrsI, there is meningeal irritation (meningism) with exudation of
serous fluid in the subarachnoid space and increased I.C.T. The
meninges arc oedematous and congested.
2. Cellular exudation (with polymorph nuclear leucocytes) occurs.
3. Later, bacterial invasion occurs with pus collection in the
subarachnoid space. Pus causes obstruction of the ventricles with
interference of C.S.F. circulation and increased I.C.T.

Clinical picture
A) Manifestations of infection
1. Constant uniform high fever
2. anorexia, malaise, headache.
3. Tachycardia, toxic facics.
B) Manifestations of meningeal irritation
1. Mental irritability, later drowsiness, stupor and coma.
2. Photophobia (patient is afraid of light).
3. Neck rigidity with severe pain on neck flexion (due to imlation o[
the basal meninges).
4. Opisthotonus position (high arched back), occurs later.
5. Weak or lost tendon reflexes.
6. Stretch signs:
a. Positive Kcrnig's sign: inability to extend the knee with
the thigh flexed on the abdomen.
b. Positive Brudziniski's sign: Flexion of the neck is
accompanied by reflex flexion of the hips and knees.
c. Positive Babiniski's sign: dorsiflexion of the toes on
stimulation of the lateral aspect of the foot.
C) Manifestations of increased I.C.T.
1. Severe generalized headache.
2. Projectile vomiting.
3. [Chirring of vision.
4. Papilloedcma.

hivestigations
1. CT scan of the brain: to exclude other complications.
2. Lumbar puncture and CSF analysis. It should be done in the
recumbent position, and CSF should not be allowed to gush
rapidly to avoid herniation of the medulla through the foramen
magnum.
 65

Also culture and sensitivity is done for the obtained CSF.

CSF Normal Meningitis
Color clear turbid
Pressure 100-150 mmH.O increased
Proteins 10-40 mg% increased (exudation)
Sugar 40-80 mg% decreased (Bacterial
utilization)
Chlorides 700-750 mg% decreased
Organisms absent (sterile) present
Cells 1-5 lymphocytes/ HPF increased especially PNI.s,
Pus cells

Treatment
First to control meningitis, and then to manage the ear pathology.
A) Medical Treatment (main line of treatment).
1. systemic antibiotics: massive parenteral antibiotics should be
started while waiting results of culture and sensitivity.
Antibiotics given should cross the BBB.
a. Sulphonamides 2-3 gm/ 4 hours I.V. drip.
b. Chloramphenicol 500 mg/ 6 hours I.V. or l.M.
c. Metronidazol 100 ml/ 8 hours I.V. drip
d. 3" generation cephalosporin
e. Ciystalline penicillin 1 million unit/ 4 hours l.M. or
intrathecal (through a lumbar puncture, now it is abandoned
due to its complications).
2 Measures to decrease I.C.T.:
a. Mannitol 20% 3 mg/kg I.V. drip
b. Lasix I.V.
c. glucose 25% I.V. drip.
d. Steroids in severe cases.
e. Repeated lumbar puncture.
3, Supportive measures:
a. Nursing in a quite dark room to lessen patient's irritation.
b. Adequate fluid and electrolytes balance.
c. Analgesics and antipyretics.
d. Care of the comatozed as described before.
II. Treatment of ear disease: (mastoid operation)
It is done as soon as possible when the general condition of
the patient allows, after subsidence of meningitis.
a. Cortical mastoidectomy in mastoiditis.
b. Radical mastoidectomy in cholesteatoma.
 It-I vr

66

Trauma of the middle ear

1. Traumatic rupture of the T.M.
2. Otitic Barotrauma
3. Temporal bone fracture
4. Ossicular dislocation
5. Surgical trauma.

Iraumatic rupture of the TM

it occurs more commonly in males as they are more liable to

trauma, and there is no special age.

Aetiology
1. Self induced as cleaning the car with a sharp object e.g. knitting
needle.
2. During removal of a foreign body especially if impacted and not
using anaesthesia or microscope, during manipulations.
.V Slap on the ear by the palm of the hand due to sudden rise of air
[pressure in the meatus.
4. During vigorous ear wash, especially if the drum is atrophic or if
there is a scar.
5. Fracture base of skull (longitudinal fracture of temporal bone).
(). Blast injury: High explosives can cause rupture of the TM as it
causes a wave of compression followed by a wave of negative
pressure.
7. Otitic barotrauma.

Clinical picture
There is history of trauma which is followed by;
1. Sudden severe otalgia radiating to the temporal and frontal
regions.
2. Deafness and tinnitus
3. Bleeding per car which is very scanty. Bleeding is only severe in
cases of fracture base and does not clot because it is mixed with
CSF that contains anticoagulants.
4. Loss of consciousness, giddiness, nausea, vomiting and vertigo
may occur.
 il-f':

61

Signs
1. TM perforation: (Fig. 17)
- It is nearly always central rarely
marginal.
- In the pars tensa and usually in the
anteroinferior quadrant of TM and Fig, 17 traumatic
less commonly in the posteroinferior perforation
and posterosuperior quadrants.
- Sharp irregular edges with blood clots
at the periphery.
2. Blood clots in the external canal.
3. Infection may set in with subsequent otitis media.
4. Tuning fork tests: conductive hearing loss.

Differential diagnosis
Pathological perforation of the TM
Traumatic perforation Pathological perforation
History Trauma O.M.
Discharge absent present and purulent
Bleeding present scanty if present
Perforation
1 - site pars tensa anywhere
- type central central or marginal
1 - size usually small any size
1 - edges irregular and sharp regular and smooth
, ' mucosa of ME normal usually congested

Treatment
A. Conservative
- Keep the ear sterile, avoid entry of water, and car drops are
prohibited.
- Instruct the patient not to blow the nose forcibly.
- Prophylactic antibiotics to guard against infection.
- Decongestant nasal drops.
In most cases the perforation heals spontaneously. Th:
average time for healing in uncomplicated cases is 25 days.
 u-»'-Li

68

B. Surgery
Indicated in persistent perforation (3-6 months).
Myringoplasty (grafting the TM) is done. The graft materials
used arc temporalis fascia (commonest), or pcricondrium from
Iragal or choncal cartilages.
~ Some surgeons prefer to graft the perforation early especially in
large perforations with everted edges.

Otitic barotrauma (aerotitis)

This is damage of the tissues of the middle ear caused by
changes in the atmospheric pressure when the Eustachian tube is
occluded. This usually occurs during diving and during descent
when Hying.

Mechanism
In the presence of Eustachian tube dysfunction, tubal
obstruction prevents air from entering the jniddle ear to equalize the
middle ear pressure, so, this results in effusion. Nonnally, the
Eustachian tube is closed, and it allows air out passively, but allows
air in, actively during swallowing (the normal person swallows 3-4
times/ minute while awake, and once/ minute while asleep).

Predisposing factors
1. Eustachian tube dysfunction.
2. Nasal allergy and inflammations.
3. Adenoids.

Clinical picture
Symptoms
1. sensation of fullness and discomfort in the ear.
2. [-'arachc
3. Deafness and tinnitus.

Signs
1. In mild cases: the TM is retracted and congested.
2. In severe cases: there may be
- Middle ear effusion with fluid level (hair line) behind the TM.
 69

-Sometimes haemorrhagic blebs on the TM, or blood behind

the drum (haemotympanum).
- In more severe cases the TM may rupture.
3. Tuning fork tests: conductive hearing loss.

Investigations
Audiogram (PTA); shows conductive hearing loss.

Treatment
A. Prophylactic
1. Avoid flying or diving in the presence of Eustachian tube
dysfunction e.g. common cold.
2. Avoid sleeping during descent of the aeroplane, and the person is
instructed to repeated trials of swallowing, chewing and active
inflation (valsalva's manoeuver).
3. Topical decongestant nasal drops and oral decongestants in
patients with nasal allergy before flying.

B. Curative
1. Autoinflation of middle ear (valsalva's manoeuver).
2. If there is severe pain, do paracentisis of the TM, or myringotomy
to equalize pressure.
3. Topical decongestant nasal drops and oral decongestants.
4. Treat TM rupture if present (as mentioned before).

Fracture temporal bone

(Fracture base of skull)

There are two types (Fig. 18)

A. Longitudinal fracture.
B. Transverse fracture (more dangerous).

I. Longitudinal fracture
More common (80% of cases).
Cause: Direct trauma to the side of the head in the temporal or
parietal regions.
The fracture line passes along the longitudinal axis of the petrous
temporal bone.
 It contains air-filled cavities {Mastoid air cells) Which are lined
by mucous membrane similar to and continuous with that of the
middle ear.
The mastoid air cells are arranged in groups:
1. The mastoid antrum: this is the largest single air cell, il is
connected with the attic of the middle ear via the aditus ad
antrum. It shows two elevations in its medial wall; the bulge
of the lateral semicircular canal, and the 2"'' genu of the facial
nerve anteroinferior to it.
2. Sinodural air cells: between the dura of the roof and sigmoid
sinus.
3. Tip cells: at the tip of the mastoid.
4. Retrofacial cells: behind the vertical portion of the facial
nerve.
5. Perisinus cells: Over the sigmoid sinus.

mastoid antrum
sinodural cells

perisinus cells

retrofacial cells
tip cells

Fig,7, mastoid process

Fig,8 types of the mastoid process

According to the degree of cellularity, the mastoid process can

be divided into three types:
1. Pneumatic; cellular.
2. Diploic; less cellularity.
3. Sclerotic; acellular.
 70

Clinical Picture
1. Bleeding per car due to rupture of the TM
2. Conductive deafness due to rupture of the TM, or ossicular
dislocation. The inner ear is not involved.
3. Facial nerve paralysis: occurs in 15- 20% of cases (less common
than with transverse fracture). It is lower motor neuron paralysis
(LMN) mostly partial due to stretch of the ner\'e and is of delayed
onset.
4. ("SI-' otorrhoea may occur if there is dural tear.
5. Otoscopy; shows a tear of the TM and skin oftheEACwith
bleeding.

II. rransverse fracture

Less common 20%
Cause A blow to the occipital region.
The fracture line passes perpendicular to the long axis of the
petrous bone (transversely across the petrous pyramid passing
through the inner ear). Bones of the middle and posterior cranial
fossae arc usually involved.
Clinical picture
1. it is more severe than the longitudinal fracture as it usually carries
a major insult to the brain.
2. There is loss of consciousness with the onset of trauma and the
patient is usually comatosed. It is due to brain oedema,
contusions, lacerations, or haemorrhage.
.V Sudden total sensorineural hearing loss (as the fracture line passes
across the inner car.
4. Sudden severe vertigo, nausea, vomiting and nystagmus due to
affection of the inner ear (vestibular affection).
5. Ilaemolympanum (bleeding in the middle ear and the TM is
intact). The drum appears bluish in colour, without external
bleeding.
(). Immediate LMN facial paralysis occurs in about 50% of cases. It
is usuallN' tluc to severe trauma, being either torn or compressed
by bone.

Investigations
1. Plain X- ray skull.
2. CT scan MRI skull and temporal bone: shows the fracture line
and associated brain insult.
 71

3. Audiogram: shows the type of hearing loss.

Treatment
1. Bed rest in the semisitting position.
2. Avoid cough and straining.
3. Cover the ear with sterile dressing and avoid application of
topical treatment, or instrumentation to avoid introduction of
infection.
4. Prophylactic systemic antibiotics especially those crossing the
BBB to guard against meningitis.
5. Special care if the patient is comatosed.
6. Surgery:
a) Tympanic membrane grafting and repair of ossicular
discontinuity (ossiculoplasty) in longitudinal fracture.
b) Facial nerve exploration, if there is associated facial paralysis.
In longitudinal fractures it usually recovers without
interference. In transverse fractures facial exploration is
mandatory to decompress any bone specule pressing on the
sheath of the nerve or to graft a severed (cut) nerve.
c) Management of associated brain injury (e.g. contusion,
lacerations, or haemorrhage) by a neurosurgeon.

Fig.18. fracture temporal bone

 72

Otosclerosis

This is a primary disease of the otic capsule (bony labryinth), in

which there is replacement of the nomial compact lamellar bone
in localized areas by abnonnal spongy bone of greater thickness,
cellularity and vascularity.
There is progressive fixation of the stapes by bony ankylosis of
its framework (footplate) or in the niche of the oval window.

Incidence
This is the commonest cause of bilateral conductive deafness.
Age: 15- 45 years.
Females are affected more than males with a ratio of 2: 1.
The process is bilateral, but it may be unilateral in 10% of cases.

Aetiology
The cause is not exactly known but it may be due to:
1. Developmental defect: postembryonic .formation of new spongy
bone to replace unossified cartilagenous cell rests.
2. lin/.ymatic theory: release of lysosomal hydrolase enzyme by
hislocytes and osteoclasts.

There arc several factors that contribute to otosclerosis:

1. Hereditary tendency: there is positive family history in 50% of
cases.
2. Endocrinal influence: the process is accelerated by thyrotoxicosis,
and puberty.
3. Pregnancy also accelerates the process, as it is related to calcium
metabolism.

Sites of otosclerotic foci

1. Anterior margin of ihe oval window (fissula antefenstram), with
fixation of the foot plate of the stapes. This is the commonest site
and represents 85%) of cases.
2. Fossula postfcnestram: this is a minute fibrocartilagenous
depression behind the oval window.
3. F^ound window.
4. Cochlear capsule.
 73

Types:
A. Stapedial otosclerosis: fixation of the footplate of the stapes and
conductive hearing loss (CHL)
B.Pure cochlear otosclerosis: affection of the endosteal layer of the
labryinth with sensorineural hearing loss (SNHL).
C. Mixed (combined) stapedial and cochlear otosclerosis. This starts
by fixation of the foot plate of the stapes, later on, the process
extends to the cochlear capsule.

Clinical picture
It has an insidious onset and slowly progressive course. In 15%
of cases the course is rapid.

Symptoms
1. Deafness: this is the most important complaint. It is bilateral and
has an insidious onset and progressive course. It is due to fixation
of the stapes.
2. Tinnitus: It may increase as the deafness progresses.
3. Paracussis willisii: this is the phenomenon of hearing better in the
presence of a noisy background, because such patients obtain
advantage than normal people from the raising of their friend's
voice in a noisy place. It is present in all cases of conductive
deafness.
4. Vertigo: may occur in \0% of cases due to involvement of the
inner ear with resultant 2ry Meniere's disease.

Signs
1. The patient has a characteristic quiet voice, although he thinks
that it is loud enough.
2. Ear examination: The TM is normal and intact. Sometimes, a
flamingo red tinge is seen due to dilated blood vessels on the
promontary (Shwartze sign) and this denotes active otosclerosis.
3. Tuning fork tests:
a. bilateral conductive hearing loss of variable degrees according
to the degree of stapedial fixation.
b. Bezold's triad:
• Rinne test is negative.
• Raised lower tone limit.
• Increased absolute bone conduction.
 74
.J*

c. Sensorineural hearing loss in pure cochlear otosclerosis,

il. Mixed hearing loss in mixed otosclerosis (i.e. cochlear
involvement).

Investigations
1. Pure tone audiogram;
a.Conductive hearing loss with an air bone gap, which varies
with the degree of stapedial fixation,
b.Sensorineural hearing loss in pure cochlear otosclerosis
c. Mixed hearing loss in otosclerosis with cochlear
involvement.
2. lympanogram: type As (stunted = stiffness eur\'e) which denotes
ossicular fixation.

I'reatment
1. No treatment in early cases with mild conductive hearing loss less
than 20 dB air- bone gap.
2. Surgical treatment: stapedectomy
This is the treatment of choice if there is conductive or mixed
hearing loss and the air bone gap exceeds 20- 25 dB. The
operation should be carried on the worse hearing ear.
3. Medical treatment: Sodium fluoride therapy.
• Il is given if there is progressive sensorineural hearing loss. It was
found to regress the process of otosclerosis
• Na fluoride is given as 30 mg enteric coated tablets (as it causes
stomach upset) t.d.s. aHer meals, up to 2 years. Calcium
carbonate 500 mg and \it. D 400 units is given with it.
• It is contraindicated in pregnancy, young age before full skeletal
development, renal dysfunction, and rheumatoid arthritis.
4. Hearing aid;
It is a good alternative to surgery' if the operation is contraindicated
(e.g. SNHL) or refused by the patient. It can be used if the operation
fails. The patient needs not to wear the hearing aid all the time.

Stapedectomy operation
" It consists of removal of the stapes superstructures, making a hole
in the stapes foot plate, then linking the long process of the incus
to the oval window by a prosthesis, thus the conductive hearing
mechanism is restored.
 rn

75

The prosthesis used may be Teflon, wire, Tef wire, Tef platinum
or gold. (Fig. 19)

Tef wire Teflon

footplate

long process of incus

Fig. 19. stapedectomy

Contraindications
1. Medical contraindications as in heart failure, however, il can he
done under local anaesthesia.
2. Old age above 50- 60 years (relative)
3. Children and young age as the lesion is still active
(otospongiosis).
4. Pregnancy: it should be postponed after delivery.
5. Occupation requiring a considerable degree of physical strain
(e.g. diggers) or a high degree of balance maintenance (e.g.
acrobatics, and those working at heights).
6. Active otosclerosis, because bleeding is more during surgery.
Active focus is suspected in
- Child bearing period and in children.
- Progressive SNHL.
- positive Shwartze sign.
7. Only hearing ear: because if surgery is done, there is a risk of
SNHL, and thus the patient may be rendered bilaterally deaf. In
this situation a hearing aid is preferred.
8. Severe SNHL with poor speech discrimination.
9. Associated Meniere's disease as it increases the incidence o'(
vertigo and carries the risk of SNHL.

Complications:
1. Sensorineural hearing loss and dead ear: the patient should be
informed as regards worsening ofhearingaftertheoperation.lt
carries an incidence of SNHL (3-5%).

ass
 •m

76

2. Persistent conductive hearing loss due to slipping of the

prosthesis or necrosis of the long process of the incus.
3. Vertigo.
4. Perilymph fistula, due to lack of sealing the defect of the oval
window around the prosthesis.
5. Facial nerve paralysis in a case of congenitally prolapsed facial
nerve.
6. Injury of the chorda tympani nerve with loss of taste on one side
of the anterior third of tongue.

N.B. The patient should be informed that there is no guarantee as

regards improvement of tinnitus by surgery.

Tumours of the middle ear

'fhe most common are:
1 .squamous cell carcinoma (Malignant).
2.Glomus tumours (Benign).

I. Squamous cell carcinoma

it arises either from the EAC or from the middle ear.
Incidence: rare.
Sex: males more than females.
Aetiology
1. Long standing chronic suppurative otitis media in more than 50%
of cases.
2. May be irradiation induced.

Clinical picture
There is a history of long standing CSOM with the following
changes:
1. Change in the character of aural discharge which becomes blood
stained, foul smelling and more profuse
2. Deep seated earache.
3. Facial nerve paralysis due to erosion of its bony canal.
4. hicreasing hearing loss. Sensorineural hearing loss occurs later,
dud to invasion of the inner ear.
5. Vertigo and tinnitus increase.
 77

6. Granulations and polypi are detected. They are nodular, friable

and bleed easily on touch.
7. Manifestations of spread:
a. last four cranial nerve palsies due to their involvement in
the jugular foramen at the base of the skull or in the
parapharyngeal space by metastasis in the node of
Rouviere.
b. ulceration of the skin.
c. extension to the tempromandibular joint and to the parotid
gland.
d. enlarged hard, fixed parotid or upper deep cervical lymph
nodes.

Investigations
1. plain x-ray mastoid: shows bone erosion.
2. CT. scan of temporal bone: shows enhancing soft tissue mass
with extensive bone destruction. It is important to show
extensions of the tumour and lymph node involvement.
3. Audiogram and tympanogram.
4. Metastatic work up: chest x ray, abdominal ultrasound and bone
scan.
5. Carotid angiography: to detect invasion of the internal carotid
arteiy.
6. Biopsy: to confirm the diagnosis.

Treatment
A. Combined surgery and postoperative radiotherapy is the treatment
of choice. Surgery consists of subtotal resection of the temporal
bone which may be extend to involve other structures (e.g. pinna,
skin, .parotid gland, T.M.J.) according to extensions of the
tumour. Radical neck dissection is done if there is enlarged
cervical lymph nodes.
B. Palliative radiotherapy for inoperable cases.

II. Glomus tumours (Paraganglioma = chemodectoma)

These are locally invasive, highly vascular, and very slowly
growing benign tumours. They arise from the non-chromaffin
paraganglionic cells in relation to nerves. These are the most
common tumours of the middle ear and there are two main types that
affect the temporal bone.
 78

1. (ilomus JLigularc: Arises in relation to the Arnold's nerve situated

on the dome of the jugular bulb.
2. Cllomus tympanicum: Arises in relation to Jacobson's ncr\e (from
the glossojiharNngeal ner\'c) on the promontoiy.

Age: usually 40- 50 years

Sex: l-eniales mueli more commoner than males.

( linical picture
I. Ololojiic njanifestations
1. I 'nilalcral gradual progressive deafness, first conductive deafness,
iind later sensorineural deafness occurs due to cochlear invasion.
2. ('nilatcral pulsatile tinnitus (characteristic).
.V Otorrhea due to 2r>' otitis media, it may be bloody.
4. Deep seated otalgia.
5. Bleeding per ear may occur when the mass erodes the TM.
6. Vertigo is rare.
7. liar examination reveals either:
a. A reddish mass behind an intact TM, occupying the
inferior portion, with the characteristic rising sun
appearance. It blanches upon compression by a pneumatic
speculum (Brown's sign).
b. A reddish vascular polyp bleeding easily on touch, may be
seen when it erodes the TM.
8. A bruit may be auscultated over the mastoid.

II. Cranial nerve palsies

1 1 owcr motor neuron facial paralysis is the earliest and most
common to occur.
2. Last four cranial nerve palsies. This occurs with glomus jugulare.
a. 9' \ 1 o' \ 11' ^ cranial nen'cs at the jugular foramen (jugular
foramen syndrome)
b. 12*^ in the hypoglossal canal.
3.5' ^ and 6 ^ cranial nerve palsies arc less common.

III. Increased intracranial tension

I leadachc, projectile \'omiting, blurring of vision and papiUoedenia.
These occur in advanced cases due to intracranial extension.
 79

Investigations
1 CT scan of temporal bone: shows the tumour as an enhancing soft
tissue mass with bone destruction. Early, there may be only
widening of the jugular foramen in glomus jugularc. It shows
extensions of the tumour.
Angiography: confimis the diagnosis (it shows the tumour blush)
and shows the feeding vessels.
MRl (Magnetic resonance imaging) and MR with angiography.
4. Audiogram and tympanogram:

Classification (Fisch)
Type A: Tumour limited to the middle ear cleft (tympanicum )
Type B: Tympanomastoid tumour without destmction of the
infralabyrinthin compartment.
Type C: Tumour invading the infralabyrinthine compartment and
extends to the petrous apex.
Type D: Intracranial extension.
Treatment
1. Surgical excision of the tumour:
a.Glomus jugulare: it can be removed by:
- Transcanal approach with drilling the
hypotympanum.
- Posterior tympanotomy or extended facial
recess approach.
- Radical mastoidectomy.
b.Glomus jugulare: it is removed by the infratemporal
fossa approach type A. For complete excision, it
entails removal of thejugular bulb, so drilling of the
mastoid tip, anterior transposition of the facial nerve
(rerooting) and ligation of the IJV in the neck are
done together with packing of the lateral sinus
superiorly.

N.B. Preoperative embolization of the feeding vessels and the

tumour bed is done 2-3 days prior to surgery in order to minimize
bleeding during the operation.
2. Embolization, radiotherapy or a combination of both is used in
inoperable cases.
 •*

III. INNER EAR

The inner ear has such a convoluted shape that is referred to
as the labryinth.
A. The bony labryinth is composed of:
• The bony cochlea.
• The bony vestibule.
• Three bony semicircular canal (Superior, Lateral and posterior).

B. The membranous labryinth which is composed of: (Fig. 9)

1. Membranous cochlear duct.
2. Utricle and saccule.
3. Membranous semicircular canals.
4. Endolymphatic duct and sac.

ViP*^ CttNMr

Fig.9. membranous labyrinth

The membranous labryinth is filled with endolymph (the only

extracellular fluid in the body, which is rich in Potassium and low
in Sodium), and it is surrounded by another fluid, the perilymph
(high in Sodium and low in potassium), which in turn is encased
in the bony labryinth.
 •v^P

so

Meniere's Disease
(Endolymphatic hydrops)
•fhis is a disorder of the vestibular labyrinth of unknown
actiolog)', which is characterized by paroxysmal attacks of a triad of
\'ertigo. deafness and tinnitus; which is due to increased volume and
pressure of the cndolymph.

Incidence
It is the commonest single cause of peripheral labyrinthine vertigo.
Males arc slightly more commonly affected than females.
Age: most often before the age of 50 years.
ll is usually unilateral, but it may become bilateral in 50% of
cases.

Aetiology
It is not exactly known and several theories were postulated.
. Sympathetic overactivity: vasospasm of the internal auditory
artery or one of its branches due to sympathetic overactivity, this
will lead to accumulation of metabolites and capillary
N'asodilatation, with excessive endolymph fonnation.
I. Autoimmune disease
Histamine sensitivity
[•iidocrinal theory
SaU and water retention.

( linical picture
Ihe classic triad of Meniere's disease consists of vertigo,
deafness and tinnitus, that occur in episodes, and between which
there are free inter\'als (remissions) of variable duration. These
episodes arc due to \'olume/ pressure fluctuation of endolymph.
1. Vertigo: sudden severe vertigo of dramatic onset that lasts fomi
few minutes to few hours. It may be associated with nystagmus
with its rapid phase to the opposite side.
2. Deafness: There is sensorineural hearing loss (Rinne test is
reduced positive). In early stages, it is fluctuant and affects the
low tones, and is reversible. Later on, it becomes progressive with
affection of the low and high tones and is permanent. The patient
 81

is highly sensitive to loud sounds (recruitment) which is

diagnostic of a cochlear pathology.
3. Tinnitus is usually present and is exaggerated during or just
before the attack.
4. In severe attacks there may be manifestations of vagal stimulation
in the form of nausea, vomiting, sweating, colicky abdominal
pains and bradycardia.

The attack lasts fonn few minutes to few hours. There may
be certain alarming symptoms before the attack (aura) in about 50%
of cases, in the form of pressure and fullness in the ear, otalgia and
appearance of or increasing tinnitus.

Investigations
1. Audiogram (PTA); early low tone fluctuant sensorineural hearing
loss and, later on, it involves the high tones and becomes
permanent.
2. Speech audiogram: poor speech discrimination matching with the
PTA (i.e. cochlear SNHL).
3. Electrocochleography is diagnostic.
4. Caloric test: hypoactive labyrinth (canal paresis) denoting
hypofunction with directional porporderance to the opposite side.
5. Dehydration test (glycerol test): It is done during the attack. First
an audiogram is done before the test, then 1.5 mg/kg b.wt.
glycerol (diuretic) is given orally with equal amount of saline and
after 3 hours repeat the audiogram. Improvement of hearing by
10- 15 dB indicates positive test (i.e. presence of hydrops).
6. CT scan of temporal bone to exclude a retrocochlear pathology
(e.g. Acoustic neuroma).

N.B.: Audiological investigations show that the type of hearing loss

is cochlear sensorineural hearing loss, in which there are:
- Poor speech discrimination matching with the PTA.
- Negative tone decay.
- Positive recruitment.
- ABR: normal wave number V.
 82

Ireatment
Medical treatment should be started at first and tried for a
long lime, and if failed resort to surgery only if the attacks arc
rrctjucnt incapacitating the patient and disturbing his work.

I. Medical treatment
Medical therapy is directed to alleviating the uncomfortable
symptoms and slowing the progression of hearing loss.
1. Bed rest with the head suppoiled.
2. Sedatives: Diazepam (valium) 10 mg IM or I.V.
3. Antiemetics: Chloropromazine (largactil) 75 mg I.M. if there is
severe vomiting during the attack.
4. Vestibular suppressants e.g.: Promethazine, medizine for vertigo.
5. Vasodilators; histamine, nicotinic acid, betahistidine.
6. Diuretics: lasix.
7. Streptomycin in toxic doses can be used in bilateral cases to
selectively destroy the vestibular end organ. It should be used
cautiously.
8. General measures:
A. Relaxation and reassurance.
B. Salt restriction in diet.
C. Avoid activities in which vertigo may be hazardous e.g. car
driving, or working at heights.
D. Avoid alcohol, smoking and coffee.
I:. Masking the tinnitus, if annoying the patient by wearing a
tinnitus masker appliance.
I\ Hearing aid, if there is permanent hearing loss with special
electric setup to nullify recruitment.
G. Vestibular rehabilitation.

II. Surgical treatment

It is indicated if the patient becomes severely disabled
because of recurrent severe vertigo, and progressive hearing loss,
despite medical management and the patient is strongly positive
towards the surgcr)'.
The operation is designed according to the hearing of the patient:
A. If good (sen'iceablc) hearing: then do either
1. Transmastoid endolymphatic sac decompression (saccus
decompression) to enhance the endolymph drainage.
 83

2. Vestibular ner\'c section (vestibular neurectomy):

Through a retrolabyrinthine, rctrosigmoid, or middle
cranial fossa approaches. It is done if the disease is strictly
unilateral.
A. If bad (non serviceable) hearing: do surgical labyrinthectomy.
N.B. Chemical labyrinthectomy by instillation of gentamycin into
the middle ear to be absorbed through the round window to cause
destruction of the endorgan may be done.

llllllllIIlllHlllllllllllllIlllllUlllllIlllllllllllllinilllllllllllllllllllllll^

Acoustic neuroma (vestibular schwannoma)

It is a benign tumour that arises from the Schwann cells
(neurilemma) of the vestibular division of the 8" nerve.
Acoustic neuroma is a misnomer because it is of \estibular origin.
Incidence
- It represents about 8% of brain tumours, and 80"/) of
cerebellopontine angle'(CPA) tumours.
- Age of presentation is about 40- 60 years, but it starts at an earlier
age and grows very slowly.

Origin Schwann cells of the vestibular nerve at the glial-

neurolemmal junction.
Site: at the internal auditory meatus (lAM) or cerebellopontine angle
(CPA).
Grossly slowly growing, encapsulated, small, smooth circumscribed
tumours.
Microscopic there are two types of cells
1. Fasiculated (Antoni type A): long fusiform cells with elongated
central nuclei, arranged in longitudinal bundles.
2. Reticular (Antoni type B): cells are arranged as a reticular
network.
This differs from Von Rickienghousen's disease (multiple
neurofibromatosis) where the nerve fibers are entangled inside tiic
tumour (like in neurofibroma).
 84

Clinical picture
A. Otological manifestations
The earliest manifestations are auditory:
1. Unilateral slowly progressive sensorineural hearing loss.
2. Unilateral tinnitus: This may be the only symptom. Tinnitus must
be taken seriously in any elderly, and investigate the case as
acoustic neuroma. This is the only way to detect early cases.
3. Vestibular manifestations:
- Transient mild unsteadiness.
- Vertigo is not marked as the condition is slowly progressive
allowing central compensation, and this is against what is
expected from a beginner.
B. Neurological manifestations
Cranial nerve palsies:
a. Trigeminal (5th nerve) is the earliest to be affected. Absent
corneal reflex is the earliest sign and later there is facial
parasthesia and numbness.
b. Facial nerve paralysis is rare to occur.
If the case presents with facial paralysis, think of other CPA
lesion as (congenital cholesteatoma).
C. Cerebellar manifestations
This occur when the tumour is large (3 cm or more).
1. Nystagmus: spontaneous, coarse and pendular
2. Cerebellar ataxia
3. Other cerebellar manifestations (see as before)
D. Terminal phase:
1. increased ICT: headache, projectile vomiting, bulbar
palsy or cerebellar herniation.
2. Coma, death.

Investigations
1. Audiogram (PTA): sensorineural hearing loss in 96% of cases.
2. Speech audiogram: poor speech discrimination, poorer than
expected from the PTA, this differentiates a cochlear from a
rctrocochlear neural lesion.
3. Auditory brain stem response (ABR.): This is an accurate
noninvasive method. There is delay of wave V (number 5) more
 85

than 0.4 m sec, greater than the other side which is highly
suggestive of a retrocochlear pathology affecting the s"' nerve.
4. CT scan of petrous bone with contrast:
- Early, there is widening of the 1AM, later it shows the
tumour.
- Small intracanalicular tumours less than 0.3 cm may not
be detected by CT scan
5. MRI with gadolinium contrast: this is the best investigation to
show the tumour especially at an early stage.

Differential diagnosis other CPA lesions

1. Meningioma
2. congenital cholesteatoma.
3. Pontine glioma.
4. Vascular loop.
5. Arachnoid cyst.

Treatment
A. Surgery: This is the main form of therapy, and the approach
depends upon the size and location of the tumour as well as the
degree of hearing loss.
1. Good (serviceable) hearing:
a. Middle cranial fossa approach if the tumour is small less
than 1 cm.
b. Retrosigmoid approach: in large tumours in the CPA.
2. Bad (non serviceable) hearing: with more than 50 dB hearing
threshold and less than 50% speech discrimination.
- Translabyrinthine approach is done, in which the labyrinth
is destroyed and the lAM is opened directly from its lateral
aspect.
B. Gamma Knife (stereotatic radiosurgery): This is recently used
with unclear results.

N.B. If Acoustic neuroma is detected in a member of a family all

other members of that family must be investigated as this may be
multiple neurofibromatosis which is hereditary.
 86

Anatomy of the facial nerve

(7th cranial nerve)

It is the motor nerve to the muscles of the lace. The facial

nerve nucleus lies in the pons. In the pons, fibres pass up to the 4''^
\'cnlriclc, forming a knee around the nucleus of the 6th nei*ve. It
leaves the pons at the junction between the pons and the medulla.
Fibres then pass in the cerebellopontine angle to enter the internal
auditory meatus. (Fig. 19)

I he intratemporal course of the facial nerve:

• (tic facial ner^^c is encased in the temporal bone for a distance of
37-45 mm. This is the longest bony enclosure of a nerve in the
body.
• Its course in the temporal bone is divided into three parts:
1. Labyrinthine segment: The facial nerve enters the internal
auditory meatus accompanied by the 8th nerve. It runs in the
internal auditory canal superior to the cochlear nerve and anterior
to the superior vestibular nerve, it then runs laterally to reach the
medial wall of the middle ear at the geniculate ganglion.
2. Tympanic (horizontal) segment: At the geniculate ganglion it
curves to form the first genu and runs backwards in the medial
wall of the middle ear above the promontory and the oval window
till the posterior wall of the middle ear.
3. Mastoid (vertical) segment: It turns inferiorly (second genu) and
lies anteroinferior to the lateral semicircular canal, where it runs
vertically downwards through the anterior border of the mastoid
process to leave the skull at the stylomastoid foramen.
• it then passes downwards and anteriorly where it enters the
parotid gland where it divides into its five terminal branches. This
is the extracranial portion.

Branches
1. The branches in the temporal bone
a. greater superficial petrosal nerve: arises at the level of the
geniculate ganglion and carries secretomotor
parasympathetic fibres to the lacrimal, nasal, and palatine
glands.
 ;-i?1

87

b. Nerve to stapedius: exits in the mastoid segment. It gives

motor supply to stapedius muscle.
c. Chorda tympani nerve: It exits just above the stylomastoid
foramen to enter the middle ear. It carries taste sensation
from the anterior 2/3 of the tongue, and secretomolor
parasympathetic fibres to the sublingual and submandibular
salivary glands.
2. Two branches: after its exit from ihe stylomastoid foramen
which give motor supply to the posterior belly of digastric and
stylohyoid muscles
3. Five terminal branches in the parotid gland
-Temporal.
-Zygomatic.
-Buccal.
-Mandibular.
-Cervical.
They supply muscles of the scalp (occiplofrontalis), muscles of
the auricle, muscles of the face, as well as platysma.
4. Sensory fibres: to supply a small area in the posterior wall of the
external auditory canal.
N.B.: The tympanic and mastoid parts of the facial nerve lie in a
bony canal (fallopian canal) which may be dehiscent.

Fig. 19, anatomy of the facial nerve

 r - •H

88

Facial nerve paralysis

Aetiology
I. Supranuclear (upper motor neuron lesion)
It is due to a lesion in the corticobulbar tract.
1. cerebrovascular stroke (e.g. thrombosis, embolism,
haemorrhage).
2. Meningitis, encephalitis.
3. Trauma to the head.
4. Brain tumours and brain abscess.

II. Peripheral (lower motor neuron lesion (LMNL)]

It is due to a lesion anywhere from the nucleus of the nerve
lo its termination.
A. Intracranial
1. In the pons: affection of the facial nerve nucleus, so, facial
paralysis is accompanied by pontine manifestations.
/aj Congenital aplasia of the facial nucleus,
pontine haemorrhage,
pontine tumours.
Basal meningitis,
c. Multiple sclerosis.
2. At the cerebellopontine angle: This is usually associated with
8th (vestibulocochlear nerve) affection.
a. Tumours (e.g. meningioma, vestibular shwannoma).
b. Arachnoid cyst.
c. congenital cholesteatoma (epidermoid cyst).
B. Cranial (intratemporal)
It is due to a lesion inside the temporal bone.
1. Traumatic
a. Birth trauma as in forceps delivery pressing on the exit of the
nerve at the stylomastoid foramen.
b. Fracture temporal bone especially of the transverse type
c. Surgical trauma: during ear surgery as in mastoidectomy,
stapedectomy, and surgery of the skull base (e.g. excision of
glomus tumours)
2. Inflammatory
a. A.O.M. with dehiscence in the fallopian canal.
b. C.S.O.M especially cholesteatoma.
 :-ii?n

89

c. Viral; herpes zoster oticus (Ramzy Hunt syndrome).

3. Tumours
a. Glomus jugulare.
b. Squamous cell carcinoma at the 1AM
c. Acoustic neuroma
4. Idiopathic; Bell's palsy. This is the commonest cause of LMN
facial paralysis.

C. Extracranial (Extratemporal) —>- ^^ftfC'X^ ^^<-^.

1. Trauma
a. cut wounds of the face in the parotid region,
h. surgeiy on the face,
c. parotid gland surgery.
2. Tumours: malignant parotid tumours.
3. sarcoidosis of the parotid gland.

D. Miscellaneous
1. Polyneuritis.
2. Diabetes mellitus.
3. Lyme disease.
4. T.B.
5. Guillane-Barre syndrome.
6. Milkersson Rosenthal syndrome.

Clinical picture of LMN facial paralysis

A. Paralysis of muscles of the face
/^^ Inability to raise the eye brows with loss of frontal corrugations
!(occipitofrontalis).
^Inability to close the eye fimily (orbicularis occuli).
3. Food collects beneath the cheek (buccinator).
•f. Inability to whistle (orbicularis oris).
S. drooping of the angle of the mouth on the affected side, dripphng
o( sali\a. loss of the nasolabial fold, deviation of the angle of the
mouth to the healthy side upon smiling (Levator anguli oris ).
^b "

ci^.pp^'- , J *-^, V / w \
fp
( C
1 T'I
• The labryinth is divided into:
1. Vestibular portion which is concerned with balance.
2. Cochlear portion which is concerned with hearing.

The cochlea
It is coiled like a snail's shell, which forms two and half
turns. The axis of the spirals is called the modiolus containing nerve
fibres and arterial supply. The nerve fibres then run through a bony
shelf called osseus spiral lamina to reach the sensory organ of corti.

The cochlear duct (35 mm long) contains endolymph and

divides the cavity of the cochlea into three portions.
1. The upper; scala vestibuli contains perilymph and is separated
from the cochlear duct by the thin Reissner's membrane
2. The lower; scala tympani contains perilymph and is separated
from the cochlear duct by the osseous spiral lamina and the
basilar membrane.
3. The middle compartment is the scala media.

The basilar membrane carries the organ of corti (Sensory

end-organ of hearing), which contains one row of inner hair cells
(300 cells) and two rows of outer hair cells (12000 cell).

The vestibular part of the inner ear

• It consists of the utricle, the saccule and the semicircular canals.
• The sensory end organs responsible for maintenance of
equilibulium are:
a. Maculae of the utricle and the saccule.
b. Crista ampularis of the semicircular canals.

Nerve supply of the ear

A. Sensory
1. Auricle and external auditory canal:
a. The auricle and the surrounding skin are supplied by
the great auricular ner\'e, 3rd and 4th cervical nerves
and to a lesser degree by the lesser occipital nerve from
the 2" and 3"^ cervical nerves.
b. The tragus, part of the eras of the helix, roof and
anterior wall of E.A.C. and the outer surface of the
 90

- It IS important to assess for:

a. fonc of the facial muscles by comparing both sides at rest.
h. Power of the facial muscles by comparing both sides during
active movement.
- Dctcnnine whether the paralysis is:
a. Partjal: There is still visi^ije voluntaiy movement.
b. Complete: absence of ajl voluntary movement.

B. Differentiation between UMN and LMN paralysis

UMNL
• Paralysis of lower'/2 of face.
• Rmotional movements (e.g.
Laughing) arc intact.
• Associated hemiplegia.
• Hypertonia (spastic).
• No fasiculation.
• No muscle atrophy.
LMNL
• Total facial paralysis.
• Emotional movements are
lost.
• No hemiplegia.
• Hypotonia (flaccid).
• Fasiculations are present.
• Muscle atrophy occurs later.

N.B.: in UMN facial paralysis only the lower half ofthefaceis

paralysed, this is because the upper part of the motor facial nucleus
supplying the upper part of the face is bilaterally represented in the
cerebral cortex.

C. Leveling of LMN facial paralysis

1. Nuclear lesion
• Total facial paralysis of the upper and lower halves of the
face.
(•associated 6' nerve palsy (diplopia and convergent
squint) and other pontine manifestations may be present.
(•jLacrimation is nomial.
0Taste sensation of anterior 2/3 of tongue is normal.
• Stapedial reflex is absent.
2. At the cerebello pontine angle and LA.M.
• Total facial paralysis.
(jjassociated 8'^ nerve affection (deafness).
• Lacrimation is lost.
• Taste sensation Lost.
• stapedial reflex absent.
 91

ft- A/-
3. At the geniculate ganglion -—i ^•/^ Q'/^ ^kp'r i<' 'f /* w ^

• Total facial paralysis.

<• Lacrimation is lost.
• Taste sensation is lost.
• Stapedial reflex absent.
4. Infrageniculate ^ -/A *^^^.6--t^t y^ / --fi.fjt p^' K^C / trr-^ \<.KC'/. ,vV-i^«

• Total facial paralysis.

•:•• Lacrimation is normal.
• Taste sensation is lost.
• stapedial reflex absent.

Investigations
A. To identify the cause
1. CT scan of brain and petrous bone to show fractures or
tumours.
2. MRI petrous bone to show tumours especially facial
neuroma.
3. Plain x-ray of mastoid for cholesteatoma.
4. Audiogram (PTA).
B. To detect the level of the lesion
1. Schirmer's test (test for Lacrimation): (Fig. 20) It is significant
when the difference between the lacrimal flow of both sides
exceed 30% of the total bilateral lacrimation, indicating a lesion
at or above the geniculate ganglion.
2. stapedial reflex: lost in any affection above the nerve to
stapedius.
3. Taste sensation:
a. Qualitative: compare taste of different staff applied to
the lateral edge of the anterior 2/3 of the tongue.
b. Quantitative: electrogustometry.
4. Submandibular salivary flow test: the amount of salivation is
compared on both sides. It is diminished on the affected side.
^'*^''^*^

Fig,20, Shirmer's test

 92

('. KIcctrodiagnostic studies: to detect the condition of the facial

iicr\'c and facial muscles. This important for diagnosis, prognosis,
and deciding the management. They are important to delect nerve
degeneration as early as possible which is useful in complete
jiaralysis. They include:

1. Nerve excitability test

Determine the minimal electrical current in milliamperes
required to produce a just \isible muscle contraction, and compare
both sides.
a. A difference less than 3-5 mAmp between both sides
indicates degeneration.
b. A difference less than 3 mAmp between both sides
indicates neurapraxia.
It is of no value if done before 3 days of injury because the
degenerated fibres can continue to respond to stimuli during this
period.

2. Klectroneuronography (ENOG), evoked electromyography

This is the measurement of the amplitude of the summation
action potentials of the muscles when a supramaximal stimulus is
applied to the nerve and compare both sides. This is important to
detect the percentage of degeneration, which is important to decide
the way of management and prognosis. It is done after 2-3 days for
the same limitation as the nerve excitability test.

3. Electromyography
This is recording of the electrical activity of the facial
muscles at rest and during active movement. This is valuable only
when degeneration of the nerve has occurred, so it is important in
the follow up to detect nerve regeneration (i.e. good prognostic but
late diagnostic lest).
a. Fibrillation potentials indicate degeneration.
b. Polyphasic potentials indicate regeneration, and these are
detected earlier than clinical recovery.

Pathology of nerve affection

A. Neurapraxia: There is only compression of the nerve leading to
physiological block. Spontaneous recovery is usually complete in
one month.
 93

B. Axonotmesis: there is damage and degeneration of axons, with

intact myelin tubes, where the axons grow into the empty myehn
tubes at a rate of 1 mm/day. Spontaneous recovery occurs in
about 2-3 months and may be incomplete.
C. Neurotmesis: loss and degeneration of axons ofmyelin tubes. As
the axons in the myelin tube regrow they may get mixed together
leading to cross innervations. Spontaneous recovery may occur in
1 year and always incomplete.

General management of facial paralysis

The treatment of facial paralysis varies according to the
cause, but there are certain lines that are followed in every case.

1. Reassurance of the patient

2. Care of the eyes: To prevent exposure keratitis and conical
ulceration due to lack of Bell's phenomenon (frequent blinking).
a. Artificial tears during the day.
b. Eye ointment by night.
c. Use of eye glasses outdoors.
d. hi prolonged cases, lateral larsorraphy or gold weight
implantation in the upper lid can be done.
3. Care of the paralysed facial muscles: to prevent disuse atrophy
and fibrosis.
a. Physiotherapy and gentle massage in a circular manner.
b. Infrared heat and galvanic stimulation.
c. When voluntary movement starts, the patient should start
active muscular exercises in front of a mirror.
4. Treatment of facial paralysis according to the cause
5. Rehabilitation
It is performed in prolonged cases with hope of spontaneous
recovery (after 1-2 years). It is either:
a. Dynamic: to improve the function of the nerve during
movement, provided there is good status of muscles.
-End to end anastmosis of the nerve, if the distal antl
proximal segments arc identified.
-Ner\'e graft: The cable graft is obtained from the great
auricular nerve in the neck, or from the sural nerve in
the leg behind the lateral maleolus.
 94

-Cross tacial anastomosis: This is an anastomosis

bciwcen the facial nerves o[ both sides, tlirough a
supralabial tunnel, using the sural nerve.
"[•i\'poglosso-facial anastomosis.
b. Static: to improve the appearance of the face at rest.
-Implaritation of fascia lata slings.
-Regional muscle transplantation e.g. temporalis muscle
implanted in the cheek.

Results of facial paralysis

C\)ntracturcs due to fibrosis of dencrvated muscles.
Tics and spasms, which are involuntary spasmodic mo\'emcnts of
the facial muscles.
Cross innervation due to misdirection of the regenerating fibres,
resulting in:
a. Synkinesis: Voluntary movement of one muscle is associated
with involuntary movement of another muscle.
b. Crocodile tears: This is lacrimati.on while eating. It is due to
mixing of the regenerating parasympathetic fibres between
the greater and lesser superficial petrosal nerves.

Important causes of facial paralysis

1. Bell's palsy.
2. Traumatic facial paralysis.
3. Herpes zoster oticus (see before).
4. Facial paralysis complicating C.S.O.M. (see before).

Bell's palsy (idiopathic facial paralysis)

This is the commonest cause of LMN facial paralysis
representing about 80 - 90% of all cases of facial palsy.

.Vetiology
Is not clearly known and several theories were suggested:
1. Vascular ischacmia theory; postulates that local vasospasm of the
vasoncrvosa supplying the facial nerve, causes oedema of the
nerve sheath with compression of the nerve in its bony canal,
leading to secondary ischaemia and more nerve damage. The
 95

cause of primary ischemia is unknown, but it may be due to

exposure to cold air draughts.
2. Viral theory: Suggests that it is a sort of isolated viral neuritis or a
single manifestation of polyneuritis. It may be due to reactivation
of neurotropic herpes simplex virus.
3. Autoimmune theory.

Clinical picture
It affects mainly middle aged adults, and affects both sexes
equally. It may be precipitated by exposure to cold air draughts,
emotional stress, or pregnancy. The diagnosis of Bell's palsy is
made by exclusion of all other etiologies of facial paralysis.

It presents as:
1. Unilateral LMN facial paralysis of sudden onset, which may be
partial or complete, and reaches a maximum in few days.
2. Retroauricular pain may occur several hours before the onset of
the paralysis.
3. A reddish chorda tympani nerve may be visible through the
posterosuperior part of the T.M.

Investigations (as mentioned before)

In prolonged cases of Bell's palsy, that do not show recovery
in a period of 6 months, investigations to exclude the presence of a
facial nerve neuroma should be done, especially MRI and CT scan
of petrous bone.

Treatment: Most cases of Bell's palsy recover spontaneously.

1. General measures: as mentioned before
2. Medical treatment:
It should be started as early as possible.
a. vasodilators: They are valuable if given in the first few hours
to relieve the primary ischaemia. These include; nicotinic
acid, histamine and beta histidine.
b. Steroids (medical nerve decompression): It is given to
decrease the oedema and inflammatory process. Oral
prednisolone is given 80 mg/day for 5 days, Then 40 mg/day
2 days, then 20 mg/day 2 days, then 10 mg/day 1 day.
Tapering of the dose is essential to avoid adrenocortical
insufficiency. Steroid therapy should be started early and if
 96

no improvement occurs after 2 weeks a second course could

be given.
N.B. The value of medical treatment is questioned by some
authors, who tried giving no treatment and obtained the same
results of recovery.
^. Surgical treatment: (decompression)
a. [ndication: More than 90%) degeneration shown by ENOG
after 2 weeks despite medical treatment. This is met with in
few cases.
b. Decompression of the facial nerve is done by exposing it in
its bony canal and slitting the sheath of the ner\^e from the
stylomastoid foramen till the level of compression as shown
by topographic diagnosis. It is performed through a
mastoidectomy approach, or a middle cranial fossa approach
or a combination of both approaches (total nerve
decompression).
4. Late cases; require facial rehabilitation, but remember to exclude
the presence of a facial nerve neuroma in such cases.
There arc certain criteria suggestive of poor prognosis:
1. Recurrent BelFs palsy.
2. Severe retroauricular pain.
3. Complete paralysis from the start.
4. Old age, diabetes and hypertension.

Traumatic facial paralysis

II ma>' be due to:
I. Fracture base (temporal bone fractures)
The pathological mechanism may be:
1. Stretch and ischaemia of the nci-vc.
2. Compression of the ncr\'e.
3. Contusion of the ncr\'e.
4. Cut (severed) nenx.

f.^z-H-U .'f ransverse fracture: It is rare (20% of fractures of the temporal

bone). Facial paralysis is common occurring in about 30-50% of
cases. The paralysis is usually immediate and complete as the
injury is usually severe. There is associated sensorineural hearing
loss.
 97

2. Longitudinal fracture: It is more common (80% of fractures of ihc _ ^ ^ <: H

temporal bone). Facial paralysis is uncommon occurring in about
15-20% of cases. It is usually delayed and partial as the injury IS
usually mild. There is associated conductive hearing loss.

Treatment
l.ir the paralysis is immediate and complete, (more than 90%
degeneration) surgical exploration is recommended to
decompress a bone spf^cule or repair a severed (cut nerve). Repair
is done either by end to end anastomosis if there is no gap or
nerve graft if there is a gap.
2. If the paralysis is partial or delayed start conservative treatment in
the fomi of systemic steroids and antibiotics, and daily follow-up
by ENOG is done. If the condition gets worse (more than 90%
degeneration in two weeks), surgical exploration is performed. In
longitudinal fractures most cases recover spontaneously, and only
few cases need surgical intervention.

II. Surgical trauma (iatrogehic)

It may occur during the following surgical procedures;
l.The labyrinithine segment is affected in middle cranial fossa
approach for removal of acoustic neuroma, or for vestibular
neurectomy.
2. The tympanic segment is injured during radical mastoidectomy
and stapedectomy operations.
0 T h e 2nd genu (this is the commonest site for injury); it occurs
while searching for the antrum during ear surgery.
4. The vertical segment; is affected in cortical mastoidectomy while
drilling the retrofacial cells, to open the facial recess.
5. During stapedectomy if the facial nerve is dehiescent or
prolapsed.
6. During excision of tumours as in glomus jugulare.
7. The extratemporal part may be injured in:
- Parotid gland surgery particularly excision of malignant
tumours.
- Injection of local infiltration anaesthesia.
~ Too long postauricular incision in children, so in infants and
young children it must be a horizontal incision (Wild's
 -n

98

incision) and never the classical postauricular incision (the

mastoid process is still underdeveloped).

Injury during surgery is predisposed to by:

1. Distortion of the normal anatomy due to the presence of a
congenital anomaly, advanced pathology (extensive
cholesteatoma), or previous surgery.
2. Inexperienced surgeon. So attending temporal bone dissection
courses is recommended before starting doing live surgery.

Facial paralysis either

A. Appears immediately after surgery: It is discovered as soon as the
patient recovers from anaesthesia. It is usually a complete
paralysis as the injury is usually severe (cut of the nerve or
laceration).
B. Delayed postoperative: This occurs after several hours or days.
The paralysis is usually partial as it is due to a minor injury like a
tight pack in the mastoid cavity, compression by a bone spicule,
or due to the effect of heat during drilling of the bone.

Treatment
A. Immediate complete paralysis
Immediate reexploration should be done before sunset. The
nerve is decompressed starting from the site of injury, and extends
both proximally and distally. Then, the nerve is either sutured (end
to end anastomosis) if both ends are identified with no or minimal
gap, or a cable graft from the greater auricular nerve or sural nerve is
taken to bridge a large gap.

B. Delayed partial paralysis

Start with conservative treatment in the form of systemic
steroids, antibiotics, and remove any tight pack. Observation is
essential with daily ENOG, and it usually recovers spontaneously.
a. If improving; continue conservative treatment.
b. If worsening (reaching 90% degeneration or more;
reexploration and decompression as in immediate paralysis.

Melkersson's Rosenthal syndrome: This is a rare disease of

unknown aetiology, usually occurring in young ages below 15 years.
 99

It is characterized by recurrent alternating LMN facial paralysis,

swollen lips and furrowed tongue (scrotal tongue). A family history
is common.

Deafness (hearing loss)

Deafness means diminution of hearing up to complete loss of
hearing. According to the degree of hearing loss in dB (decibel), it is
classified into mild, moderate, severe and profound hearing loss.

Hearing loss always indicate a disease in the acoustic

pathway from the external ear up to the cerebral cortex.

Types of hearing loss

I. Conductive hearing loss.
II. Sensorineural (perceptive) hearing loss.
III. Mixed hearing loss.
IV. Hysterical (functional) hearing loss.

I. Conductive hearing loss (CHL)

There is interference of transmission of sound waves along
the conductive apparatus (the external and middle ear).

Causes
A. Occlusion of the external auditory canal
This may be due to
1. Congenital: congenital meatal atresia or stenosis.
2. Acquired atresia: secondary to external otitis or trauma.
3. Foreign body in the external canal.
4. Inflammatory:
a. External otitis (due to oedema)
b. Large furuncle
c. Otomycosis (fungal ball).
d. Polyp, coming out from the middle car.
5. Neoplastic:
c. Large exostosis
f Malignant tumours
g. Other neoplasms
6. Impacted wax: This is the commonest cause of CHL.
 100

B. Perforation of the TM
This may be due to
i. Traumatic rupture of the TM.
2. Suppurati\e otitis media.

( . ( iuiscs in the middle car

1. Congenital;
a. Atresia of the middle ear
b. Congenital ossicular fixation or deformity e.g. congenital
fool plate fixation.
2. Traumatic;
a. Dislocation of the ossicles
b. Barotrauma
c. Longitudinal fracture of the temporal bone
-V Indammator}';
a. Acute suppurative otitis media.
b. Chronic suppurati\'e otitis media.
c. Chronic non-suppurative otitis media e.g. chronic secretory
otitis media, chronic adhesive otitis media, middle ear
atelectasis.
4. Neoplastic:
a. Glomus tumours
b. Carcinoma
>, Otosclerosis;
This is one of the most important and common causes.
6. Tympanosclerosis

D. Causes in the Eustachian tube

Due to Eustachian tube obstruction by:
1, Hypertrophy of nasopharyngeal adenoid tissue
2. Tubal catarrh
-T Tumours of the nasopharynx e.g. carcinoma, lymphoma,
angiofibroma, and sarcoma.
4, Otitic barotrauma.
\ Cleft palate due to deficient structure and function of tensor and
ic\ ator palati muscles (openers of the E.T.).
f' Scarriim of the tubal orifice after adenoidectomy.
 01

II. Sensorineural hearing loss (SNHL)

It results from defects either in the conversion of sound
energy into electrical impulses in the cochlea, or in the transfer of
these impulses along the eighth nerve and the central connections to
the auditory cortex (i.e. in the auditory pathway).

A. Cochlear causes (sensory)

1. Congenital
Hearing loss, dates since birth or shortly after. It may be
1. Hereditary: due to genetic predisposition.
a. Uscher's syndrome (SNHL + retinitis pigmentosa).
b. Penderd's syndrome (SNHL + goitre).
c. Alport's syndrome (SNHL + nephritis).
2. Prenatal:
a. Maternal infections as rubella in the 1st trimester.
b. Drug intake in the 1st trimester e.g. quinine and
aminoglycosides and salicylates.
3. Natal: (during labour)
a. Hypoxia or anoxia of the foetus.
b. Birth trauma as in forceps delivery.
4. Postnatal:
a. Neonatal infections.
b. Eiythroblastosis foetalis (Rh incompatibility).

2. Traumatic
1. Transverse fracture of temporal bone involving the labryinth.
2. Acoustic (noise) trauma:
a. Acute: exposure to single severe noise as in explosions and
fireshots causes penrianent SNHL of the high tones in the
exposed ear.
b. Chronic: prolonged exposure to noise as in industries and
a ire rafts.
3. During ear surgery as in stapedectomy.
4. Concussion without fracture.
 102

3. Inflammatory (Labyrinthitis)
1. Infective:
a. Viral: measles, mumps, influenza, typhoid. Here the deafness
occurs after the febrile stage. It may be unilateral or bilateral,
asymmetric and affects more the high tones.
b. Syphih'tic labyrinthitis: deafness is progressive, asymmetric
and may be associated with vestibular symptoms (i.e.
vertigo),
c. Bacterial:
-Labyrinthitis secondary to suppurative otitis media.
-Meningitis: deafness is bilateral and profound,
oxic:
a. Ototoxic drugs: quinine, aminoglycosides, salicylates,
cthacr>'nic acid (Edecrine, a diuretic), and chemotherapeutic
agents used for cancer therapy.
b. Metabolic: uraemia, diabetes, thyrotoxicosis.

4. Vascular
Internal auditory artery occlusion due to spasm, thrombosis
or embohsm. It causes sudden hearing loss.

5. Miscellaneous
a. Presbycusis (senile deafness).
b. Meniere's disease.
c. Pure cochlear otosclerosis
d. Perilymph fistula: It may occur after stapedectomy, or it may
be spontaneous after severe straining. It causes fluctuant
SNHL.

B. Fictrocochlear causes
Due to lesion anywhere cither in the vestibulocochlear nei^e
or in the auditory pathway.
1. Vestibulocochlear nerve affection:
a. Cerebellopontine angle lesions as in acoustic neuroma, and
congenital cholesteatoma.
b. Meningitis.
c. Vascular loop.
2. Central: due to lesion anywhere in the auditory pathway. It is
rare.
 103

a. Multiple sclerosis.
b. Meningitis, encephalitis.
c. Cerebrovascular accidents e.g. thrombosis, haemorrhage or
embolism.
d. Brain tumours.

III. Mixed hearing loss

1. Congenital meatal atresia with inner ear anomaly.
2. Fracture base of skull.
3. Complicated CSOM with labryinthitis.
4. Combined otosclerosis i.e. (footplate fixation, cochlear
otosclerosis).

Congenital deafness
It is either hereditary due to genetic predisposition, or
acquired (non genetic) due to intrauterine affection in the 1st
trimester or a problem in the perinatal period.

I. Hereditary (genetic)
A. Deafness occurring alone
1. Mickel's deafness: total lack of development of the inner ear.
2. Mondini's dysplasia: partial aplasia of the bony and the
membranous labyrinth with flattened cochlea. The cochlea makes
1 Vi turns instead of 2V2.
3. Scheibe's deafness: maldevelopment of the saccule and the
cochlear duct.

B. Deafness with other abnormalities (as a part of a syndrome)

1. Waardenberg's syndrome: SNHL, partial albinism B (white lock),
heterochromia of the iris, laterally displaced medial canthi.
2. Penderd's syndrome. J. ^-^• K- L* -v 'S.^-i'^
3. Uschcr's syndrome. ^^-^•'^-'- \^-U y i^<KJ^\X^^ ^\a ^•^^\->s^.\
4. Albinism.
5. Treacher Collin's, syndrome: retinitis pigmentosa, SNHL due to
hypoplasia of the external canal and middle car, receding
mandible, occular deformity.
 104

II. Acquired (non genetic)

0 Rubella infection in the 1st trimester^ The rubella syndrome
consists of ^§NHL, caTdiac_,def^^ "^mcii^l^retardation, and
bliadil^. Hearing loss is due to hypoplasia of the organ of corti.
nAFrvthroblastosis foetalis: SNHL, jaundice, mental retardation and
cerebral palsy (kemicterus).
QljXlmjsm; mixed conductive and SNHL. with delayed physical
and mental retardation.
r4j)Hirth ir|jiirv due to hypoxia, prematurity, toxaemia of pregnancy
and anaesthesia.
r_SjQtotoxic druus intake in the first trimester e.g. thalidomide,
quinines and amnoglycosides.
(f^MeningitjS leading to labyrinthitis.

Deafness in children

Good hearing is essential for adequate development of

language and speech. If in early childhood the child has a
considerable diminution of hearing, it will interfere with proper
acquisition of speech and he may not be able to talk (Deaf-mute).

Causes
A. Causes of congenital hearing loss.
F^. Other causes:
Qj Ljibryinthitis:
a. Viral: measles, mumps.
b. Congenital syphilis.
c. Meningitis.
(2) F.rvthroblastosis foetalis.
Q^i Acute infectious diseases e.g. scarlet fever, typhoid, diphtheria.
\\hooping cough, pneumonia, rheumatic fever.
(4) Birth trauma.
® Ototoxic drues e.iz. aminoglycosides, etc...
<SV ASOM, CSOM, secretory QM-.
The most common causes are meningitis, measles and mumps.
 05

Assessment of hearing in infants and children

Special hearing tests arc needed as they are uncooperative.
1. Under 2 years: (distraction method) The infant can look for and
respond to a source of sound which is either a loud sound e.g. a
bell or a quiet sound e.g. a spoon and a cup or a rattle. Then
obsene the infant looking or turning his head to the source of the
sound.
2. 2 - 5 years: (Play audiometry) The child is learned to make a
specific movement as pressing on a coloured button, or pickmg
up a toy in response to a sound stimulus.
3. Above 5 years: The same as adults.
a. Tuning fork tests
b. Audiogram
4. Objective tests: It is done for uncooperative children or adults,
lor detection of the hearing threshold. They include
a. Evoked response audiometry
-Auditory brain stem response (ABR).
-Electrocochleography (EChoG).
-Evoked cortical audiometry.
b. Impedance audiometry.
c. Otoacoustic emission.

Sudden sensorineural hearing loss

Causes
1. Infections
a. Mumps, measles, cytomegalovirus, influenza, adenovirus.
b. Herpes zoster neuronitis of the 8th nerve.
c. Meningitis.
2. Trauma
a. Barotrauma.
b. Acute acoustic trauma.
c. Head injury with or without fracture base.
d. Electrical ir jury.
e. Surgical trauma.
3. Vascular
a. Occlusion of the internal auditory arter>'due to vasospasm,
thrombosis, embolism.
b. Coagulopathies.
 106

c. Cerebrovascular strokes.
4. Meniere's disease.
5. Acoustic neuroma in 10% of cases.
6. Perilymph fistula.
7. Ototoxic drugs.
8. Multiple sclerosis.
9. Malignant tumours (primary or metastatic).
10. Autoimmune.
1 1 .idiopathic.

( linical picture
The patient typically gives a history of an abrupt onset of
hearing loss over minutes or hours. Depending on the severity and
rapidity of hearing loss, associated symptoms may be vague.
1. Sudden hearing loss.
2. Tinnitus is often present.
3. Vertigo of brief duration may occur.
4. No pain.
5. Examination: is usually free except for:
- Tuning fork tests: reduced Rinne positive.
- Known preexisting pathology.

Investigations
1. Audiometry: Full audiological assessment to detect the seventy
and the type of SNHL (cochlear or retrocochlear).
2. hnestigations to detect the cause.

Treatment
it should be started as early as possible because early
treatment carries a good prognosis.

i. Vasodilators: Trental, histamine IV drip.

2. High dose steroids: 60 - 80 mg/day for 4 days, to be tapered over
two weeks. Steroids are contraindicated in TB, peptic ulcer,
hypertension, diabetes and pregnancy.
3. Excessive intake of oral fluids.
4. Control the underlying cause if detected.
- 50% - 60%) usually recover spontaneously and completely,
particularly in young age with residual mild hearing loss.
 107

Psychogenic (hysterical deafness)

There is an atypical history of sudden unexplained onset of
hearing loss or unexplained fluctuations in hearing, which is related
to emotional stress. In this condition there is marked discrepancy
between the hearing threshold obtained by PTA and the speech
reception threshold. Most of these cases improve by psychotherapy.

Tests of hearing
A. Clinical speech testing
By whispering simple words into an ear at different intensities, and
at different distances from the ear. The patient is asked to repeat the
spoken words. The other ear should be masked by producing noise
in it using a Barany's box.

B. Tunning Fork tests

These help to define the normal from abnormal hearing, the type of
hearing loss, and the frequency range of the hearing loss. They
provide good estimates but are not substitute for an audiogram. They
are unsuccessful under the age of 5 years. Several forks can be used
64, 128,512, 1024, and 2056 HZ.

l.Rinne test (Fig, 21)

It is the comparison of air
conduction (A.C.) with bone conduction
(B.C) in the same ear. The tunning fork
preferably chosen is the 512 HZ because it
is equally beared and felt. The fork is
struck on a dull surface as the patella or
elbow to obtain a tone of moderate
intensity, then it is placed firmly on the
mastoid (B.C.), and then placed near the
E.A.C. at 8 mm distance with the two
prongs of the fork aligned with the
direction of the E.A.C. (A.C). Then the
patient is asked to state which position
sounds louder.
 108

Results:
1. Normal: A.C. is heared better than B.C. and this is called Rinne
positive.
2. Conductive deafness: B.C. is heared better than A.C. and is called
Rinne negative. If B.C. is heared equal to AC. This means mild
conductive deafness with the difference of A.C. to B.C. less than
15dB as in E.T. obstruction.
3. Sensorineural deafness: A.C. is heared better than B.C. but both
are reduced when compared to the normal ear, and this is called
reduced Rinne positive.
4. Severe or profound sensorineural deafness: Actually, the patient
does not hear A.C. or B.C., but if the test is done the patient states
that he hears B.C. and not A.C, because the cochlea of the
normal or better hearing ear is stimulated due to transcranial
spread of vibrations through the skull bones, and this is called
false Rinne negative.

2. Weber test (Fig. 22)

This is a purely bone conduction test that compares the bone
conduction in both ears simultaneously. It tests the symmetry of
hearing to decide which is the better hearing ear. The tunning Fork is
placed on the vertex in the middle of the forehead or on the clenched
tcclh between the two central upper incisors, or on the tip of the
chni, then the patient is asked to report in which ear the tone is
louder (i.e. Weber central, or lateralized to the right or to the left).

Results
A. Normal: the sound is heared in the midline (doesn't
lateralize) or heared equal in both ears (Weber central).
B Conductive deafness: the sound lateralizes to the diseased ear
in unilateral cases or to the ear with more conductive
deafness in bilateral cases.
C. Sensorineural deafness: the sound lateralizes to the normal or
better hearing ear.
1 .Unilateral SNHL: lateralizes to the normal car.
2T^ilatcral SNIIL: lateralizes to the car with less SNHL.
 109

Fig 22 Webber test

3. Schwabach's test
This is comparison of B.C. of that of the patient to that of the
examiner.
l.If B.C. of the patient is prolonged more than that of the
examiner, this indicates conductive deafness.
2.If B.C. of the patient is shorter than that of the examiner, this
indicates sensorineural deafness.

Audiological assessment

Sound characteristics
sound has two physical characteristics:
a. Frequency: This is the number of oscillations of sound waves per
second. It is measured in Hertz (HZ) or kilohertz (kHz). The
normal human ear can percieve sound with a frequency range
between 16 to 20,000 HZ.
b. Intensity: This is the amplitude of sound energy. It is measured in
decibel (dB). Normal persons can hear sounds as low as 10 dB.
Sounds louder than 140 dB are perceived as pain and may cause
damage to the structures of the inner ear.

Audionietery
This is the measurement of hearing by the use of a spccutl
apparatus (audiometer) for studying the degree of hearing at
different intensities and different frequencies. The resultant data are
recorded as an audiogram.
 110

Value
i.To detect the hearing threshold of the patient (the intensity of
hearing in dB at different frequencies in HZ).
2. Detect the type of hearing loss (conductive, sensorineural, or
mixed).
3. Detect the degree of hearing loss (mild, moderate, severe, or
profound).
4. Selection of a hearing aid if needed.
Types
A. Pure tone audiometry: (PTA) (Fig. 23)
1 .It is the measurement of the patient's hearing threshold by
using pure tones of a single frequency
2.The test is done once with the ear phone to determine AC
curve and once with a B.C. vibrator over the mastoid to
determine B.C. cur\'e. The hearing threshold is obtained at
8 frequencies (250, 500. 1000, 2000, 4000,6000.8000
HZ).
3.The hearing threshold is the minimum intensity of sound
that the person can hear. Normally it varies from 0-20 dB
at all frequencies.
4.The resultant two cur\'es (A.C. curve and B.C. cur\'e) are
plotted on a graph (audiogram) and this will show the type
of hearing loss.
Results
1. Conductive hearing loss: elevated A.C. threshold, while B.C.
threshold is normal (i.e. Air/ bone gap).
2. Sensorineural hearing loss: Both A.C. and B.C. thresholds are
elevated without an air/ bone gap.
3. Mixed hearing loss: Both A.C. and B.C. thresholds are elevated
but with an air/ bone gap (i.e. A.C. threshold is elevated more.
To determine the degree of hearing loss:
The average of A.C. threshold at 500, 1000, and 2000 HZ is
obtained then the degree of hearing loss is obtained as follows:
1. Normal: 0-20 dB
2. Mild hearing loss: 20- 40 dB
3. moderate hearing loss: 40- 60 dB
4. Severe hearing loss: 60- 80 dB
5. profound hearing loss: more than SO dB
Ill
 112

B. Speech audiometery
This is the hearing assessment using spoken words presented
to the patient through earphones, and he is asked to repeat those
words. It ptxn'ides an idea about the ability to communicate.

Speech tests include

1 Speech reception threshold (SRT)
It is the level (in dB) at which the patient can correctly repeat
."lit".. o\' the presented speech material. It should match wMth the
hearing threshold level obtained by PTA.

2 Speech discrimination
It is the percentage of the correctly repeated speech material
h> [he patient to that presented to him. Scores of 90- 100% are
normal. In SNHL there is reduced score (i.e. poor speech
discrimination). In the cochlear type of SNHL it is poor but
malciiing with PTA, while in retrocochlear SNHL it is poorer than
expected from the PTA.

X'alucs of speech audiometery

1. confirms results of PTA.
2, Selection of a hearing aid.
V Detects malingerers.
4. Diftercntiates between cochlear and retrocochlear SNHL.

('. lympanometcry
This is the measurement of middle ear pressure, through
measuring the mobility (compliance) of the T.M. It gives an idea
about the integrity of various middle ear structures, mobility of the
ossicular chain and patency of the E.T, so it helps in the
identification of different middle ear pathologies. According to the
amplitude (compliance) of the tympanogram, the peak, and the
middle ear pressure, it is classified into: (Fig. 24)
1. Type A tympanogram: (normal)
The pressure is around 0 (-100 to+150) and the compliance
is between 0.5- 1.75 mm H^O.
2. Type As tympanogram: (stiffness curve).
The pressure is nonnal but the compliance is reduced below
0.5 mm H^O. It occurs in cases of ossicular fixation as in
otosclerosis, and tympanosclerosis.
 113

3. Type AD tympanogram: (Hypermobile or flail)

The pressure is normal, but the compliance is increased
above 1.75 mm H2O & it may exceed the limits of the
machine. This occurs in ossicular disruption or dislocation.
4. Type B Tympanogram: (Flat curve)
This occurs in secretory otitis media.
5. Type C Tympanogram:
Normal compliance witn negative pressure. This occurs in
ET dysfunction.
N.B.: Oscillating tympanogram occurs with glomus tumours.

-200 200
PHESSUHt Kxn H j O

Fig 24 tympanometry

D. Evoked response audiometery

This is recording of the action potentials anywhere in the
auditory pathway from the cochlea up to the auditory cortex. They
include:
1. Electrocochleography.
2. Auditoi7 brain stem response audiometry.
3. Cortical evoked audiometry.

Auditory brain stem response (ABR)

It records the electrical activity in the auditory pathway (from wave I
to V).
\ alue:
1. Objective detection of hearing threshold level.
2. It differentiates between cochlear and retrocochlear, a delay in
latency of 0.4 m.sec. between the wave number V of both sides is
suggestive of a retrochlear pathology (e.g. Acoustic neuroma).
 ^T1

114

K. Otoacoustic emission (OAES)

These arc low intensity waves produced in the cochlea and recorded
in the EAC. They arc classified into;
1. Spontaneous OAES: recorded in the E.A.C. without a provoking
stimulus.
. 2. Evoked OAES: recorded in response to a provoking stimulus
(tones or clicks).
They arc very sensitive to any cochlear abnormality and can detect
any cochlear affection vcr>' early. It is used in hearing threshold
detection espccialh' in infants and children.

( oclilear implants
This is a new advance in treating patients with severe to
profound hearing loss. It depends on the fact that even if all the hair
cell function is lost, and the patient can't hear even with powerful
Iicaring aid, you can electrically stimulate residual fibres of the
cochlear nerve. In 60% of patients, it allows discrimination of
speech without vision and it enhances lip reading in the remaining
40"/o.

The device consists of:

1. Multichannel implant, contains 22 to 24 electrodes on a silicone
rubber (flexible thread). It is passed through a tiny hole made in
the cochlea (cochleostomy) deep into the scala tympani to reach
vicinity of all remaining dendrites of cochlear nerve. One
indifferent electrode is inserted deep to the temporalis muscle to
complete the electric circuit.
2. Speech processor (outside appliance) which is a body worn box
that contains a microphone to receive sound, amplifiers and
frequency selective filters. The signals go through a wire to a
plug placed over the postauricular skin overlying the mastoid
process. The signal is transmitted through the skin to the other
plug which is fixed over the mastoid bone (under the skin) and is
connected to tlic implanted electrodes in the cochlea.

N.B. The results arc better in postlingual deaf patients (i.e. deafness
has been acquired aHer acquisition of speech), than in prelinguals.
 115

Otalgia (earache)
Earache may be due to a local cause in the ear or n\ the
periauricular area, or it may be radiating from a distant sue
(refened otalgia). Because the ear receives innervation from the
cranial nerves V, VII, IX, X and XI and cer\acal ner\'es C. aiui
C3, so according to the convergence- projection theory areas
innerx^ated by these nerves can refer pain to the ear.
Infants can not complain of pain at all, but rolling the head from
side to side is suggestive of earache.

A. Local causes (In the ear or periauricular area)

l.The auricle:
-lesions in the skin:
- auricular haematoma
- frost bite
- erysipelas
- Gouty tophi may be painful.
• - Rodent ulcer, and carcinoma
-Lesions of cartilage: perichondritis.
2.The external auditory canal:
-Furunculosis
-Diffuse otitis externa
-Malignant otitis externa
-Otomycosis
-Haemorrhagic blebs of bullous otitis externa
-Herpes Zoster oticus (Ramzay- Hunt's
syndrome)
-Foreign body
-Radium necrosis (postradiotherapy)
-Tumours: rodent ulcer, carcinoma.
3.The tympanic membrane and middle ear cleft:
-Traumatic rupture of the T.M.
-Otitic barotrauma.
-Bullous Myringitis
-Acute otitis media.
-Acute mastoiditis
 116

-Complications of suppurative otitis media

especially mastoiditis, extradural abscess, and
sinus thrombophlebitis.
-Malignant tumours (intractable pain).
4.Periaucular area (around the auricle):
- Lymphadenitis: preauricular or postauricular
due to scalp infections.
-Parotid gland lesions e.g. tumours, mumps.
-FMbrositis of suboccipital muscles.

II. Referred Otalgia

to dctcnnine the cause of earache when the ear appears
normal, the areas supphed by 5' , 7^\ 9' and lO' cranial nerves, and
ihc 2'" and 3" cer\'ical ner\'es should be examined.
A. Oral cavity: (along the 5'^ nerve)
1.Dental caries, dental infections, un-erupted or
impacted third molar (wisdom tooth).
2.Glossitis, stomatitis (particularly herpetic).
3.Malignant tumours of the tongue, tonsils, and oral
cavity.
4.Calculi of the parotid (wharton's) duct.
5.Temporomandibular joint arthritis, dislocation, or
dysfunction due to muscle spasm.
B. Nose: (Along the 5' nerve)
1.Sinusitis
2.Barotrauma of sinuses
3.Tumours of the nose and paranasal sinuses.
C. Pharynx: (Along the 9^^ nerve)
1.Tonsillitis, Quinsy, pharyngitis and retropharyngeal
abscess.
2.Malignant tumours especially of the tonsils, pyrifomi
fossa and nasopharynx.
3.Postadenoidectomy and post tonsillectomy.
D. Larynx: (Along the 10 ner\'c)
l.Non specific laryngitis.
2.Epiglottitis.
3.T.B. Laryngitis.
4.Perichondritis
5.Malignant laryngeal tumours.
 117

6.Cricoarytenoid joint arthritis.

E. Oesophagus: (Along the lO'*'nerve)
l.F.B.
2.Oesophagitis
3.Malignant tumours.
F. Cervical: (along the 2'^ and 3"^^^ cervical nerves)
1.Spondylosis.
2.Osteoarthritis of cervical spine
3.Secondary malignant cervical lymph nodes.
G. Miscellaneous:
1. Acute thyroiditis
2.Great vessel aneurysm
3.Migraine
4. Angina pectoris
5.Long styloid process.

III. Neuralgias
th
1 .Trigeminal neuralgia (5 nerve).
Ih
2.Geniculate ganglion neuralgia (7'" nerve).
3.Glossopharyngeal neuralgia (9' nerve).
4.Occipital neuralgia (C2 and C3 nerves).
S.Superior laryngeal neuralgia (10 nerve).

IV. Psychogenic: this is diagnosed by exclusion of all other

etiologies.

Otorrhoea

Types
A. Watery: Cerebrospinal otorrhoea , due to:
1.Trauma either fracture base of the skull or after
stapedectomy.
2.Meningitis.
3.Tumours.
B. Serous:
1.Bullous myringitis (due to rupture of blebs)
2.Eczematoid dermatitis of the external canal.
C. Mucopurulent:
1. Acute suppurative otitis media.
 IS

2.Tubo- t\'mpanic type ot'C.S.O.M .

I). Purulent;
1 .(^lolcstcaloma.
2.Tubot)'mpanic C.S.O.M, with bone necrosis.
3.1-urunculosis and otitis externa.
! l^lo(>d>':
i.Trauma:
-Foreign body or lacerations of the E.A.C
-Fracture base ofthe skull.
-Traumatic rupture ofthe T.M.
2.Tumours:
-Glomus tumours.
-Malignant tumours.
3.Bullous myringitis.

Vertigo
Vertigo is a subjective sensation of motion, usually in the
form of rotation either ofthe patient himself or his surroundings,
aciually it is a hallucination of movement. It may be the only
symptom of an ear disease or it may be combined with deafness,
tinnitus, and otalgia.

Causes
A. Physiological
Due to stimulation ofthe labyrinth by rotation or themial
stimulation (Caloric test).
13 Pathological
1 Peripheral Due to either affection of the labyrinth (inner
car) or the vestibular nerve.
-Labyrinthine
a. Mcmete^disease.
l2^ Perilymph fistuhi.
c. Trauma:
(1) Head trauma with transverse fracture of the
skull base involving the labyrinth.
(2) Postoperative, after stapedectomy (Perilymph
gush).
 119

d. Labyrinthitis^
(1) Viral: measles, mumps, influenza.
(2) Bacterial:
(a) meningitis
(b) complication of suppurative otitis media
(acute or chronic) especially
cholesteatoma eroding the lateral^
semicircular canal.
(3) Chemical (toxic):
(a) Tobacco, alcohol, quinines.
(b) Salicylates, dihydrostreptomycin,
aminoglycosides.
(c) Uraemia, diabetes.
e. Vascular: Spasm, thrombosis, or embolism of the
internal auditory artery supplying the labyrinth.
^' Bengin paroxysmal positional vertigo. This is very
common. It may occur after head trauma, infection
or spontaneously. There is vertigo with the head in a
certain position, no hearing loss or neurologic
symptoms. There is positional nystagmus. The
disease is self limiting, lasting 6 months or less.
Vestibular rehabilitation and avoidance of the
precipitating head position is usually sufficient,
otherwise operative section of the nerve supplying
the posterior semicircular canal (sm^larjierye) is
advocated in persistent cases. Disease lasting longer
than 6 months particularly in young ages, should be
reevaluated for central causes.
^Vestibular
a. Vestibular neuronitis: It is characterized by sudden
severe vertigo without deafness lasting for a few
days. There is associated nystagmus. A viral cause is
suspected. It is treated by antivertiginous drugs and
steroids. In rare instances, vestibular nerve seciion
can be beneficial.
b. Acoustic neuroma (rare)
c con gen it al cholesteatoma of the CPA.
d. Basal meningitis.
 120

2. Central
Due to affection oi' the vestibular nuclei or the
\ cstibular connections in the brain stem or cerebellum. It is
associated with other neurologic manifestations.
-Vertebrobasilar insufficiency (brainstem ischaemia)
^Cerebrovascular strokes: e.g. thrombosis, embolism.
-Cerebellar tumours, and abscess.
(gMultiplc sclerosis.
-Basilar aricn' migraine
- lipilcpsy.
-Lateral medullar\' syndrome (occlusion of the posterior
inferior cerebellar artcr\')
^Meningitis, encephalitis.

Clinical approach to a case of vertigo

A. History
^-^c^
/v.Jo ^__ 1 fvlakc sure that the patient is actually describing \ertigo
(sense of rotation).
d' '' /^"-''' <— 2.Timing of vertigo; occurs in attacks or persistent.
-_— 3.it should be detemiincd whether vertigo is provoked by
certain positions, as in bengin positional vertigo,
c— 4.Associated symptoms of nausea, vomiting and
diarrhoea indicating the severity of vertigo.
,3) -I •'...J.v^>^ -(^— 5.Loss of consciousness should raise the possibility of
epilepsy.
0— 6.Symptoms of ear disease: deafness, tinnitus, earache,
and discharge.
j I (- 7.Neurological symptoms: Headache, weakness,
parasthcsia, diplopia, ataxia and in co-ordination, may
suggest a central cause.

Examination
A. Cjeneral exam.: pulse B.P. for atherosclerosis, pallor for
anaemia, and cachexia.
U. I-'ull neurological examination:
C. cranial nerves examination.
1). Vestibular examination:
 121

1.Examination of eye movements (observation for

nystagmus).
-Nystagmus is an involuntary deviation of the
eyes away from the direction of the gaze
followed by return of the eyes to the central
resting position.
-Classification:
a. Physiologic (optokinetic): the rapid phase is
towards the center.
b. Pathologic:
(1) Occular: rotatory or pendular.
(2) Vestibular: has a rapid and slow
phase, and the rapid phase is
directed towards the side of the
lesion.
(3) Central: vertical.
-It is detected by: (observation for spontaneous
nystagmus)
a. direct observation by looking into the eyes.
b. observation using Frenzel glasses to abolish
the optic fixation.
c. Electronystagmography and videonystagmo-
graphy.
2. Examination of balance and co-ordination;
Evaluation of the vestibular system, vision,
proprioception and cerebellar function is mandatory as they
all share in maintenance of balance.
-Romberg test: the patient is asked to stand
with the feet together and aims in front of the
chest, first with eyes open, then closed. If
obvious uncontrollable falling occurs this
indicates positive test (i.e. vestibular or
cerebellar cause).
-Gait test: for ataxic gait.
-Tests for asynergia and dysmetria (signs of
cerebellar affection).
 ^

122

Investigations
A. Vestibular assessment: (observation for evoked nystagmus).
1.Positional testing:
The patient is seated with the head in 7 different
position, and observe for nystagmus in each position
to detect canal pariesis.
2.Caloric test:
The patient lies supine with the head flexed 30^, the
ear is washed with cold water (30°C) and then with
warm water (44°C), for 30- 40 seconds each time.
-Normally: Vertigo occurs, with nystagmus
lasting about 90- 120 seconds.
"Nystagmus is detected by direct looking in the
eyes, or using Frenzel glanes or by
electronystagnagraphy. According to a certain
formula we can detect normal functioning,
hypofunctioning (canal pariesis) or dead
labyrinth (no response).
3.Rotation test: Stimulation of the semicircular canals
by rotating the patient on a chair, and observe for
nystagmus as in caloric test.
4.Posturrography.
B. Audiological assessment:
1. Audiogram (FTA) and speech audiometry
2. Tympanometry
3.Auditory brain stem response (ABR)
4.0toacoustic emission.
C. Other investigations:
1 .CT scan: brain and CPA.
2.Fasting blood sugar.
3.Complete blood picture.
4.Thyroid function tests (T3, T4, TSH).
5.Serum cholesterol.
6.Serology for syphilis.
 -n

123

Tinnitus
It is the sensation of noise in the ear and/' or the head, it may
be continuos or intermittent with variable intensity and character.
A. Tinnitus with deafness; due to a local cause in the ear either
in the external canal, middle ear, or inner ear. Any cause of
conductive or sensorineural hearing loss may be associated
with tinnitus.
B. Tinnitus without deafness:
1.Subjective: (It is audible only by the patient)
-Temporomandibular joint affection.
-Impacted wisdom tooth.
-Cervical spondylosis.
-Blood diseases: anaemia, polcythaemia.
-Hypertension, atherosclerosis, hypotension.
-Heart failure.
-Thyrotoxicosis.
-Alcoholism.
2.0bjective:'It is audible by the patient and can be
auscultated by the examiner.
-Intracranial vascular tumours.
-Aneurysm of the internal carotid artery.
-Arteriovenous fistulae.
-Clonic contractions of tensor tympani.
 \^'

124

Ear operations

Myringotomy

Incision of the tympanic membrane.

Indications
1. Acute suppurative otitis media with:
• Failure of medical treatment after 48 hours.
• Bulging drum (i.e. impending rupture).
• Infants and young children with severe A.S.O.M. without
bulge in the T.M.
• Too small or high perforation (inadequate drainage).
• Complicated A.S.O.M. especially facial paralysis.
2. Chronic middle ear effusion: myringotomy is done followed by
insertion of ventilation tubes.
3. Otitic barotrauma.
4. In association with cortical mastoidectony in cases with
mastoiditis.

Procedure
Anesthesia
• General anesthesia; in children.
• Local anesthesia in adults. The local anesthetic used is
composed of equal parts of xylocaine, carbolic and mentol
crystals. A small pledget of cotton is soaked with this
solution and is applied on the T.M. for about 30 minutes
till the dnmi becomes blanched and relatively insensitive.

Technique
It is done using a microscope.
Incision: It is done using a myringotomy knife (special
angular knife). The incision is done in the posteroinferior
quadrant of the T.M., midway between the handle of
malleus and the periphery of the T.M. The incision is
done from below upwards to avoid catching the incudo-
stapedial joint if it is done from above below.
After incision a swab from the discharge is taken for
culture sensitivity. Then suction of the middle ear fluid is
 125

done. Then the ear is dried with apiece of gauze soaked

with alcohol introduced down to the lips of the incision.
Alcohol is hygroscopic, it prevents oedema of the edges
and leaves the wound patent.

N.B.: In cases of grommet tube insertion for chronic secretory

otitis media the incision is done in the anterosuperior quadrant as
it has the least migratory epithelium, so there is no early extrusion
of the tube.

Postoperative care
1. Repeated local cleaning and suction of discharge.
2. Sedatives, analgesics.
3. Antibiotics according to culture and sensitivity.
4. Observe the patient until the drum heals spontaneously.

Advantages
1. Immediate relief of pain and toxic manifestations in
uncomplicated eases. •
2. Allows rapid resolution without residual deafness.
3. The incision heals better (Primary intention) than that of
spontaneous perforation with less scarring and fibrous tissue
formation.

Complications
1. Ossicular disruption (dislocation of incudo-stapedial joint).
2. Injury of a high jugular bulb (dehiscent floor). It appears as bluish
coloured inferior portion of the T.M.
3. Residual perforation.
4. Injury of a dehiscent facial nerve.

Cortical mastoidectomy (Schwartz operation)

This is a drainage operation of the mastoid with exentralion

of all the mastoid air cells.

Indications
1. Acute mastoiditis with:
a. Persistent pain, tenderness, and fever more than 48 hours despite
medical treatment in the form of antibiotics and myringotomy.
 126

b. Positive reservoir sign.

c. Sagging of the mcatal wall.
d. Persistent suppuration more than four weeks.
c. Progressive deafness.
Development of complication e.g. facial paralysis, labyrinthitis
and other cranial and intracranial complications.
Masked mastoditis.
Mastoid abscess, bezold's abscess, zygomatic abscess.
4, As an approach to various ear operations:
• Facial exploration.
• Labyrinthectomy.
• Saccus decompression in Meniere's disease.
• Translabyrinthine approach in acoustic neuroma.
• Posterior tympanotomy and extended facial recess
approaches.

Procedure
• Anesthesia; general.
• Technique
A curved postauricular incision starting from above the
auricle down to the tip of the mastoid., 1.5-2 cm (one finger breadth
behind the postauricular groove, incising skin fascia, and periostium.
It is superficial in the upper part avoid injury of temporalis muscle,
while it is deep in the lower part. In young children and infants the
incision is short, more transverse (wilde's incision) to avoid injury
of the facial nerve which is more superficial after its exit from the
stylomastoid foramen.

The periosteum is elevated exposing the root of zygoma above

and the tip of the mastoid process below.
Identify the lateral wall of mastoid antrum (McEwen's triangle).
Superiorly, it is bounded by the suprameatal crest, anteriorly, the
posterosuperior metal wall, and posteriorly a tangential line to
the posterior meatal wall.
Search for the antrum, open il, and remove all mastoid air cells.
Pack the EAC with a piece of gauze to prevent stenosis.
Closure of the wound in two layers; the periostium and skin. A
small drain is left for 48 hours.
 127

N.B. If an abscess is encountered a specimen of pus is obtained an

sent for culture and sensitivity.

Complications
1. Injury of the:
• Dura of the middle fossa.
• Lateral venous sinus (sigmoid sinus).
• Dislocation of the incus.
• Facial nerve injury while searching for the antrum or
during drilling of the retrofacial cells.
2. Persistent discharge due to:
a. Performing the operation too soon before localization of
infection.
b. Presence of cholesteatoma.
c. coalescent mastoiditis.
3. Mastoid fistula.

Radical mastoidectomy

This is exentration of the mastoid air cells, and all contents

of middle ear except the stapes (if present). Thus the middle ear and
the mastoid are converted into a single cavity. (Fig. 25)

Indications
1. Cholesteatoma with severe sensorineural hearing loss.
2. Cholesteatoma with-development of complications.
3. Tumors:
• glomus tympanicum.
• Carcinoma.
4. Tuberculous otitis media.

Procedure
• Anesthesia: General.
• Technique: As cortical mastoidectomy with the following
procedures.
a. Removal of the posterosuperior bony metal wall (bridge) and
the outer attic mass.
b. Lowering the facial ridge (posterior meatal wall).
 128

c. Removal of all cholesteatoma matrix, polypi, granulations,

mucous membrane of the middle ear and remnants of the T.M.
• The E.T. is obliterated by cartilage, muscle or Teflon.
• At the end of the operation mcatoplasty is done to widen
the external auditory meatus, so as to accommodate the
large mastoid bowel.

( oriiplications Fig 25, radical mastoidectomy

1. Injur}' of the:
a. Facial nerve.
b. Dura, sigmoid sinus.
c. Lateral semicircular canal.
2. Mastoid cavity problems (see before).
3. Recurrence of cholesteatoma.

Tympanoplasty

It is an operation to eradicate irreversible pathological

changes in the middle ear and to reconstruct the middle ear
conducive hearing mechanism. It may be combined with
mastoidectomy (this called tympanoplasty with mastoidectomy).

Indications
1. Chronic suppurative otitis media.
2. Congenital middle car anomalies causing conductive deafness.
3. Traumatic rupture of the T.M.
4. Middle car trauma causing conductive deafness.

C ontraindications
1. Complicated suppurative otitis media as open drainage is
essential to avoid intracranial extension of infection.
 129

2. Cholesteatoma; radical or modified radical mastoidectomy should

be done.
3. Poor E.T. function.

• Anaesthesia; either general or local anaesthesia.

• Technique
1. Incision; either postauricular or endaural incision. It may be done
through the external auditory canal (permeatal), if mastoidectomy
will not be performed.
2. Eradication of all diseased mucosa, or any granulation in the
middle ear and mastoid.
3. Reconstruction of the hearing mechanism by:
A. Myringoplasty; to repain a tympanic membrane perforation,
using a graft material which acts as a supporting framework for
regeneration of the outer epithelial and inner mucosal layers of
the tympanic membrane. The graft may be placed under the T.M.
and the annulus (underlay) or between the epithelial and mucosal
layers of the T.M. (onlay).
• The graft material used may be:
a. Temporalis fascia (the most commonly used).
b. Perichondrium (from the tragus or concha).
c. Vein graft (rarely used).

B. Ossiculoplasty; which entails reconstruction of fixed, damaged

or absent ossicular chain, in order to restore its conductive
mechanism.
Reconstruction of the ossicular chain is performed either by:
a. Cartilage grafts; tragal cartilage, conchal cartilage, or nosal
septal cartilage.
b. Bone grafts; bone chips from the mastoid cortex or the patient
own ossicles.
c. Prosthesis; TORP (total ossicle replacement prosthesis) PORP
(partial ossicle replacement prosthesis), or Teflon.

Wullestine types of tympanoplasty (Fig. 26)

Type I: Myringoplasty only, for reconstruction of a T.M.
perforation.
Type 11: The T.M. graft is placed on the incus (i.e. absent malleus).
 r"

130

Type III: The T.M. graf\ is placed on the head of stapes (absent
malleus and incus.
Type IV: The T.M. graf^ is placed on the footplate of the stapes
(absent stapes suprastructures).
Type V: The T.M. graf^ is placed over an artificial fenestra on the
lateral canal, or stapedectomy due to fixed foot plate of the stapes.

" ''' E lyp.^

0 iyp«IV

Fig.26 Types of tympanoplasty

 r
- 131 -

THE NOSE AND PARANASAL SINUSES

Anatomy of the Nose and Paranasal Sinuses
Anatomy of the nose
I. External nose (Fig. )
It is roughly pyramidal in shape. The upper attachment of the nose
at the forehead is known as the root of the nose, and the free lower angle
is the apex or tip of the nose. The rounded ridge connecting these two
parts is the dorsum nasi, and it's uppermost part, supported by the nasal
bones is the bridge of the nose. The lateral surfaces of the nose are
expanded below to form the alae, that are separated by the columella.
Skeleton of the external nose (Fig. 27 )
A. Bony framework
It forms the upper 1/3 and is made up of:
1. Two nasal bones, narrow and thick above; wide and thin below.
2. Nasal process of the frontal bone which articulates superiorly with
the nasal bones.
3. Nasal processes of the maxilla articulates laterally with the nasal
bones.
B. Cartilagenous framework
It fomis the lower 2/3, and is made up of:
1. Upper lateral nasal cartilages above.
2. Lower lateral nasal cantilage below. It has a medial and lateral
cms.
3. Alar cartilages that support the nasal alae.
4. Septal quadrangular cartilage.

Fig,27, Ext nose

 - 132-

//. Interior of the nose (Nasal cavity)

There are two nasal cavities (nasal fossae), that are separated by the
nasal septum. They extend from the anterior opening (anterior nares or
nostril), to the posterior opening (choana).
- Nasal valve : This is the area of greatest narrowing in the nasal
cavity at the level of juncdon between the upper and lower lateral
nasal cartilages.
Walls of the nasal cavity
A. Roof : Formed by the cribriform plate of the ethmoid bone
separating it from the anterior cranial fossa.
B. Floor : Formed by the hard palate consisting of the palatine process
of the maxilla and the horizontal plate of palatine bone, on both
sides.
C. Medial wall (Nasal septum); is formed of the following: (Fig. 28 )
1. Perpendicular plate of the ethmoid bone posterosuperiorly.
2. Vomer bone posteroinferiorly.
3. Rostrum of the sphenoid far posteriorly.
4. Nasal crest of the maxilla inferiorly.
5. Quadrangular septal cartilage,anteriorly.

PvpaniUculV

euHag*

Th« luul icfXvn

Fig.27 Medial wall of the nose

D. Lateral wall: (Fig.2 g)

- It is formed by the medial wall of the maxilla, ethmoidal labryinth
and perpendicular plate of the palatine bone. It bounds most of
the paranasal sinuses and receives their openings. It shows the
following features:
1. Three bony projections : superior, middle and inferior
turbinates or conchae.
 -133-

Superior
turblnat*
concha) Sphenoid
slnw
Mkldk
turblnitt
(concha)

tnlarlor
turbhnatff
(concha)
Oattonof
Euatachlan
tuba

Utddl* and
Inferior Maatua

Fig.28.a. lateral wall of the nose

Ana* ti
^ —
Htm konui duct .CU Mlact «l S<««to EthmoU
**AtJt
Cw( turite*
glUttwlt
O t i M D Of

OiMteca
Fig.28. lateral nasal wal

Fig.28. Lateral nasal wal

 -134-

2. Four spaces in relation to the turbinates: the space below each

turbinate is known as the meatus. So, there are superior,
middle and inferior meati, and one space above the superior
concha called the sphenoethmoidal recess.
a. Inferior meatus : lies below the inferior turbinate (which is
a separate bone and contains dense venous plexus). The
nasolacrimal duct opens in the anterior portion of the
inferior meatus.
b. Middle meatus : Lies below the middle turbinate (which is
a part of the ethmoid bone), it shows the following
features :
- Bulla ethmoidalis : rounded projection that carries the
openings of the anterior ethmoid air cells.
- Hiatus semilunaris : a curved groove infront and below the
bulla ethmoidalis.
- Opening of the maxillary sinus : in the posteroirferior
portion of the hiatus semilunaris.
- Opening of the frontal sinus : in the highest anterior part of
the hiatus semilunaris (frontal recess areal).
- Uncinate process : a sharp ridge of bone below the hiatus
semilunaris.
N.B : The ethmoid infundibulum : opens in the hiatus
semilunaris. It varies in depth. From 0.5 to 10mm. The
anterior ethmoid air cells and the maxillary sinus open in it
(as above). Posteriorly, it is continuous with the middle
meatus. The medial wall of the infundibulum is the uncinate
process and its lateral wall is the lateral wall of the nose.
c. Superior meatus : lies below the superior turbinate, and the
posterior ethmoid air cells open in it.
d. Sphenoethmoidal recess : lies above the superior turbinate,
and carries the opening of the sphenoid sinus.
Blood supply
A, Arterial supply
From branches of the internal carotid artery (I.C.A) and external
carotid artery (E.C.A.).
1. The external nosq is supplied by :
a. Nasal branch of the facial artery from EGA.
b. Dorsenasal branch of the ophthalmic artery from I.C.A.
 -135-

c. Twigs from the infraorbital branch of the maxillary artery from

E.C.A.
d. Twigs from arteries supplying the nasal septum.
2. The nasal cavity is supplied by the following arteries :
a. Anterior and posterior ethmodial arteries from the ophthalmic
artery, a branch from the I.C.A. They supply the superior part.
b. Sphenopalatine artery from the maxillary artery from the E.C.A.
It supplies the posterior part.
c. Greater palatine branch of the maxillary artery.
d. Superior labial branch of the facial artery. It supplies the
anteroinferior part.
B. Venous drainage
1. Sphenopalatine vein.
2. Anterior and posterior ethmoidal veins.
3. Angular vein.
These veins are connected with the cavernous sinus either through
the ophthalmic vein or through the pterygoid plexus of veins, so
infections of the nose may lead to cavernous sinus thrombosis.
N.B. : The dangerous triangle of the face extends from the root of the
nose superiorly (nasion), to the lateral comers of the mouth on each
side. Infections in this area might extend to the cavernous sinus.
Nerve supply
1. Sensory : 5th (trigeminal nerve) via the anterior and posterior
ethmoidal branches of the sphenopalatine ganglion (maxillary
division of 5th nerve).
2. Olfaction : 1st cranial nerve (olfactory n.)
3. Autonomic supply, (through the sphenopalatine ganglion)
a. Parasympathetic : (Facial nerve) By the greater superficial
petrosal nerve which forms the nerve of pterygoid canal (vidian
nerve), which relays in the sphenopalatine ganglion and
postganglionic fibres carry secretomotor parasympathetic
innervauon.
b. Sympathetic : preganglionic fibres from the upper thoracic
segment relay in the superior cervical ganglion and
postganglionic fibres form a plexus around the ICA from which
the deep petrosal nerve arises to form with the greater superficial
petrosal nerve the nerve of the pterygoid canal which supplies
the nasal blood vessels.
 - 136-

Lymphatic drainage
1. Anterior portion : submandibular lymph nodes.
2, Posterior portion : Retropharyngeal lymph nodes.
And both finally drain into the upper deep cervical lymph nodes.

Histology
Tlie lining of the nose is divided histologically into three parts :
1. The vestibule : This is the dilated anterior space. It is surrounded
by cartilage and lined by stratified squamous epithelium containing
stiff hair (vibrissae).
2. The respiratory portion : It is lined by respiratory mucosa
(pseudostratified columnar ciliated epithelium with goblet cells and
seromucinous glands). It lines the following areas :
a. all tlie nasal cavity except the olfactory portion & vestibule.
b. Eustachian tubes.
c. Nasopharynx till the level of soft palate.
d. Paranasal sinuses.
3. The olfactory area : It is lined by olfactory neuroepithelium cells,
which appear yellowish or faint blue. It covers the superior portion
of the nasal cavity :
a. Superior turbinate.
b. Portion of middle turbinate (medial side).
c. Lateral surfaces over the ethmoid sinuses.
d. Upper portion of the septum.

Functions of the nose

1. Respiratory passage.
2. Olfaction.
3. Voice resonator.
4. Portection; through the following mechanisms :
a. Humidification and warmth of the inspired air by moisture
supplied by the mucous blanket covering the nasal mucosa.
b. Vibrissae which filter large particles.
c. Ciliae moving the mucous blanket backwards filter small
particles.
d. Reflex sneezing.
e. Lysosymes in the nasal secretion have a bacterolytic effects.
 -137-

The mucous blanket: The goblet cells and the seromucinous glands of
the nose produce mucus that forms a continuous blanket throughout
the nose and sinuses. This blanket is composed of a superficial thick
mucous layer, and deep thin preciliary layer. It collects dust, bacteria,
viruses and pollens. By the ciliary action the blanket is carried back to
the pharynx and swallowed. Lysosyme in the mucus intiates bacterial
destruction.
The ciliary action : Cilia beat at a rate of 10-20 times per second at
room temperature. This beat has a characteristic biphasic motion; a
rapid effective stroke and a slower recovery stroke. The mucous layer
is conveyed in the direction of effective stroke (i.e. backwards towards
the pharynx).
The normal ciliary activity is inhibited by :
a. dryness
b. drugs (eg. cocaine and adrenaline).
c. excessive heat or cold.
d. hypertonic and hypotonic solutions.
e. nicotine (i.e. smoking).
f. fumes (eg. sulfur dioxide, & carbon monoxide).
g. infection.

Anatomy of the paranasal sinuses (Fig.29)

- The paranasal sinuses are air filled spaces present within the skull
bones, and lie around the nasal cavity. They open into the lateral
nasal wall.
- Lining : The paranasal sinuses are lined by mucous membrane
similar to, and continuous with that of the nasal cavity. It is
pseudostratified columnar ciliated epithelium with goblet cells and
seromucinous glands. The goblet cells and seromucinous glands
secrete the mucous blanket layer, which is transported by the beat
of ciliae towards the sinus ostia.
- There are four pairs of sinuses : the frontal, maxillary, ethmoid, and
sphenoid sinures. They vary greatly in size between different
individuals.
- Anterior group of sinuses : include the maxillary, frontal, and
anterior ethmoid sinuses.
- Posterior group of sinuses : include the posterior ethmoid and
sphenoid sinuses.
- Each sinus communicates with the nasal cavity through an opening
known as the ostium.
 -138-

A. The maxillary sinus

- It is the only sinus present at birth, and it is contained within the
body of the maxilla.
- It is pyramidal in shape with its base at the lateral wail of the nose,
and the apex at the zygomatic process. It has the following
boundaries :
a. Roof: Floor of the orbit, the infraorbital nerve traverses it in a
special canal.
h. Floor : alveolar part of the maxilla (hard palate). The 1st molar
and the 2nd premolar teeth are related to it. It lies at a lower
level then the floor of the nose.
c. Anterior: chctk.
d. Posterior : pterygopalatine fossa.
e. Medial: lateral nasal wall.
- The ostium of the sinus lies high up in its medial wall (against
gravity). It opens in the ethmoid infundibulum of the middle
meatus (posterior part of hiatus semilunaris). It is about 3-4 cm in
diameter. An accessory ostium may be present posteriorly.
B. Frontal sinus
- It is not developed at birth, and starts to appear at the age of 2-4
years. It consists of an excavation into the diploe of the frontal
bone.
- The two sinuses are of unequal size, and are separated by bony
septum which lies in the midline.
- Relations:
a. Anteriorly to the forehead.
b. Posteriorly to the anterior cranial fossa.
c. Inferiorly to the orbit.
d. laterally to the opposite sinus.
- The ostium of the sinus opens into the frontal recess in the anterior
portion of the middle meatus.
C. Ethmoid sinuses
- These are 7-17 small air cells within the ethmoid bone, lying
between the orbit and the nasal cavity. They are divided into
anterior ethmoid cells and posterior ethmoid cells.
- The ostia of the ethmoid sinuses are inconsistent in location. The
anterior ethmoid cells generally drain into the ethmoid
 -139-

infundibulun of the middle meatus or in the region of the ethmoid

bulla. The posterior ethmoid cells drain into the superior meatus.
D., Sphenoid sinus
- It lies within the body of the sphenoid bone and is divided by a bony
septum into right and left halves,
- It is related to :
a. Pituitary gland superiorly.
b. Nasopharynx inferiorly.
e. Optic nerve, internal carotid artery and the cavernous sinus
laterally,
- The ostium of the sinus lies in its anterior wall and opens into the
sphenoethmoidal recess.

Middle

*^'^*>*^**v Cribitoni.
\ plate
OfWal
cavity -

Hiatus
semilunaris

Wertor
turbinate

Fig.29. Paranasal sinuses

Functions of the paranasal sinuses

1. Lighten the weight of the skull.
2. Humidification and warming of the inspired air.
3. Secretion of mucus to keep the nasal chambers moist.
4. Improving vocal resonance.
5. Absorption of shock to the face or skull.
6. Regulate the intranasal pressure.
What is the osteomeatal complex ?
The osteomeatal complex is a term used to describe the region of
the uncinate process, maxillary ostium, middle turbinate, bulla
ethmoidalis and ethmoid infundibulum. It is important because the
 - 140-

frontal, maxillary, and ethmoid sinuses ail drain in this area which
contains a very narrow cleft. Any mucosal thickening or anatomical
variat-ion is likely to produce obstruction, stenosis, and recurrent
infection of these sinuses. Functional endoscopic sinus surgery is based
on the concept that the osteomeatal complex must be cleared to restore
and enhance normal sinus drainage.
 -141-

History and physical examination of the nose

/. History
1. The main complaint should be first established with regard to onset,
course, duration and recurrence.
2. Enquire specifically into the likely presenting symptoms and these
include :
a. Nasal obstruction : unilateral or bilateral.
b. Nasal discharge : mucoid, serous, watery, sanguinuous, its odour,
and relation to head position, and whether unilateral or bilateral.
c. Epistaxis : severity, relation to trauma, any bleeding disorder,
atherosclerosis or hypertension, and whether it is unilateral or
bilateral,
d. Facial pain and headache : site, severity, relation to posture and
periodicity.
e. Abnormalities of smell: hyposmia (decreased smell), anosmia (loss
of smell), cacosmia (bad smell), parosmia (altered smell), uncinate
fits (hallucinations of smell).
f. Proptosis, visual defects and diminished vision.
g. Mouth breathing and Halitosis (bad breath),
h. Snoring and sleep aponea.
3. Symptoms of cranial nerve palsies.
4. Previous medications, or nasal surgery : when and where it is done?
5. Past history of general medical problem.

//. Physical examination (Fig.30)

A. External examination ; for tenderness, swelling, scars, deformities
(twist of nasal bones, or depressed bridge).
B. Interna! examination
It may be difficult due to mucosal oedema, septal deviation or polyps.
7. Anterior rhinoscopy : using the nasal speculum (thudicum's
speculum), the nasal cavities are examined through the anterior
nares. The anterior part of the nasal cavity, septum, anterior parts of
the middle and inferior turbinates are visualized. In infants and
young children pinching the nasal tip with the thumb is enough for
visualization.
2. Posteior rhinoscopy : (Fig.31) using a post nasal mirror to visualize
the nasopharynx, posterior part of nasal cavities, posterior end of
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infcrior turbinate, Eustachian tube opening, and the septum. It is

sometimes difficult and annoying to the patient.
3. Nasal endoscopy : using rigid endoscopes 0°, 30°, and 70° is ideal to
examine various compartments of the nose under local anasthesia.
4. Digital examination : to palpate the nasopharynx and choana.

ExankiMtonbrblatwy

Fig 30. Examination of the nose

Fig.31. posterior rhinoscopy

 -143-

Congential diseases of the nose

Congential choanal atresia
This is congenital atresia of the posterior choana due to persistence
of the embryonic bucconasal membrane. It may be unilateral or bilateral,
and it may be bony (90%), or membranous (10%) atresia.
Clinical picture
A. Unilateral atresia
It may not be symptomatic at birth, and may be missed except if put in
mind. It is detected in early childhood by :
1. Chronic unilateral nasal obstruction.
2. Unilateral persistent mucoid nasal discharge.
B. Bilateral atresia
- This presents as an emergency situation at birth, the newborn
depends totally on the nasal airway for breathing (nasal breathers)
and then, learns mouth breathing by the age of 6-8 weeks. The
newborn cannot reflexly open his mouth, and to acquire mouth
breathing; it needs gradual nasal obstruction.
- The condidon is detected at birth by :
a. Bilateral nasal obstruction.
b. Bilateral nasal discharge.
c. difficult suckling.
d. Cyanosis or pallor unless the newborn cries (i.e. opens his
mouth). If an oral airway is not established he might pass into
asphyxia and die.
Signs
1. Coloured drops (eg. Mercurochrome in water) instilled in the nose
donot appear in the pharynx.
2. Failure of passage of a rubber catheter through the nose into the
pharynx.
Investigations
1, X-ray with lipidol : the dye is retained in the nose with failure of
passage to the pharynx.
2. CT scan of the nose and nasopharynx shows the atresia, and
differentiates between bony and membranous ones.
 - 144-

Treatment
A. Bilateral atresia
1. Emergency management is essential to provide an airway. This can
be done by :
a. Insertion of a plastic oral airway or a McGovern rubber nipple
into the infant's mouth to keep it open.
b. Emergency transnasal endoscopic perforation of the atresia.
2. When the infant is stable, the atresia can be excised by :
a. Transnasal route : using an endocsope, the atretic plate is
excised.
b. Transpalatal route : resection of the atretic plate and posterior
end of the septum. It is done in late childhood and adolescence.
A silastic tube is placed to maintain the opening for at least 4-6
weeks.
B. Unilateral atresia
Transnasal or transpalatal operation is done. It is better postponed
till the patient is stable.

Traumatic conditions of the nose

1. Fracture nasal bones.
2. Foreign body in the nose.
3. Cerebrospinal rhinorrhoea.
4. Oroantral fistula.

Fracture nasal bones

Cause
Direct trauma to the nose e.g. in boxers and car accidents. The
prominent position of the nose makes it susceptible to isolated injury.
Clinical picture
Symptoms
1. History of trauma (ask about time and type of injury).
2. Pain.
3. Epistaxis is usually present, due to mucosal lacerations.
4. Nasal obstruction due to oedema, haematoma, or depressed nasal
bridge.
5. Swelling and deformity of the external nose.
 -145-

Signs
1. External deformity in the form of deviation, or depression of the
nasal bridge.
2. Oedema and ecchymosis.
3. Localized tenderness and crepitus.
4. Subcutaneous emphysema if there is associated fracture of the
ethmoid.
5. Associated septal trauma (haematoma, fracture, or dislocation).
6. Accumulated clotted blood in the nasal cavity, and mucosal
lacerations may be present.
Investigations
Plain x-ray of the nasal bones (two lateral views) may show the
fracture line. This is important medicolegally.
Treatment
First control the epistaxis if present; and further management
depends upon the timing of injury and degree of oedema.
A. If the patient is seen shortly after trauma :
1. If there is no marked oedema : reducdon of the nasal bones is done
manually or by the use of
walsham's forceps under
general anaesthesia (Fig.32).
External fixation is done by
nasal splint or a plaster of paris.
- Straightening of the septum
may be done by Ashe's
forceps.
- A nasal pack is placed for
24-48 hours for support and
Fig.32. Reduction of fractured
to maintain the nasal bones nasal bones
in posiuon.
2. If there is marked oedema : Antibiodcs, analgesics, and hot foments
are applied for 5-7 days till oedema subsides then do reduction
and external fixadon.
B. If the patient is seen late :
After 2 weeks of trauma, the fracture is left to heal and rhinoplasty
is performed after 3-6 months. Rhinoplasty is done is cases of old
malunited fractures with callus formation and external deformity.
C. Prophylactic antibiotics : are given in all cases.
!
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Foreign body in the nose

• It is seen in children and mentally retarded adults.
• It may be iatrogenic as neglected nasal pack.
Foreign bodies may be :
1. hard : glass beads, buttons.
2. Soft: paper, vegetable, seeds, beans, cotton, artificial form.
Clinical picture
1. lintially, there may be sneezing, pain, or sense of discomfort and
may be mild epistaxis.
2. Unilateral offensive mucopurulent or sanguineus nasal discharge.
4. Examination (anterior rhinoscopy): The F.B. is seen near or on the
I I
floor of the nose, because it is prevented from slippage backwards
by the nasal valve, which is the narrowest area in the nasal cavity at
the level of the anterior end of inferior turbinate. Trials to remove
the F.B. may push it backwards.
5. A hard F.B. may be felt by probing.
6. Sometimes fiberoptic endoscopy is needed to visualize a more
posteriorly situated F.B.
Investigations
Plain x-ray may show a radiopaque F.B.
Complications
A. Neglected F.B. leads to :
1. Infection : rhinitis and sinusitis.
2. Pulmonary complications as lung abscess and respiratory
obstruction. This happens if the F.B. slips back to the choana
(wide roomy space) and becomes inhaled,
3. Rhinolith or nasal stone : Calcium, and magnesium salts are
pericipitated on the F.B. with blood clots, mucus, and pus.
Treatment
1. The F.B. is removed carefully by a hook, forceps or by suction, if
the child is cooperative and the F.B. is well seen.
2. It is done under general anaesthesia (never inhalation anaesthesia) if
the child is not cooperative or the F.B. is deep. The nasopharynx is
packed to avoid falling of the F.B. backwards.
3. Later rhinotomy may be needed to remove a large rhinolith.
 -147-

Cerebrospinal rhinorrhea
- Tliis is leakage of cerebrospinal fluid (C.S.F.) from the nose.
- The origin of leakage may be from the :
a. Roof of the nose (cribriform plate).
b. Roof of the ethmoid sinus (fovea ethmoidals), frontal sinus, or
sphenoid sinus.
c. Middle ear cleft (CSF otorhinorrhea); CSF passes through the
E.T. to the nasopharynx and then to the nose. This is rare.
Aetiology
A. Traumatic : (There must be a dural tear)
1. Accidental: Fracture base involving the floor of the anterior cranial
fossa.
2. Surgical : endoscopic sinus surgery, removal of large tumours of
the skull base and transsphenoid pituitary hypophysectomy.
B. Spontaneous :
1. Neoplastic : Tumours eroding the floor of the anterior cranial fossa
e.g. carcinoma of the nose and olfactory neuroblastoma.
2. Infection : Osteomyelitis, syphilis, midline lethal granuloma.
3. Congenital defect in the cribriform plate. This may be associated
with meningocele or encephalocele.
4. Idiopathic : This may be due to increased intracranial tension, e.g.
in brain tumours.
Clinical picture
1. Unilateral nasal discharge which is clear, watery with salty taste
\ (due to the high chloride content of CSF). It increases on leaning
forwards, coughing, sneezing and straining. It doesnot stiffen in a
handkerchief as it contains no mucus.
2. Headache : It may be due to lowered CSF pressure due to
continuous leakage or increased CSF pressure in cases of brain
tumours or meningitis.
3. Anosmia if the cribriform plate is involved.
4. Features of the cause : history of head trauma, sinus or nasal
surgery.
5. Features of complications if they arise :
a. Meningitis.
b. Intracranial aerocele.
 -148-

Investigations
1. Biochemical analysis of nasal discharge ; CSF is :
- Clear, colourless, doesnot contain mucus or albumin.
- Specific gravity is 1005-1010.
- It contains glucose which is detected by :
a. Reducing Fehling's solution.
b. Reduces glucose impregnated oxidase strips.
c. 30 mg% glucose concentration is confirmatory.
- The normal nasal secretions contain saccharides, so it reduces
Fehling solution, but the glucose level never reaches 30 mg%.
- CSF contains P2 transferrin which is not found in plasma.
2. CT scan of the skull base with I.V. contrast (metrizamide):
This is the investigation of choice, as it detects accurately the site
of the leak.
3. Intrathecal dyes : Intrathecal injection of fluorescine (it stains CSF
yellow-green), through a lumbar puncture, and then examine the
nose by endoscopy. It helps to localize the site and the size of the
leak.
4. Radiostopic studies.
Treatment
A. Conservative measures : Should be tried in all cases of acute CSF
leaks, as the majority of posttraumatic CSF fistula heal spontaneously;
this consist of:
1. Bed rest in the head-up position.
2. Avoid coughing, sneezing, straining or nose blowing.
3. Avoid any local intranasal treatment e.g. nasal packing.
4. Prophylactic antibiotics especially those crossing the blood brain
barrier. .
B. Surgical :
- Indicated in :
a. Persistent chronic leaks or recurrent leaks,
b. Failed medical treatment in 2-3 weeks.
- It entails exploration of the skull base and repair of the defect by :
a. Tissue graft (fat, muscle, or fascia).
b. Flap : mucoperiosteal septal flap rotated superiorly.
 -149-

- The approach for repair may be :

a. Intracranial: If the defect is large or if the site of the leak cannot
be accurately localized, and if there are multiple defects.
b. Extracranial : If the site of the leak is accurately localized,
especially if the defect is involving the anterior ethmoid roof,
and the approach is through an external frontoethmoidectomy.
c. Endoscopic : If the site of defect is well localized endoscopically
and is of small size, or if the fistula occurred accidentally during
endoscopic sinus surgery.
Adhesive sealing materials as histoacryl, fibrin glue, and
microfibrillar collagen can be used for further support of the graft
or the flap.

Oroantral fistula
This is a fistula between the oral cavity and the maxillary sinus. It
occurs usually on the alveolar margin (alveolar), but it may be sublabial
presenting on the anterior wall of the maxillary sinus. (Fig.33)
Aetiology
1. Traumatic : This is the commonest cause.
a. Dental extraction of the 2nd premolar and first molar teeth
especially if there is dehiescence of the bony floor of the antrum
and the roots of the teeth are only covered by the lining
respiratoy mucous membrane.
b. Excision of dental or dentigerous cyst.
c. Penetrating wounds of the upper jaw.
d. Radical antrum operation, if the sublabial incision does not heal
spontaneously.
2. Neoplastic : Erosion by malignant tumours of the palate or the
maxillary sinus.
3. Inflammatory : osteomyelitis of the maxilla, syphilis, and non
healing granulomas.

Fig,33. oroantral fistula

 '-rr

-150-

Clinical picture
1. Regurgitation of fluids and occasionally food particles from one
side of the nose.
2. The patient can blow air from his nose into his mouth.
3. Purulent foetid discharge through the fistula,
4. Maxillary sinusitis with purulent offensive nasal discharge,
5. A probe can be passed through the fistula from the mouth to the
antrum, but this is not advisable as it may damage an attempt of
healing. It is done only in doubtful cases.
Investigations
1. Plain x-ray sinus view; shows maxillary sinusitis, F.B, or retained
tooth fragment in the antrum.
2. CT scan of the paranasal sinuses; localizes the site of the fistula.
3. Fistulography; injection of contrast material into the fistula to
outline its track.
Treatment
A. Recent cases : "Discovered within 24 hours eg. after tooth
extraction"
a. Small fistulae usually heal spontneously.
b. Large fistulae need "surgical repair by suturing the mucosa in two
layers or by the use of rotational buccal flap, or palatal flaps.
In both cases antibiotics and decongestants are given, and avoid
nose blowing.
B. Late cases : "after 8 weeks"
Spontaneous closure is not expected due to epithelialization of the
track. Surgical repair is done by excising and trimming of the bony
edges of the fistula, then either, suturing primary in two layers, or
using a rotational mucoperiosteal flap (buccal, palatal or a
combination). Radical antrum operation is done as a part of the
procedure.
C. In failed repair : We can use a prosthesis to cover the fistula eg.
dental obturator.
 -151-

Inflammations of the nose

I. Acute:
1. Fumculosis,
2. Vestibulitis.
3. Rhinitis : - Non specific : - common cold.
- Influenza
- Exanthemata.
- Specific : - diphtheria.
II. Chronic : - Non specific : - Atrophic rhinitis.
- hypertrophic rhinitis.
- Specific - Rhinoscleroma.
- lupus.
- syphilis.
- leprosy.
- Sarcoidosis

Furnculosis of the vestibule

This is an acute infection of a hair follicle in the vestibule of the
nose (hair bearing area) by staphylococcus aureus.
Aetiology
It may be due to :
a. Mechanical trauma as in nose picking.
b. Lowered immunity as in diabetics.
Clinical picture
1. Pain and swelling of the tip of the nose.
2. The furuncle is seen in the vestibule of the nose as a hard, tender,
red, hot nodule, with surrounding oedema. Later, it enlarges and,
becomes more painful, fluctuant and it may show pointing. It may
be multiple and recurrent in diabetics.
3. The majority show spontaneous discharge in the vestibule and
resolve, but occasionally, complications may occur, and these
include :
a. Facial cellulitis,
b. Septal abscess.
c. Cavernous sinus thrombosis (as it lies in the dangerous area of
the face.)
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Treatment
1. Systemic antibiotics.
2. Local antibiotic cream.
3. Local moist heat.
4. Analgesics.
N.B. : squeezing of a nasal furuncle should be avoided to prevent the
occurrence of cavernous sinus thrombosis.

Nasal vestibulitis
This is an inflammation of the skin of the vestibule due to infection
by pyogenic organisms, or irritant dermatitis (as in common cold
secodnary to excoriating nasal discharge). There is dryness of the nasal
vestibule with crustations, fissurring and severe pain.
Treatment
1. Local antibiotics ointment. It may be combined with steroids.
2. Systemic antibiotics.

Common cold (coryza)

- This is an acute non-specific viral rhinitis, which is caused by
rhinoviruses of more than 100 different types.
- It spreads by droplet infection.
- Predisposing factors :
a. lowered immunity particularly in children.
b. exposure to cold, chills, and temperature changes.
c. overcrowdness.
Clinical picture
- It is a symptom complex of the upper respiratory tract, in which the
nasal symptoms are more predominant.
I

- The incubation period is 1-3 days.

- The disease passes into the following stages :
A. Stage of ischaemia; (vasoconstriction)
1. There is burning sensation and dryness in the nose, and
sneezing.
2. Generalized bony aches.
- Remember that direction of air current to the back especially if
there is sweat causes vasconstriction in the nasal blood nasal.
 -153-

B. Stage of congestion; (vasodilatation and secretion)

1. Slight fever, malaise, and headache.
2. Nasal obstruction.
3. Excessive watery nasal discharge.
4. There may be cough.
- It lasts about 3-5 days, and recovery may occur after tliis stage.
C. Stage of secondary bacterial infection; (suppurative rhinitis)
- Due to infection by 2ry bacterial invaders especially,
staphylococcus, streptococcus pneumoniae, and haemophilus
influenza. It may last up to two weeks, showing :
1. Increased constitutional manifestations with high fever.
2. Nasal discharge which becomes thick and mucoid, then
mucopurulent and purulent.
3. Nasal obstruction.
4. Diminished taste and smell sensations.
D. Stage of resolution : during which recovery occurs within 3-5
days.
On examination :
- The mucosa of the nose is red, congested with oedema. There is
mucoid, mucopurulent or purulent discharge.
- redness of the nostrils and upper lip due to sniffing and repeated
nose blowing.
Complications
1. Sinusitis, pharyngitis, otitis media.
2. Laryngitis, laryngotracheobronchitis.
3. Bronchitis and pneumonia.
4. Permanent anosmia.
Treatment
A. Prophylaxtic :
1. Avoid overcroudedness, exposure to cold or temperature
changes.
2. Vaccination : several vaccines have been developed but of
doubtful effect, due to the very large number of vimses.
B. Curative:
1. Bed rest, and plenty of fluids.
2. Analgesics, and antipyretics.
3. Systemic antibiotics to avoid secondary bacterial infection.
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4. Repeated douching with alkaline nasal lotion.

5. Oral decongestants.
6. Antihistaminics.
7. Vitamin C.
8. Steam inhalation.

Influenzal rhinitis
- This is an acute non specific viral rhinitis, similar to common cold
but more severe. It is caused by influenza viruses, types A, B, and
C. It is rather a systemic disease complex.
- Clinical picture; similar to common cold with the following
differences.:
1. Severe headache^ malaise and high fever.
2. Rhinorrhoca and sneezing are mild.
3. Secondary bacterial infection is more frequent.
4. Complications as in common cold may occur, but they are more
severe and in addition pneumonia, myocarditis, and
meningoencephalitis may occur.
- Treatment
1. As in common cold.
2. Vaccination of high risk groups.
Rhinitis of viral exanthemata
- Rhinitis is frequently, a prodromal symptom of measles, rubella, and
chicken pox. It often preceeds the exantliemata by 2-3 days.
- Secondary bacterial infection and complications are more common
and severe than with common cold.

Chronic hypertrophic rhinitis

Tliis is a form of chronic nonspecific rhinitis which is characterized
by hypertrophy of the mucous membrane of the nose especially that of
the turbinates.
Aetiology
1. Repeated attacks of acute rhinitis with irreversible changes in the
form of hypertrophy and hyperplasia of the mucosa and
submucosa,
2. Vasomotor rhinitis.
3. Allergic rhinitis.
 -155-

Clinical picture
Symptoms
1. Nasal obstruction.
2. Mucoid nasal discharge and post nasal drip.
Signs
Enlarged inferior turbinate with swollen congested mucosa. The
size of tlie inferior turbinate doesn't shrink with the application of a
vosoconstrictor indicating irreversible changes.
Treatment
1. Control of pedisposing factors.
2. Topical steroids may be tried.
3. Reduce the size of the inferior turbinate by :
a. Submucous diathermy (electrocoagulation).
b. Partial inferior turbinectomy.
c. Laser turbinectomy.

Chronic atrophic rhinitis

This is a chronic nonspecific rhinitis associated with progressive
atrophic changes of the nasal mucosa (including glands and blood
vessels), and the bony turbinates.
Aetiology
I. Primary : (Idiopathic or Ozaena)
The cause is not known exactly, it may be due to :
1. Endocrinal imbalance as it is more in females.
2. Infections, secondary to purulent rhinitis and sinusitis in young
ages. The organism may be klebsiella ozaenae.
3. Deficiency of iron and vitamin A.
4. Autoimmune disease.
5. Autonomic imbalance : due to sympathetic overactivity and spasm
of the feeding blood vessels.
II. Secondary :
There is destruction of the nasal mucosa with subsequent squamous
metapalsia of the epithelium and subepithelial fibrosis. This may occur in

1. Chronic specific rhinitis (Nasal granulomata) : Scleroma, syphilis,

lupus, leprosy.
 -156-

2. Postoperative : excessive removal of nasal mucosa as after inferior

turbinectomy.
3. Postirradiation.
Pathology
Tliere are atrophic changes which present as:
• a. degeneration of the epithelium and loss of cilia.
! b. squamous metaplasia.
c. The submucosa show dgeneration of the serous glands and the
nerve endings, endarteritis and periarteritis of terminal arterioles
and fibrosis.
d. Atrophy of the underlying bone.
Clinical picture
- It is bilateral, and more common in females at the age of puberty.
Symptoms
1. Nasal discharge : viscid, thick^ crusty, greenisji or blackish, Foetor
is marked and is due to secondary infection by anaerobs, and
putrefaction under the crusts. Foetor is not perceived by the patient
due to the accompanied anosmia.
2. Nasal obstruction inspite of the roomy nasal passages. It is due to
dullness of sensation of air on the atrophic nasal mucosa, with
atrophy of nerve endings.
3. Anosmia due to degeneration of the olfactory mucosa.
4. Mild epistaxis may occur on separation of crusts.
5. Sorcethroat due to associated atrophic pharyngitis, and loss of
moisture of the inhaled dry air.
6. Chocking if detached crusts slip into the larynx.
Signs
1. Tlie nasal mucosa is dry, pale, glazed and atrophic.
2. Roomy nasal passages.
3. Atrophic turbinates.
4. greenish or blackish crusts with marked foetor, and on removal,
may cause bleeding.
5. Associated signs related to the cause in secondary atrophic rhinitis.
Treatment
A. Treatment of the cause in secondary atrophic rhinitis.
B. Medical
1. Repeated nasal douching with alkaline nasal wash. It dissolves
the crusts, helps their separation and decreases the foetor.
 / /

-157-

2. Frequent removal of crusts by forceps or suction.

3. Menthol paraffin (oily) nasal drops after removal of the crusts to
prevent adherence of new crusts, and to decrease the foetor,
4. 25% glucose in glycerine applied as a pack for 15 minutes. It
inhibits proteolytic organisms and decreases foetor.
5. Local oestrogen drops to stimulate secretion by the
seromucinous glands.
6. Postassium iodide, 5 grains t.d.s. to stimulate secretion by the
glands.
7. Iron and vitamin A supplementation.
9. Mucolytics.
' V.

C. Surgical
T^ To narrow a wide nasal cavity :
a. Medial displacement of the lateral wall of the nose.
b. Submucosal implantation of grafts e.g. bone, cartilage,
dermofat or teflon.
(2. Temporary occulusion of one of both nostril:; by a plastic
operation. Using raised mucosal folds from the vestibule, or the
floor of the nose, then suturing them together. It is left for six
months up to 2 years. (Young's operatoin)

Rhinoscleroma
- This is a chronic specific inflammatory granuloma of the upper
respiratory tract. It affects the nose, pharynx, and larynx. It is the
\ commonest granuloma in Egypt. It is endemic in Sharkayia,
Menofea and fayoum.
- It is caused by Klebsiella rhinoscleromatis (gram -ve Frisch
bacillus).
- Infection requires long and intimate contact. Bad hygiene and
lowered immunity have a role. u
- Age : 15-35 years.
- Sex : It is more in females.
Pathology
A. Atrophic stage
- Similar to atrophic rhinitis. There is degeneration of ciliated
epithelium and seromucinous glands.
 ••f

-158-

- Chronic inflammatory cellular infiltration by lymphocytes, plasma

cells, Rusdbpdies, and macrophages.
B. Nodular (active) stage
The submucosa shows rich vascularity and cellular infiltration by
Mikulicz cells, Russel bodies, lymphocytes, macrophages, and plasma
cells.
^^^ikulicz celtsy These are the cheif component of the infiltrate
(characteristic cells). They are large vacuolated cells with foamy
cytoplasm and small central nucleus. Within the vacuoles, the
bacilli may be demonstrated. These cells are macrophages that
undergo hydropic degeneration.
•Russel bodies : These are plasma cells with hyaline degeneration.
They appear bright red, oval or rounded and without nucleus.
C. Fibrotic stage
There is increased proliferating fibroblasts and co^Ia^en fibres with
dense fibrosis and decreased cellularity and vascularity.
Clinical picture
- It has an insidious onset and slow course. It passes into several
stages and there may be more than one stage at a time.
A. Invasive stage; similar to acute nonspecific rhinitis.
B. Atrophic stage; similar to atrophic rhinitis.
Signs
1. Tlie nasal cavity is roomy with thin pale dry mucosa.
2. There are yellowish or greenish foetid crustations that bleeds on
removal.
3. occasional small scattered granulonatous mases.
C. Active nodular stage
Signs
Bilateral submucosal hard cartilagenous nodules starting at the
mucocutaneous junction (between the nasal mucosa and skin of the
vestibule). They are first discrete, but later on, they coalesce together to
form a lage mass filling the nasal cavity and expanding the nose. First,
they are bluish red, and later on pale grey. The granulomata may
infiltrate the collumella, the alae feel firm to hard and cause great
defomity.
D. Fibrotic stage
1. Persistent nasal obstruction.
 -159-

2'. Dense fibrosis with narrowing which may lead to complete

obilteration of the nased cavity.
3. hard alae.
Sequalae
A. Extension during the active nodular stage
1. Subcutaneously to involve, the tip of the nose, collumella, and may
be the upper lip.
2. Extension to the lacrimal passage (dacryoscleroma) causing
epiphora and may be proptosis.
3. To the pharynx and larynx.
4. Externally, to form localized firm masses on the dorsum of the
nose.
5. Cervical lymph nodes are very rarely involved. The favourable
diagnosis in such a situation is sinus histiocytosis (Rosai Dorfman's
disease) and not scleroma.
B. Fibrosis ; leading to stenosis of the nasal cavity and deformities (eg.
collapse of the tip of the nose).
C. Malignant transformation ; is very rare, but reported.
Investigations
1. Biopsy and histopathological examination ; Shows the
characteristic microsopic picture of each stage. It is diagnostic in
the active nodular stage but nonspecific in the atrophic and fibrotic
stages.
2. Culture ; shows the characteristic frisch's bacilli.
3. Electron microscopic examination ; may be positive in some
cases with negative biopsies examined by light microscopy.
Treatment
A. Medical
7. Rifampicine (Rimactan) : 600 mg orally taken daily before meals,
for 8-10 weeks and up to 3 months
side effects ; hepatotoxic and redcolouration of urine and sweat.
2. Streptomycine : Igm I.M., daily for 40 days.
side effects ; ototoxic vestibulotoxi (tinnitus, vertigo, and
deafness), and nephrotoxic
Frequent examination of 8th nerve and PTA during treatment
should be done.
3. Other antibiotics that may be used :
 -160-

a. Ampicillin 250 mg 4 times daily 20-30 days.

b. Third generation cephalosporins.
N.B. : The antibiotics donot reach the organism easily as it is
intracellular (inside the macrophages).
4. Local:
a. Repeated nasal douching with alkaline nasal wash.
b. Remove crusts by forceps or suction.
c. Aueromycin oint. 20% for 1 year.
B. Surgical :
1. Removal of a localized mass within the nose to allow
recanalization, followed by insertion of polyethelene tubes for 6-8
weeks to keep it patent,
2. Fibrotic narrowing can be widened by CO2 laser.
3. Plastic reconstruction if there is deformity, with limited chances of
success.
C. Deep x-ray therapy ; Which is no more used as it is carcinogenic,
and furthermore the lesion is bengin, and the patient is young with a
great chance developing an irradiation induced malignancy later on,
e.g. ca. thyroid.

Syphilis of the nose

- Organism : Treponema pallidum (one of the spirochaetes).
- It is either :
a. Acquired ; primary, secondary or tertiary stages.
b. congenital; due to transplacental infection.
A. Primary acquired syphilis
- Chancer of the nose is very rare, when it occurs, it appears in the
vestibule. It is hard indurated raised reddish papule, later it
ulcerates to form a painless ulcer with sharp edges and dull red
floor, that heals without scar formation.
- Enlarged, submandibular and preauricular lymphnodes. They are
rubbery, discrete and painless.
- There is swelling and irritation of the nose, but with no pain.
B. Secondary acquired syphilis
- There is persistent catarrhal rhinitis with fever and malaise.
- Nasal vestibulitis with crustations and fissuring.
 -161 -

- Mucous patches : appear in the nose and pharynx as painless, flat

or slightly raised, oval or rounded, regular, white plaques
surrounded by a red margin. Later, they ulcerate and coalesce
together to form a snail track ulcer.
- generalized symmetrical pleomorphic skin rash.
- Condylomate lata.
- generalized lymphadenopathy especially epitrochlear, splenic and
posterior cervical.
C. Tertiary syphilis
- This is the commonest nasal manifestation of syphilis.
- It affects the bony part of the septum, and less commonly the
lateral nasal walls and floor. It doesn't affect the cartilagenous
septum as syphilis is a disease of vessels, and cartilage is devoid
of vessels, and thus gummatous perforation of the septum occurs
posteriorly and not anteriorly.
- Nasal obstruction.
- Nasal discharge, first mucoid, and later on becomes offensive,
blood stained with crustations, and secondary atrophic changes.
- Headache which is worse at night, but without pain.
- Gumma ; reddish, illdefined rubbery swelling, single or multiple,
localized or diffuse. Later, it ulcerates to form a deep ulcer with
punched out edges, irregular indurated margins and yellowish
necrotic floor.
- Fibrosis then follows.
- Tenderness over the nasal bridge.
Complications
1. Secondary infection with pyogenic organisms.
2. Sequestration.
3. Perforation of the bony septum, or hard palate,
4. Collapse of the nasal bridge (saddle nose deformity).
5. Scarring and stenosis of the nasal cavity.
6. Secondary atrophic rhinitis.
7. Intracranial complications due to involvement of the meninges.
Investigations
1. Serological tests for syphilis; Wasserman reaction (W.R.), Kahns's
test, Treponema pannidum immobilization test (TPI). They are
positive in secondary and tertiary syphilis, but unreliable in Iry
syphilis.
 -162-

2. Direct smear ; demonstrates the motile spirochaetes.

3. Biopsy is characteristic (endarteritis obliterans).
4. Response to antisyphilitic treatment is so marked in they 2ry stage
so that it can be used as a diagnostic test.
Trcalrncnt
1. General antisyphilitic treatment (Penicillin).
2. Alkaline nasal wash.
3. Mercuric ointment.
4. Plastic surgery for septal perforadons.
Congential syphilis
It is transmitted by transplacental infection.
A. Early form ; (firt 3 months)
- It resembles secondary acquired syphilis.
- There is rhinorrhoea with thick purulent nasal discharge,
sometimes blood stained.
- Snuffles, noisy respiration and snoring.
- Fissuring of the vestibule and upper lip (rhagades).
B. Late form ; (from the 3rd year of life)
- It resembles 3ry acquired syphilis.
- There are localized or diffuse gummata.
- Other stigmata of congenital syphilis ; Hutchinson's teeth,
interstitial keratitis, sensorineural hearing loss and positive
serological tests for syphilis.
Treatment
1. General antisyphilitic treatment.
2. Local antiseptics.

Lupus of the nose (lupus vulgaris)

- Lupus vulgaris is an indolent or chronic form of tuberculous
infection that affects skin and mucous membrane. It is caused by
attenuated T.B. bacilli of low virulence.
- It is more common in females.
Clinical picture
1. Nasal discharge and obstruction, followed by crusting and occa-
sional epistaxis.
2. Nodules (Apple - jelly nodules) develop on the skin of the vestibule
 -163-

at the mucocutaneous junction and on the butterfly area of the face.

Tliey are reddish and fimi with crustations and foetor.
3. later, the nodules ulcerate to form shallow ulcers with undermined
edges, bluish margins. This may cause perforation of the
cartilagenous portion of the septum.
4. There is marked deformity of the tip of the nose, alae and skin of
the face (as if the face is eaten by a wolQ.
Complications
1. Secondary atrophic rhinitis.
2. Pulmonary tuberculosis in small proportion of cases.
3. Dacryocysitis, corneal ulceration and nasopharyngeal lupus.
4. Epithelioma.
Investigations
1. Biopsy is characteristic.
2. Bacterologic examination shows theT.B, bacilli.
Treatment
1. Specific antituberculous therapy and calciferol (vitamin D2)
150,000 unit daily for 6-9 months.
2. Repeated douching with alkaline nasal wash.
3. Surgical repau" for residual nasal deformities.

Leprosy
This is a chronic granulomatous disease caused by Mycobacterium
leprae, it is 5% acid fast. It affects skin, mucous membrane and
peripheral nerves, leprosy is a disease of peripheral nerves and needs
cold climate to grow.
Three main types of leprosy are recognized :
1. Tuberculoid leprosy ; anaesthetic cutaneous patches may extend to
the nasal vestibule. Isolated cranial nerve palsies (eg. VI and VII)
may occur.
2. Lepromatous leprosy ; there is diffuse infiltration of skin (piniu,
chin, nose and brows), nerves, and mucosa. The nasal mucosa is
involved early in most cases and the nasal secretions contain a very
large number of the bacilli.
3. Borderline leprosy ; a midway between tuberculoid and
lepromatous types.
 -164-

Clinical picture
1. Nasal obstruction and blood stained nasal discharge with
crustations.
2. Nodular thickening of the nasal mucosa. The nodules have a yellow
tinge and affects the anterior end of the inferior turbinate at first.
Later, they ulcerate and end in fibrosis, and stenosis of the nasal
cavity. Perforation of the cartilagenous part of the septum may
occur.
Investigations
1. Scrappings from the nasal mucosa show the acid-fast bacilli.
2. Biopsy.
Treatment
1. Rifampicine 600 mg / day before breakfast.
2. Clofazimine 100 mg/two days.
3. Dapson 100 mg/day.
A triple therapy of the above mentioned drugs is preferred.
4. Alkaline nasal wash.
 -165-

Diseases of the nasal septum

Deviated nasal septum
Septal deviations are extreemly common, but are not usually severe
enough to affect the nasal functions. A perfectly straight septum is rarely
found.
Aetiology
A. Developmental
1. Growth abnormality due to excessive ossificadon of one plate of the
vomer more than the other.
2. Affection of other parts of the nose ; a high arched palate reduces
the space of the nasal chamber, so that the thin pliable septum
cannot develope normally.
3. Excessive development of the middle and inferior turbinates
pushing the septum to the opposite side.
B. Traumatic
1. Intrauterine trauma.
2. Birth trauma.
3. Accidental acquired' trauma, which is usually assocaited with
fracture nasal bones.
4. Surgical trauma.
Pathological variants
A. Deviations; (Fig.34) more
marked in the cartilagenous
portion of the septum, and may
involve the bony part. It may be
C-shaped, S-shaped, angular or
irregular.
B. Spurs ; sharp angulations like a Fig.34. deviated
septum
crest or spine at the junction
between cartilage and bone,
usually between the septal
cartilage and the nasal crest of
the maxilla.
C. Dislocation ; the lower border of the septal cartilage is displaced
from its medial position and projects into the nostril.
Clinical picture
Most of the septal deformides are asymptomatic and only gross
ones impair the nasal functions and produce symptoms.
 -166-

1. A^a^a/ obstruction ; This is the dominant symptom. It is usually

unilateral, but it may be bilateral in S shaped deviations, or if there
is reactive hypertrophy of the inferior turbinate in the side opposite
to the deviation.
2. Hyposmia due to nasal obstruction.
3. Mucoid nasal discharge and postnasal drip due to contact of the
mucosal surfaces or recurrent sinusitis.
4. Epistaxis due to congestion and angulation of the vessels over the
deviation or spur.
5. Recurrent otitis media.
6. Secondary atrophic rhinitis with scabbing and crustations.
7. Neuralgia and headache in markedly deviated septum, due to
pressure on the lateral nasal wall (contact headache) or interference
with aereation of the frontal and ethmoidal sinuses (vaccum
headache).
8. Examination
- Septal deformity, spurs, and atrophic rhinitis.
- Posterior deviations involving the bony septum are best seen
endoscopically.
Investigations
1. Plain x-ray sinus view.
2. CT scan of the paranasal sinuses, if there is associated sinusitis.
Ireatmcnt
Surgical correction of the septal defonriity.
Indicated in ;
1. Symptomatizing cases with permanent nasal obstiuction.
2. Sinusitis.
3. Recurrent epistaxis.
Operations
1. Submucous resection (SMR) of the septum (Fig.35)
- It is designed by Killian.
- It is done under local or general anaesthesia.
- A vertical incision is made in the mucoperichondrium of the
septum 1cm behind the anterior end of the septum. The
mucoperichondrial flap is elevated from the cartilage on one
side, then the incision is deepened through the cartilage, and the
flap of the opposite side is elevated. The deviated portion of the
 -167-

septal cartilage and bone is removed, then the

mucoperichondrial flap is repositioned again in the midline. A
nasal pack is placed to be removed after 48 hours.
The operation should not be done in children (so as not to
disturb facial growth).

Fig.35 submucous resection

2. Septoplasty
Here no cartilage is removed, and the deflected part is straightened
by linear incisions.
- Indicated in :
a. Correction of septal deviation in childien.
b. Anterior septal dislocation.
- Advantages :
a. Lesser incidence of septal perforation.
b. No supratip depression of the external nose.
3. Removal of associated septal spurs.
4. Treatment of associated sinusitis eg. F.E.S.S.
5. Reduction of the size of the inferior turbinate if needed.
Complications of septal surgery
1. Postoperative haemorrhage.
2. Septal haematoma and abscess.
3. Postoperative infection and sinusitis.
 -168-

4. Septal perforation especially during

SMR, if there is a mucoperichondrial
tear which is bilateral and overlapping.
5. Collapse of the nose and supratip
depression (Fig.36), if no supporting
^
cartilage is left.
6. Persistent obstruction due to inadequate
Fig.36 saddle
correction or if the hypertrophied nose
turbinates are not reduced in size.
7. CSFrhinorrhoea.
8. Complications of anaesthesia.

Septal haematoma
. This is collection of blood between the mucoperichondrium and
septal cartilage. (Fig.37)
Aetiology
1. Traumatic
- Accidental; a blow to the nose.
- Surgical; SMR and Septoplasty.
Fig 37. septal
2. Spontaneous ; less common. haematoma
- In haematologic disorders with
bleeding tendency.
- In elderly patients especially, those taking aspirin regularly for
cardiac conditions.
Clinical picture
1. History of trauma or nasal operation.
2. Bilateral nasal obstruction.
3. Examination reveales a fluctuant swelling on both sides of the
septum and on aspiration with a needle it brings blood.
Complications
1. Septal abscess due to secondary infection.
2. Organization of the haematoma with permanent thickening of the
septum.
3. Supratip depression after evacuation.
Treatment
Incision and evacuation of all blood clots. The incision is done

_ = j .
 •Tl

- 169-

vertically on one side and horizontally on the opposite side to avoid

septal perforation. A nasal pack is placed for 24 hours to avoid
recollection. Antibiotics are given to avoid infection.

Septal abscess
Aetiology
1. Infection of a septal haematoma (commonest cause).
2. Extension from vestibulitis.
It occurs more in diabetics.
Clinical picture
- Usually there is a history of trauma.
1. Fever, headache, malaise.
2. Pain first dull aching, later becomes throbbing with pus formation.
3. Bilateral nasal obstruction.
4. Purulent nasal discharge if the abscess ruptures spontaneously.
5. Oedema of the skin covering of the nose.
6. Examination reveals symmetrical, bilateral, fluctuant severely
tender swelling on both sides of the septum. Tenderness is marked
over the tip and dorsum of the nose particularly at the junction
between the cartilage and bone. (Fig.38)
Complications .^Aticaii

1. Cavernous sinus thrombosis.

2. Necrosis of the septal cartilage which
may lead to septal perforation or nasal
deformity (saddling and supratip
depression).
Treatment Fig.38 septal
abscess
1. Systemic antibiotics.
2. Incision and drainage of the abscess.

Septal perforation
Perforations of the septum are fairly common, and persons may be
not aware of their presence.
Aetiology
1. Traumatic ; the commonest
a. Habitual nose picking (localized perichondritis), or idiopathic,
this is the commonest cause.
 -n

-170-

b. Postoperative ; after operation (e.g. SMR and septoplasty), after

excessive cauterization of little's area especially if performed on
both sides simultaneously or repeated, therefore, an interval of 2
weeks should elapse between successive cauterization.
c. Bullet or stab wound (very rare).
2. Innammatory
a. Septal abscess and septal haematoma (the perforation is large).
b. Lupus, (anterior perforation in the cartilagenous portion).
c. Leprosy, (anterior perforation in the cartilagenous portion).
d. Syphilis, (posterior perforation in the bony portion).
e. Midline granulomata e.g. Wegener's granuloma.
3. People working in copper, arsenic, and chromic acid industry.
4. Addicts to cocain snuff, because it causes severe vasoconstriction
and anaesthesia.
5. Malignant neoplasms.
Clinical picture
1. Many cases are asymptomatic.
2. Recurrent epistaxis and crust formation.
3. Sensation of dryness of the nose and dull aching pain over the
dorsum.
4. Passage of inspired air produces a whistling sound.
5. Traumatic perforations are usually in the cartilagenous portion, with
sharp clean edges.
6. Apart from traumatic cases, septal perforations are preceded by
ulceration.
Treatment
Septal perforations never heal spontaneously, but fortunately, most
of them do not cause symptoms, and therefore do not require treatment.
1. Repeated nasal douching with alkaline nasal wash if crusts and
bleeding are troublesome.
2. Closure of the perforation by ;
a. Closing the perforation by an obturator, which is button like, and
made of silastic, or teflon.
b. Surgical repair ; the perforation is closed by grafts (e.g.
temporalis fascia) or a rotational mucosal flap from the lateral
wall of the nose, inner mucosa of the upper lip, and floor of the
nose. The procedure is difficult and the results are
unsatisfactory.
 - 171 -

Acute sinusitis
This is an acute inflammation of the mucosal lining of the paranasal
sinuses. It may be involving one or more than one sinus. Rhinitis is a
common association, so it is better called rhinosinusitis.
Aetiology
1. Recurrent viral upper respiratory tract infections (i.e. acute rhinitis),
as in common cold and influenza. This is the commonest cause.
Then viral sinusitis is followed by 2ry bacterial infection.
2. Viral exanthemata e.g. measles and mumps.
3. Neglected foreign body in the nose.
4. Iatrogenic ; intranasal packs, nasotracheal and nasogastric tubes.
5. Dental causes : These represent 10% of cases of maxillary sinusitis.
One should always search for a dental cause in isolated unilateral
maxillary sinusitis. The bone which separates the sockets of the
teeth from the antrum is thin. These causes include :
a. Dental infections eg. periapical abscess, and periodontitis.
b. Oroantral fistula.
6. Trauma :
a. Facial fractures especially compound ones as they disturb the
normal sinus drainage.
b. Sinus barotrauma in which there is oedema and occlusion of the
sinus ostium.
c. Penetrating foreign body e.g. gunshot.
Predisposing factors:
1. Locally : - deviated septum, septal spurs.
- Nasal allergy and polypi.
- disturbed mucociliary clearence as in cystic fibrosis
(mucoviscidosis).
2. Lowered general resistance as in children and diabetics.
3. Overcrowdedness, air pollution (dust, fumes)
Causative organisms:
- Streptoccous pneumoniae, and haemophilus infhienza are the
commonest. Others, as staph, strept, and gram -ve bacilli may be a
cause.
- Anaerobic organisms (e.g. fusibacterium, and bacteroids) are the
commonest in maxillary sinusitis due to dental causes.
- In children moraxella catarrhalis and H. influenza are common.
 - 172 -

Pafhology
- It usually starts by catarrhal followed by suppurative rhinosinusitis.
- There is congestion and oedema of the sinus mucosa, this leads to
occlusion of the sinus ostium, with impairment of normal
physiologic sinus drainage and mucociliary clearence, thus the
secretion accumulates within the sinus lumen with stasis and
subsequent infection and pus formation.
Clinical picture
Manifestations depends upon the sinus or group of sinuses
involved. One sinus or more may be affected.
Symptoms
1. History of acute rhinitis, and in early cases it is difficult to
differentiate from sinusitis.
2. Fever, malaise and anorexia. Fever is uaually mild and high fever
indicates a complication.
3. Unilateral or bilateral nasal obstruction.
4. Unilateral or bilateral nasal discharge. According to the patency of
the sinus ostium, discharge may be profuse (if the ostium is patent)
or scanty in amount, (if the ostium is occuluded). It is
mucopurulent or purulent.
5. Postnasal drip with irritative cough.
6. Pain and headache ; the location of facial pain and headache will
vary and is related to the sinus involved (Fig.39). It is usually
severe and may be throbbing, related to posture, and it increases on
coughing, bending forwards, walking and sudden head movement.
Children are less likely to complain of facial pain and headache
than adults.
7. Facial oedema and swelling.
8. Symptoms of complications if they arise.
Signs
1. Pyrexia, is higher in children and if complications arise. There is
associated tachycardia.
2. Tenderness over the affected sinus on presure or percussion.
3. Oedema, and reddness over the affected sinus. This is more
common in children and in severe cases.
4. Anterior rhinoscopy ; shows :
a. congestion and oedema of the nasal mucosa.
 -173-

b. mucopurulent or purulent nasal discharge. It's location varies

according to the affected sinus. Pus in the middle meatus
(anterior group of sinuses); pus in the superior meatus (posterior
ethmoids); pus in the sphenoethmoidal recess (sphenoid).
6. Postnasal purulent or mucopurulent nasal discharge.

Fig. 38. sites of referred pain from sinuses

A. Acute maxillary sinustis

Symptoms
In addition to the symptoms previously described there are special
features :
1. History of dental infection or extraction.
2. Nasal discharge may be mucopurulent or purulent. It may be
offensive in sinusitis of denaU origin (anaerobic infection).
3. Facial pain and headache ; it is situated over the antrum and may
refere to the ear and temple. Dental pain involving the upper teeth
is usually present.
4. Oedema over the cheek and lower eyelid.
Signs
It shows the following characteristics :
1. Tenderness over the cheek and upper teeth.
2. Oedema and redness over the cheek.
3. Purulent discharge is seen in the middle meatus.
4. Oral examination may reveal dental infection or an oroantral
fistula.
 -174-

//. Acute frontal sinusitis

It is usually associated with anterior ethmoiditis and maxillary
sinusitis, as the frontal recess drains in the middle meatus.
Clinical picture
It shows the following characteristics:
1. Pain and headache arc felt in the supraorbital region or across the
forehead. Pain has a characteristic periodicity, it starts usually in
the morning and becomes worse by midday, then gradually lessens
at the end of the day.
2. Oedema over the upper eyelid and occasionally the forehead.
3. Tenderness above the eyebrow, the forehead, and on the floor of
the sinus.
4. Mucopurulent or purulent discharge is seen in the anterior part of
the middle meatus.
C Acute ethmoidal sinusitis (ethmoiditis)
' In adults, it always accompany frontal sinusitis and may be
maxillary sinusitis, while isolated ethmoiditis is more common in
children and frequendy presents as orbital cellulitis.
Clinical picture
It shows the following characteristics :
1. Pain and headache are felt between the eyes, over the bridge of the
nose and reu*o-orbital. It may be referred to the parietal region.
2. Oedema in the region of the inner canthus.
3. Tenderness is detected by pressure over the inner canthus,
4. In children, the lateral wall of the ethmoid sinuses is thin (lamina
papyracea) and hence extension of infection to the orbit with orbital
complication and proptosis are common.
5. Mucopurulent or purulent discharge is seen in the middle and
superior meati.
D, Sphenoidal sinusitis
Acute isolated sphenoidal sinusitis is rare, it is usually associated
with infection of other sinuses (i.e. as a part of pansinusitis).
Clinical picture
It shows the following characteristics :
1. Severe retro-orbital pain and headache which is frequently referred
to the vertex and basiocciput.
2. The mucopurulent or purulent discharge is seen in the region of the
sphenoethmodial recess.
 -175-

Investigations
1. Plain x-ray : occipitomental (sinus view) and occipitofrontal view,
Shows sinus opacification or airfluid level. The ethmoid sinuses
and the ostiomeatal complex are poorly visualized.
2. Transillumination of the maxillary and frontal sinuses. Which is
done by placing light inside the mouth and observing the amount
of light transmitted through the sinus. The affected sinus looks
opaque. This technique is of little value and is not done
nawadays.
3. CT scan of the paranasal sinuses : This is the investigation of
choice. It shows sinus opacity, affection of ethmoid sinuses,
condition of the ostiomeatal complex, and evaluation of
anatomy prior to surgery. It is particularly indicated if
complications are suspected,
4. Culture and sensitivity of the discharge.
Treatment
A. Medical
1. Rest in bed, light diet, and plenty of fluids.
2. Analgesics, and antipyretics.
3. Mucolytics.
4. Local decongestant nasal drops e.g. oxymetazohne hydrochloride
(Afrin).
5. Steam inhalation and warm foamentations.
6. Systemic antibiotics :
- Should be started rapidly to avoid progression of the disease and
to avoid complications.
- It is best given according to culture and sensitivity, but start with
broad spectrum antibiotics while waiting the results.
- Commonest antibiotics used include ; amoxycillin, amoxycillin
with clavulanate ((i-lactamase inhibitor), third generation
cephalosporins e.g. cefuroxime. They are continued 10-14 days,
and clinical improvement is expected in 48-72 hours.
- Hospitalization and massive parenteral andbiotics in severe cases.
B. Sugrical
- Surgical drainage is indicated in :
1. Failed medical treatment.
2, Present or threatening complications.
 -176-

- The aim of surgery is to establish adequate drainage. It should be as

conservative as possible to avoid progression of infection.
- The fQllQwing prgcgdurcs are dong:
1. Maxillary sinusitis : Antral puncture and lavage,
2. Frontal sinusitis : External frontal trephine operation (through
the sinus floor), and establish draniage for few days by a tube.
(Fig.40)
3. Ethmoiditis : ethmoidectomy (endoscopic or external).
4. Sphenoiditis : sphenoethmoidectomy (endoscopic or external).
N.B. : Nowadays the functional endoscopic sinus surgery is highly
effective in draining the affected sinus.

0 » » n k . ( M rw*r •

Fig.40. frontal trephine operation

Chronic sinusitis
This is a chronic inflammation of the mucoperiosteal lining of the
paranasal sinuses with complex irreversible pathological changes.
Aetiology
1.Repeated attacks of acute sinusitis with incomplete resolution is the
cause, which may be due to :
a. Persistence of predisposing factors with inadequate drainage and
poor ventilation of the sinuses (persistent obstruction of the
ostiomeatal complex).
b. Inadequate treatment with residual infection.
2. High virulence of the organism, or low resistance of the patient.
Pathology
- TTie mucosa is oedematous, congested, and my be polypoidal.
- Degeneration of ciliated epithelium, with loss of cilia and
metaplasia.
 -'-*•<.-"-rrawMT-II

-177-

- Microabscesses and granulation tissues.

- Excessive fibrosis.
' Round cell and PNLs infiltration of the submucosa.
- In late cases the mucosa is either atrophic or hypertrophic, and at this
stage the condition is irreversible.
The region of the ostiomeatal complex is the key area for different
sinuses affection. It's obstruction will eventually result in maxillary,
ethmoidal and frontal sinuses infection.
Clinical picture
Symptoms
1. Persistent or intermittent nasal obstruction.
2. Nasal discharge ; mucopurulent or purulent and may be offensive.
There is postnasal drip with irritative cough.
3. Hyposmia and cacosmia (bad smell).
4. Facial pain and headache :
- recurrent, periodic, more in the morning, localized and dull
aching.
- Its site varies according to the affected sinus (see before).
- Increases on bending forwards, coughing, and straining.
5. Symptoms of septic focus, low grade fever, fatigue, bone and joint
pains.
6. Symptoms of descending infection :
a. Recurrent rhinitis.
b. Otitis media especially in children, and E.T. dysfunction.
c. Recurrent pharyngitis due to postnasal dripping.
d. Laryngitis, bronchitis, and chest infecnon.
7. Symptoms of complications if they arise.
Signs
1. Tenderness over the affected sinus on deep pressure.
2. Anterior rhinoscopy ; shows :
a. Mucosal oedema and congestion.
b. Mucopurulent or purulent discharge in the middle meatus.
c. Nasal polypi may be seen in chronic ethmoiditis.
• Diagnostic nasal and sinus endoscopy is now in common use. It is
perfect in visualizing the sinus ostia, purulent discharge in different
areas, detect ethmoidal polypi, and predisposing anatomical variations
(e.g. concha bullosa).
 1-

-178-

Investigations
1. Plain x-ray ; shows sinus opacification, fluid level or thickened
mucosa.
2. Culture and sensitivity for the discharge.
3. Diagnostic antral puncture and lavage.
A. CT scan of the paranasal sinuses ; This is the most reliable
investigation nowadays (see acute sinusitis).
r Treatment
A. conservative
1. Systemic antibiotics according to culture and sensitivity, they
should be continued for at least 14 days and up to 4 weeks,
2. Oral decongestants (contraindicated in glaucoma, hypertension, and
prostate enlargement).
3. Local decongestant nasal drops.
4. Mucolytics.
5. Analgesics.
6. Control of predisposing factors e.g. nasal allergy, deviated septum,
and nasal polypi.
7. Repeated douching with alkaline nasal wash.
8. Moist heat and steam inhalation.
B. Surgical
It is indicated if medical treatment (up to 4 weeks) fails, or there is
mechanical obstruction (e.g. Deviated septum or anatomical variadon).
/. Chronic maxillwy sinusitis :
a. Repeated antral puncture and lavage up to six times.
b. Endoscopic middle meatal antrostomy (widening of the natural
ostium of the sinus after removal of the uncinate process.
c- Intranasal inferior antrostomy is obsolete now, being replaced by
F.E.S.S.
d. Caldwell luc's (radical antrum operation) is restricted nowadays
to removal of large polypoid mucosa or cysts and during closure
of oroantral fistula.
2. Chronic frontal sinusitis :
a. Endoscopic clearance of the frontal recess. Previously external
frontal operation was the procedure frequently done, where the
floor of the sinus is opened and the diseased mucous membrane
removed.
 -179-

b. Osteoplastic flap operation in chronic and recurrent cases. The

. sinus cavity is obliterated by fat,
3. Ethmoiditis :
a. Intranasal ethmoidectomy either endoscopic or microscopic.
b. External frontoethmoidectomy if there are complications
especially orbital ones.
4. Sphenoidal sinusitis;
Intranasal sphenoethmoidectomy either endoscopic or microscopic.
* Functional endoscopic sinus surgery :
- This is the standered surgical procedure done nowadays for chronic
sinusitis. It is based on restoration of the functional physiology of
sinus drainage by correction of any obstruction of the ostiomeatal
complex which is the key area for different sinus infections.
- It is done using 0\ 30" and 70" rigid endoscopes,
- The FESS procedure consists of :
1. Exenteration of anterior ethmoid cells (anterior ethmoidectomy).
2."Widening the ostium of the maxillary sinus (middle meatal
antrostomy).
3. Clearance of the posterior ethmoid cells if needed (posterior
ethmoidectomy).
4. Sphenoid sinus clearance if needed (sphenoidotomy).
5. clearance of the frontal recess area to help drainage of the frontal
sinus.
- An accurate preoperative C.T. scan of the paranasal sinuses is
mandatory to identify the anatomical landmarks and the diseased
areas.
- The FESS procedure has the following advantages :
1. Precise identification and eradication of the diseased areas with
excellent magnification and illumination.
2. Allows removal of the diseased mucosa and preserves the
nonnal mucosa.
3. Preserves natural anatomy and physiology of the nose.

Sinusitis in children
- Sinusitis in children is somewhat different from adults, and this
difference is due to anatomical variations, and to the fact that the
tissues of the child are growing.
 r
-180-

- Age incidence : 5-8 years.

- The maxillary and ethmoid sinuses are the commonset to be affected.
Aetiology
Predisposing fflglprs [
1. Repeated viral respiratory tract infections are common.
2. Exanthemata (e.g. measles, and mumps) are common.
3. Cystic fibrosis (mucoviscidosis) with disturbance of the
mucociliary clearance. It is associated with nasal polypi in 50% of
cases.
4. Kartagner's syndrome (immotite cilia syndrome). It consists of
bronchiectasis, sinusitis, and sterility.
5. Immune deficiencies (e.g. laekemia, and immunosuppressive
drugs).
6. local : Adenoids, choanal atresia, foreign body, and dental
infections.
Causative organisms :
The commonest are streptococcus pneumoniae, haemophilus
influenza, and Moraxella catarrhalis.
Clinical picture
A, Acute sinusitis
- Similar to that in adults with special features as :
1. High fever, and the child is irritable.
2. Pain, reddness, and swelling over the affected sinus.
3. Periorbital oedema.
4. Purulent nasal discharge.
r
5. Complications especially orbital and facial cellulitis are more
frequent and run a more rapid course.
B. Chronic sinusitis
~ It presents mainly as :
1. Persistent mucopurulent or purulent discharge.
2. Persistent laryngitis and chronic irritative cough especially
nocturnal.
3. Recurrent otitis media due to excessive postnasal discharge.
Therefore sinus and aural examination should be done in
children complaining of symptoms in either area.
4. In general, children are less likely to complain of facial pain and
headache.
 -181-

Treatment
A. Medical
As in adults, especially antibiotics. This can be sufficient to resolve
the condition.
B. Surgical
r " It is reserved for ;
\~ I. Complications : orbital, intracanial.
r ~ 2. Unresolved infections after maximal medical therapy.

Complications of sinusitis
It denotes extension of infection from the mucosal lining of the
paranasal sinuses into and beyond their bony walls.
Classification
I. Orbital complications
1. Orbital cellulitis.
2. Subperiosteal abscess.
3. Orbital abscess.
4. Isolated optic neuritis.
5. Superior orbital fissure syndrome.
6. Orbital apex syndrome.
II. Cranial complications
1. Osteomyelitis of the frontal bone and the maxilla.
2, External fistula (especially of ethmoid origin).
III. Intracranial complications
1. Extradural abscess.
2. Subdural abscess.
3. Meningitis.
4. Frontal lobe abscess.
5. Cavernous sinus thrombosis.
IV. Other complications
1. Mucocele, and pyocele.
2. Lower respiratory tract infections; bronchitis, pneumonia,
bronchopneumonia, bronchial asthma.
3. Upper respiratory tract infections; pharyngitis, and laryngitis.
4. Ears ; E.T. dysfunction, and otitis media.
5. Focal sepsis.
 r

-182-

Aetiology
1. Severe acute sinusitis ; especially in children and immunocompro-
mized.
2. Acute exacerbration on top of chronic sinusitis.
Routes of spread of infectoin
A. Direct spread through bone
1. Osteitis in compact bone and osteomyelitis in cancellous bone.
2. Osteoporosis causing dehiescence in the bony walls.
3. Congenital dehiescence; or a fracture line as a result of
accidental or surgical trauma.
B. Venous spread
1. Septic venous thrombosis in the diploic veins.
2. Retrograde thrombophlebitis ; from veins draining the sinus
mucosa which communicate with the dural veins.
C. Perivascular lymphatic spread,
D. Perineural spread; along the olfactory filements to the
subarachnoid space.

Orbital complications
These are the commonest complications of sinusitis (about 75% of
orbital infections are due to sinusitis).
Aetiology
1. Ethmoiditis especially in children. The ethmoid sinuses are
separated from tlie orbit by a thin plate of bone called the lamina
papyracea.
2. Pyocele
- Maxillary sinusitis is less likely to cause orbital complications.
Clinical picture
There are five stages of orbital complications : (Fig.41)
/. Orbital oedema
Mild inflammatory reactionary oedema of the orbital contents due
to venous obstruction. Tliis is the commonest to occur especially in
children. The upper eyelid is swollen. There is no proptosis,
chemosis, diminution of vision or ophthalmoplegia).
//. Orbital cellulitis
There is diffuse oedema where the inflammatory cells and bacteria
 -183-

invade the orbit but without pus formation. There are the following
features:
1. Severe pain in the eys, aggravated by eye movement.
2. Chemosis (conjunctival injection).
3. Proptosis ; due to oedema of orbital contents.
4. Ophthalmoplegia (limitation of eye movements).
5. Diminution of vision may be present, but reversible.
///. Subperiosteal abscess
There is pus collecting on the medial side of the orbit beneath the
periosteum, which normally,acts as^abarrier, when it ruptures
infection flares up in the orbital compartments, with the formation
of orbital abscess. There are the following features :
1, Severe throbbing pain in the affected eye.
2, Chemosis.
3. Proptosis; downwards and laterally.
4. Progressive diminution of vision, but reversible.
l y . Orbital abscess
There is collection of pus within the orbit, due to rupture of a
subperiosteal abscess. There are the following features :
l^ Severe throbbing pain.
2. Marked proptosis.
3. Total opthalmoplegia.
4. Progressive impairment of vision, that may end in irreversible
blindness.
V. Cavernous sinus thrombosis :
It is due to thrombosis of the superior and inferior ophthalmic veins
(mentioned later).
Finally septicemia and pyemia may occur.
Investigations
1. Urgent C.T. scan of the paranasal sinuses and orbit.
2. Fundus examination; shows engorged retinal veins and
papilloedema in cavernous sinus thrombosis.
Treatment
1. Hospitalization.
2. Massive parenteral antibiotics to cover all the possible organisms.
- Then, monitor the response by; daily measurement of visual acuity
and C.T.scan.
 -184-

3. Surgical Treatment
Surgical drainage of a subperiosteal abscess is indicated if there is :
a. Progressive decrease in visual acuity,
b. Progression of symptoms over 24 hours, or no improvement after
48 hours despite treatment.
c. CT scan showed a subperiosteal abscess.
Approaches :
a. External frontoethmoidectomy in ethmoiditis.
b. External frontal drainage (trephine) in frontal sinusitis.
c. Endoscopic drainage may be tried.
4. Steroids if not contraindicated can be given to reduce oedema and
to save vision.
5. Surgical treatment of sinusitis after subsidence of infection.

SubfWioslMl
AteoM

OrWil
AtaCMS

Fig.41 Orbrtal complications of sinusitis

 -185-

Orbitai complications due to infection

of posterior group of sinuses
/. Orbital apex syndrome
Affection of structures passings jhroughjhe superiororbital fissure
(ophthalmic veins, ophthalnriic branch of 5th nerve, 3rd, 4th, and 6th
cranial nerves), and the optic foramen (optic nerve). There is proptosis
total ophthalmoplegia, progressive loss of vision that may end in
blindness, and pain along the distribution of the ophthalmic division of
5th nerve.
//. Superior orbital fissure syndrome
As in orbital apex syndrome, but the vision is normal.
///. Isolated optic neuritis (very rare).
Treatment
1. Medical treatment as before.
2. Steroids.
3. Drainage of the affected posterior group of sinuses, (i.e. posterior
ethmoid and sphenoid).

Osteomyelitis of skull bones

Osteomyelitis occurs in diploic bones (frontal bone and maxilla). It
is due to direct extension of infection to bones or due to thrombophlebitis
of diploic veins.
A. Frontal osteomyelitis
- There is fever, malaise, loxamia and chills. Localized severe
forehead pain, tenderness and marked oedema. The swelling
may become large and fluctuant (subperiosteal abscess) and may
rupture to produce a fistula. Sometimes, the infection is
fulminant with rapidly spreading oedema over the whole scalp
and accompanied by diffuse headache.
- Plain x-ray; shows an opacified sinus with moth-eaten appearance
of its posterior wall and the presence of bone sequestra.
- CT scan of the paranasal sinuses is important.
Treatment
1. Hospitalization and massive parenteral antibiotics.
2. External frontal drainage operation (trephine of the floor of the
frontal sinus), and a catheter is fixed for drainage until infection
subsides.
 -186-

B. Osteomyelitis of the maxilla

- It may follow maxillary sinusitis. dg_ntal infections, radiotherapy
for aatraUiimours and trauma. It usually affects children and
diabetic adults, and it is rare.
- There is pain, oedema and tenderness over the cheek. A
subperiosteal abscess forms over the canine fossa and palate
which may rupture to form an oroantral fistula.
- There is purulent nasal discharge and oedema of the lower eyelid.
- Plain x-ray and CT scan shold be done.
Treatment
1. Hospitalization with massive parenteral antibiotics.
2. Drainage of subperiosteal abscess and removal of bone
sequestra.

Meningitis
This is the commonest intracranical complication of sinusitis. The
source' of infection is most often the sphenoid and posterior ethmoid
sinuses.
Clinical picture refer to otology chapter
Investigations
1. Lumbar puncture and CSF culture.
2. CT scan should be done before lumbar puncture.
Treatment
1. Hospitalization and high dose antibiotics crossing the blood brain
barrier.
2. Surgical drainage of the affected sinus if there is no improvement
within 48 hours despite treatment.

Extradural abscess
- It most commonly follows frontal sinusitis and frontal bone
osteomyelitis.
- There is low grade fever, headache and malaise. There is pain and
tenderness over the frontal sinus. There may be manifestations of
increased intracranial tension, but without neurologic deficit.
- Investigations; CT scan paranasal sinuses and brain.
r"
-187-
t

- Treatment
Hospitalization and massive parenteral antibiotics, followed by
drainage through an osteoplastic flap.

Brain abscess (frontal lobe abscess)

r~
It occurs due to frontal or ethmoidal sinusitis, and is fatal in
20-30% of cases. It is due to septic cortical veins thrombophlebitis.
Clinical picture
There is headache, fever, malaise and anorexia. Behavioral and
personality changes are marked. The abscess may rupture before it is
large enough to cause UMN paralysis.
Investigation; CT scan of the paranasal sinuses and brain.
Treatment
L Hospitalization and antibiotics.
2. Drainage by a neurosurgeon.

Cavernous sinus thrombosis

Aetiolgoy
Spread of infection to the cavernous sinus from :
1. Skin sepsis of the face, nose and forehead (e.g. furuncle or
squeezing of a boil). Infection extends via the facial veins to the
ophthalmic veins then to the cavernous sinus.
2. Sinusitis.
3. Orbital cellulitis secondary to ethmoiditis.
4. Pharyngeal suppuraton (e.g. quinsy). Infection spreads to the
pterygoid venous plexus, and then to the cavernous sinus.
5. Lateral sinus thrombophlebitis complicating C.S.O.M. Organisms
are, pneumococci, streptococci, and staphylococci.
Clinical picture
1. High fever, rigors, toxic facies, anorexia, nausea with severe
generalized headache and rapid deterioration of the general
condition.
2. The ipsilateral eye shows;
- Swelling and oedema of the upper eyeUd.
- Forward proptosis which may be pulsating.
- Chemosis (conjunctival injection).
r
T -188-

J - Total ophthalmoplegia due to paralysis of the 3rd, 4th and 6th

r^ cranial nerves.
- Fundus examination shows papilloedema and engorged retinal
r veins.
^ - Finally, blindness may occur.
r 3. Tlie other eye may be affected (bilateral).
4. Severe oedema over the forehead and upper face in late cases.
r 5. If untreated, the patient passes into coma and death from
^^ meningitis, cereberal thrombophlebitis, and extension of
r thrombosis to the sagittal sinu. Mortality is about 30%.
'^ Investigations
r 1. Blood picture; marked leucocytosis, and increased ESR.
"^ 2. CT scan of the brain with contrast.
'^ 3. MRI with angiography (MRA and venous phase carotid
angiography.
Treatment
^ 1. Hospitalization.
r^ 2. Massive parenteral antibiotics crossing the blood brain hairier.
3. Anticoagulants and fibrinolytics.
4. Care of the comatosed.
5. If the condition is controlled, then treat sinus infection.

Mucocele
A mucocele is an expajition of the frontoethmoid air cells or rarely
sphenoid and maxillary by accumulation mass of mucoid
secretoins.
Aetiology
It is either;
A. Secondary mucocele : due to obstruction of sinus, ostium by :
1. Inflammation (oedema), and excessive scarring of the draining
T duct.
2. Osteoma and nasal polypi.
3. Trauma, accidental or surgical.
B. primary mucocele ; secondary to cystic dilatation of mucous
glands.

I
 -189-

Sites
r
L Frontal sinus is the commonest
2. Frontoethmoid is the next common.
3. It is rare in the maxillary and sphenoid sinuses.
Pathology
- Obstruction of the sinus ostium with retention of secretions.
- The cyst expands and the bony walls become thinned out and finally
destroyed, so that the cyst enlarges, and displaces the orbit and may
expose the dura.
- Histologically, it is lined by cuboidal epithelium and contains viscid
sterile mucus.
Clinical picture
1. A slowly progressive painless swelling related to the orbit; at the
inner canthus (ethmoidal) or at the medial half of the orbital roof
under the supraorbital ridge (frontal). It is hard and cannot be
T compressed; but occasionally an egg-shell crackling sensation is
felt if the bone is thinned out, and later, fluctuation can be elicited
if bone is destroyed.
2. Proptosis, downwards and outwards, due to displacement of the eye
globe by a large mucocele.
3. Frontal headache is common.
4. When infected (i.e. mucopyocele), the overlying skin become red
and hot with oedema, and tenderness. There is purulent nasal
discharge. A mucopyocele may rupture at the inner canthus to
produce a fistula, and may lead to orbital complications and
intracranial complications if the dura is exposed.
5. Pulsations indicate exposure of the dura of the frontal lobe.
6. Occasionally, a mucocele or a mucopyocele is seen in the middle
meatus.
Investigations
1. Plain x-ray; shows sinus opacity, the affected sinus is larger than
the opposite side, deficient bony roof of the orbit, rarifaction of
bone, and loss of the scalloped appearence of the fronal sinus.
2. CT scan and MRI of the paranasal sinuses are diagnostic.
Treatment
The aim is to evacuate the mucocele and to establish adequate
drainage to avoid recurrence.
 -190-

1. Frontal mucocele
a. External frontal operation (trephine of the floor of the frontal
sinus).
b. Osteoplastic frontal flap operation in recurrent cases with
destruction of the posterior table of the frontal bone.
2. Ethmoidal or frontoethmoidal mucocele
a. External frontoethmoidectomy.
b. Endoscopic intranasal drainage, if it is large and bulges in the
middle meatus.
- A tube or a catheter should be placed in the sinus ostium for
2-3months in order to establish drainage and to maintain its patency
and prevent recurrence.
3. Mucocele of the maxillary sinus; endoscopic middle meatal
antrostomy.
4. Sphenoidal mucocele; endoscopic intranasal removal of the
anterior wall of the sphenoid sinus.
5. In mucopyocele; drainage, with massive preoperative and
postoperative antibiotic coverage.
 -^

-191-

Allergic rhinitis
Allergy is a state of exaggerated susceptibility to various foreign
substances and physical agents, that are harmless to normal individuals.
Allergic rhinitis is an IgE-mediated hypersensitivity disease of the
mucous membrane of the nose upon exposure to an antigenic substance
to which the individual was previously sensidzed, and is characterized by
sneezing, itching, watery nasal discharge and a sensation of nasal
obstrucdon.
Incidence
It is extreemly common, affecting 10-20% of the populadon.
Allergic rhinitis is either;
a. Seasonal e.g. summer hay fever.
b. Perennial (allover the year).
c. Perennial widi seasonal exacerbadons.
Aetiology
Predisposing factors:
1. Genetic predisposition : (in 50% of cases). Allergic rhinius occurs
in atopic paUents. Atopy is the tendency to develop an exaggerated
IgE antibody response, and allergy is the clinical expression of
atopic disease, (e.g. rhinitis, asthma, and eczema). Atopy is
inherited among families.
2. Changes in temprature and humidity.
3. Repeated and persistent infections.
4. Psychogenic : It is claimed to occur in neurotic patients.
Exciting factors : (Environmental allergen).
1. Inhalants (areoallergens): This is the commonest factor.
- Tree and grass pollens (seasonal rhinids).
- House dust mites and domestic pets (perennial rhinitis).
- Occupational e.g. flour among bakers, wood among carpenters
and latex among nurses and doctors (occupauonal rhinitis).
2. Infectants : parasitic, fungal and bacterial andgens.
3. Injectants ; e.g. penicillin and insulin.
4. Ingestants : (food and drug induced rhinius). Food e.g. milk, fish,
eggs, (food preservatives, drugs e.g. Aspirin, and
anuhypertensives).
5. Contacts : e.g. face powders.
 -192-

- Usually susceptible individuals are allergic to multiple allergens.

- Air pollution has a great role.
Pathogenesis; (Type I hypersenstivity reaction)
- Upon exposure to a specific allergen for the fu-st time, production of
allergic specific IgE antibodies will occur, that will bind to a
specific receptor site on the surface of mast cells present in the
nasal mucosa, and thus they will be sensitized to that specific
allergen.
- On re-exposure to the same allergen, it will bind to the fixed IgE on
the surface of mast cells with subsequent degranulation of the cells
and release of their chemical mediators.
- These mediators will act upon the target organs in the nasal mucosa
producing the characteristic inflammatory reaction and increased
air-way resistance.
- Tliis reaction consists of :
a. Vascular vasodilatation and increased capillary permeability with
exudation of plasma.
b. Increased secretions by seromucinous glands.
c. Cellular infiltrations especially eosinophils.
d. Smooth muscle contraction.
e. Oedema of the mucous membrane with the formation of polypi.
- The chemical mediators released are, Histamine, bradykinine,
serotonine, slowly reacting substance of anaphylaxis (SRSA),
leukotrines, vasoactive substances, and enzymes e.g. tryptase.
N.B.: - The mucosa of the nose is continuous with that of the sinuses,
so they are usually involved (i.e. allergic rhinosinusitis).
Clinical picture
Symptoms
The allergic response starts by a rapid onset on exposure to a
specific allergen (which is usually difficult to identify) and it consists of:
1. Sense of itching in the nose and palate.
2. Repeated paroxysmal prolonged sneezing.
3. Bilateral profuse watery nasal discharge.
4. Bilateral nasal obstructoin.
5. Other manifestations of associated allergy :
- Conjunctival congestion and excessive lacrimation (watery itchy
eyes) due to associated allergic conjunctivitis.
- Bronchial asthma, eczema, urticaria.
6. There is positive family history in 50% of cases.
 -193-

Signs
1. The nasal mucosa is oedematous, moist and pale blue.
2. Swollen oedematous turbinates.
3. Excessive mucoid thin secretions.
4. Nasal polypi may be present in the middle meatus. They arise from
the ethmoid sinuses.
Investigations
1. Nasal cytology; examination of nasal secretion shows eosinophilia.
2. Skin prick testing (sJin sensitivity test):
- The skin of the forearm is pricked with a needle passed in extracts
of suspected allergens. A positive test is detected by the
development of a central wheel surrounded by erythema.
- Value :
• rapid, fairly accurate and can be done for a variety of antigens.
• diagnose or exclude atopy,
• provides a helpful and supportive evidence for the history.
3. Nasal challenge test: An allergen is applied in a spray form to the
nose. Positive reaction is manifested by sneezing, rhinorrhea, nasal
obstruction and lacrimation.
4. Radioallergosorbency test (RAST) : Incubation of patient's serum
(containing antibodies) with specific concentrations of specific
antigens. The IgE level is measured by radioimmunoassay.
5. High IgE levels in serum by radioimmunoassay.
Treatment
A. Allegen avoidance; avoiding exposure to the offending antigen.
B. Medical Treatment
1. Antihistaminics e.g. Astemizole, Loratidine, and cetrizine.
- They are given orally. Recently avialable as spray (azelastine).
2. Topical decongestant nasal drops for temporary relief of nasal
blockage. They should be used only for short periods as
prolonged use may cause rhinitis medicamentosa.
3. Oral decongestants.
4. StgrQJds;
a. Topical steroid preparations eg. spray or drops as
beclomethazone.
b. Short courses of systemic steroids can be used in severe cases.
c. Local steroid injection into the inferior tubinate has been tried.
 -194-

5. Mast cell stabilizer eg, sodium chromoglycate used as spray or

oral, to prevent degranulation of mast cells.
6. Recently antileukotrincs are tried eg. Zuflo.
C. Immunotherapy; (allergen hyposensitization)
This is done by injecting gradually increasing doses of extracts of a
specific allergen over a long period of time. This will lead to production
of IgE (blocking antibodies), which binds to the antigen, and prevents it
from binding with IgE. This is useful in seasonal allergy,
D. Surgery
1. Reduction of the size of
the inferior turbinates if
grossly hypcrtrophied, by
partial turbinectomy,
submucous diathermy
(Fig.42), or laser.
2. Nasal polypectomy for
associated nasal polypi. f^ig 42 submucous
diathermy of the inferior turbinat

Nasal polyps
These are projections of oedematous pedunculated prolapsed
r' -
mucosa of the nose or ethmoid sinuses. A special type occur in the
maxillary sinus (antrochoanal polyp).
Aetiology
1. Allergy; this is the most accepted cause, as 90% of nasal polyps
show eosinophilia, furthermore bronchial asthma is present in
20-40% of cases, and allergic rhinitis is uaually present.
2. Inflammatory; especially chronic ethmoidal sinusitis.
3. Mixed allergy and 2ry bacterial infections.
4. It may accompany malignant neoplasms of the nose and
nasopharynx. It is due to lymphatic obstruction and biopsy from the
polyp is always negativefor biopsy so, a deeper biopsy must be
taken in order not to miss the diagnosis.
5. Vasomotor imbalance.
6. Allergic fungal sinusitis (Aspergillosis).
 -195-

N.B. ; Some patients have the triad of aspirin sensitivity, bronchial

asthmna, and nasal polypi, and the cause is claimed to be
alteration of prostaglandins synthesis.
Sex : It affects males more than females (3:1).
Age: - Adults.
- It is rare in children, but if it affects a child between 2-10
years cystic fibrosis (mucoviscidosis) should be suspected.
/. Ethmoidal (allergic) nasal polypi
These are the most common. They arise from the ethmoid sinuses
or from the middle meatus. This region bears the brunt of the allergic
reaction and in addition there is a very loose submucosa in this area.
Pathology
The polypi are covered by ciliated columnar epithelium with areas
of squamous metaplasia due to chronic irritation. The loose submucosa is
grossly distended by tissue oedema. The cellular infiltrate is formed
mainly of plasma cells, lymphocytes, macrophages, and eosinophils.
Early, oedema is reversible, but later, it becomes irreversible.
Clinical picture
Symptoms
1. Bilateral continuous nasal obstruction is the leading symptom.
2. Watery nasal discharge and sneezing may be present.
3. Mucopurulent nasal discharge if there is secondary infection.
4. Hyposmia and alterations in taste.
5. Facial pain over the bridge of the nose and vertex. Headache may
be present.
6. Epiphora due to obstruction of the nasolacrimal duct.
7. Postnasal drip.
8. Infrequent epistaxis» but this is not common.
Signs
1. Distension of the nose and broadening of the nasal bridge
(hypertolirism) in long standing cases and in children with cystic
fibrosis before fusion of the nasal bones.
2. Anterior rhinoscopy shows; bilateral multiple insensitive masses,
that are soft, smooth, mobile, glistening, pale or greyish white, and
pedunculated (probe can be passed all around). They arise in the
region of the middle meatus. If the polypi are large and protrude
externally, they become exposed to trauma with secondary
infection and ulceration.
 T

-196-

Investigations
1. CT scan of the nose and paranasal sinuses; to detect the extent of
polypi, condition of the sinuses, and the anatomical landmarks
prior to surgery.
2. Investigations for allergy.
3. Investigations for cystic fibrosis in children (sodium level in sweat).
Treatment
It is usually a combination of medical and surgical treatment.
A. Medical
7. Steroids
- A trial of systemic steroids (5-30 mg/day for 10 days to be
tapered gradually) may be sufficient in small non obstructing
polypi.
- Topical steroid e.g. beclomethasone spray.
2. Antibiotics if there is secondary infection.
3. The rest of antiallergic treatment as mentioned before.
B. Surgery
1. Simple polypectomy by
avulsion snare. (Fig.43)
2. Intranasal ethmoidectomy
either endoscopic or by the
aid of microscope.
- Preoperative steroids
(topical and systemic)
and antibiotics are
advisable to decrease
oedema and congestion.
- There is a high rate of
recurrence after surgery
reaching 40%, in 9 Fig,43. polypectomy using a snare
months to 2 years.
//. Antrochoanalpolyp (Killian polyp)
~ This is a single unilateral polyp which arises from the mucosa of the
maxillary sinus, and prolapse through the ostium of the sinus into
the nose, where it passes through the choana to reach thQ
nasopharynx. (Fig.44)
- It is more common in males, and occurs mostly in children and
young adults.
 -197-

Pathology; similar to ethmoidal polypi, but the cellular infiltrate lacks

eosinophilia.
Clinical picture
Symptoms
1. Unilateral nasal obstruction, later it reaches up to complete
obstruction when the polyp reaches the nasopharynx.
2. Accumulated mucoid or mucopurulent discharge in the obstructed
side of the nose.
3. Snoring and rhinolalia clausea.
Signs
1. Anterior rhinoscopy shows :
- Swollen inferior turbinate.
- Accumulated mucoid secretions on the floor of the nose.
- Sometimes the greyish, soft. Jelly-like polyp is seen.
2. Posterior rhinoscopy and digital palpation; show the smooth, soft,
greyish white spherical mass occupying one choana and projecting
into the nasopharynx. It should be differentiated from
angiofibroma,
3. When the polyp is large it may cause sagging of the soft palate or
even appear in the oropharynx.
Investigation
1. Plain x-ray; shows unilateral maxillary sinus opacity.
2. CT scan of the paranasal sinuses is conclusive.

Fig.44 Antrochoanal polyp

 - 198-

Treatment
1. Removal of the polyp from the nose gently to withdraw the part in
the maxillary sinus. Tliis can be done by the use of an endoscope or
microscope.
2. Radical antrum operation (Caldwell luc's) in recurrent cases.

Vasomotor rhinitis
It is also called intrinsic rhinids or non allergic perennial rhinids. It
may be related to drugs (e.g. antihypertensives and contracepdves)
or hormonal imbalance at menopause.
Clinical picture
1. Nasal obstrucdon and watery nasal discharge, which is often
precipitated by temperature changes, and dusty atmosphere.
2. Examination; shows swollen, oedematous turbinates, with excessive
mucoid secretions.
Treatment
It is often unsatisfactory.
1, Topical steroids may be beneficial.
2. If the turbinates are markedly swollen we may do submucous
diathermy or submucosal injection of long acting steroids.

Fungal infections of the nose and sinuses

- It is divided clinically into four categories :
A. Mycetoma.
B. Indolent (chronic) form.
C. Allergic fungal sinusitis.
D. Fulminant (invasive) form.
- Tredisposing factors :
A. Local
1. Obstruction of the sinus ostium.
2. Defective mucociliary clearance.
B. General :
Decreased general resistance in;
1. Patients on prolonged course of antibiotics and steroid therapy.
2. Patients on immunosuppressive therapy.
3. Diabetes, malignancies, leukaemia, and AIDS.
 -199-

A. Mycetoma
This is an isolated condition with minimal symptoms, in which
there is collection of mucus within the maxillary sinus together with
hyphae of the fungi. The condition only becomes symptomatic when
there is obstruction of the sinus ostium and secondary bacterial infection,
B. Indolent (chronic) form;
This usually passes undiagnosed as it manifests as chronic bacterial
sinusitis.
Treatment of mycetomas and indolent forms
1. Treat the bacterial infection.
2. Proper drainage of the sinus.
C. Allergic fungal sinusitis
- The organism is an aspergillus in most cases.
- There is usually a history of nasal allergy and bronchial asthma.
Nasal allergic polypi are always seen in addition to greenish brown
mucoid nasal discharge. It may cause bone expansion towards the
orbit or intracranial extension.
- CT scan of the paranasal sinuses, show the characteristic
heterogenous opacity with mottled appearance.
Treatment
1. Treatment of allergy; short course of systemic steroids and topical
steroids.
2. Systemic antifungal therapy e.g. oral fluconazole is used.
Amphotericin B is given if there is intracranial extension, or orbital
involvement.
3. Surgical excision either endoscopic if it is localized or through an
external approach if there is massive invasion or failed endoscopic
surgery.
D. Fulminant (invasive) form; Rhino-orbital and Rhino-cerebral
mucormycosis).
- This usually occurs in diabetics with ketoacidosis or
immunosuppressed patients receiving cytotoxic chemotherapy.
- There is necrosis with gangrenous blackish discolaration of the
middle and inferior turbinates, that may extend to the palate and
skin. It is due to subintimal haemorrhage and vascular ischemia.
- There is serosangineous nasal discharge.
- There is a high tendency towards intravascular extension;
 -200-

a. to the orbit with proptosis, diminution of vision and finally

blindness.
B. intracranially, leading to neurological deficits, cranial nerve
palsies and may end in coma and death.
CT scan the paranasal sinuses is essential and diagnostic.
Treatment
1. Control diabetes or stop immunosuppressive drug.
2. Systemic antifungal therapy; I.V. drip of amphotericin B
(fungizone) is the drug of choice. It is hepatotoxic and nephrotoxic,
daily liver and kidney function tests should be done.
Amphotericin B may be applied locally as a nasal wash where 50cc
of fungizone are disolved in 500 ml saline.
3. Surgery; surgical drainage of the sinus involved, debridement and if
needed orbital exenteration.
 -201-

Tumours of the nose and paranasal sinuses

Pathological Classincation
Benign Intermediate Malignant

Epilhelial papilloma Inverted papilloma squamous cell carcinoma

adenoma leukoplakia Adenocarcinoma
neavus Adenoidcystic carcinoma
olfactory neuroblastoma

Mesenchymal Haemangioma osteoclastoma Angiosarcoma

osteoma chordoma osteosarcoma
chondroma haemangiopericytoma Ewing's surrcoma
fibroma Teratoma Chondrosarcoma
neurofibroma Fibrosarcoma
schwannoma lymphoma

Oodontogenic Dental and dentig- Adamantinoma

erous cysts Odontogenic,
Keratocyst

Metastatic From carcinoma in the

lung, prostate, kidney,
breasts, (rare)

Benign tumours
The most common Benign tumour is osteoma, and the next
common are haemangioma and papilloma (skin warts of the nasal
vestibule).
/. Osteoma
This is the most common benign tumour of the nose & sinuses. It
possibly ar.ses from persistent embryonal periosteum
particularly ia areas where endochondral and membranous bone
meet (e.g. at the junction between the frontal & ethmoidal
sinuses).
Age : young adult 15-30 years.
 -202-

Sites
Frontal sinus (70%) ethmoids.(25%), maxillary and sphenoid (5%),
and nasal bones (5%).
Types
A, Ivory (compact) osteoma
This is the commonest type. It affects the frontal sinus which arises
from membranous bone. Microscopically, it is fromed of compact
lamellar bone and few fibroblasts.
B, Cancellous (spongy) osteoma
This usually affects the ethmoidal and maxillary sinuses.
Mircoscopically, it is formed of irregular trabeculae of spongy bone
separated by excess fibrous tissue.
Clinical picture
1. Many cases are asymptomatic, and are discovered accidentally on
x-ray examination of the sinuses done for an unrelated cause.
2. Facial pain and headache due to bone expansion.
3. Bony swelling at the medial canthus and proptosis due to
enchroachment upon the orbit.
4. Gradually increasing nasal obstruction as it involves the nasal
cavity.
5. Secondary mucocele or mucopyocelc may occur due to obstruction
of the sinus ostium.
6. Intracranial extension due to pressure atrophy of the posterior table
of the frontal bone, with the occurrence of pressure symptoms.
7. CSF rhinorrhea may occur due to pressure necrosis of the
cribriform plate.
8. Examination of the nose may reveal a hard, rounded, well defined
pedunculated or sessile mass, often pinkish in colour and is slowly
growing.
Investigations
1. Plain x-ray; shows a rounded well defined mass.
2. CT scan of the paranasal sinuses; shows the osteoma and its
extension. It is important step before surgical excision.
Treatment
Surgical excision if large and symptoinatizing, or rapidly growing.
It is done by an external approach.
1. Frontal osteoma; frontal trephine operation if small, or frontal
 -203-

osteoplastic flap if large and destroying the posterior table of the

frontal bone.
2. Ethmoidal osteoma; external frontoethmoidectomy. If small, it can
be removed endoscopically.
3. Maxillary osteoma; Cadlwell-Iuc's approach.
N.B. : Gardner's syndrome : This is the association of craniofacial
osteomas, soft tissue masses (e.g. sebaceous cyst, subcutaneous
fibroma) and colonic polyposis. The mandible is the commonest
site of osteoma, but the sinuses can be also affected. It is an
inherited defect, and the colonic polypi may turn malignant if
untreated.
//. Fibrous dysplasia (ossifying firboma = fibrous osteoma)
- This is not a true neoplasm. It affects teen agers and females are
affected more than males. Microscopically, it is formed of fibrous
tissue, and cancellous osseous tissue (woven bone) in various
proportions. When active, the fibrous tissue is predominant, and as
it matures the osseous tissue increases (i.e. stabilized).
- The cause of fibrous dysplasia is unknown, but it may be
developmental.
Site
It affect the mandible and the maxilla.
Types
1. Monostotic (localized): involving a single site e.g. maxilla.
2. Polystotic : involving several facial and cranial bones unilaterally.
3. Albright syndrome : This a syndrome that affects females. It
consists of unilateral polystotic fibrous dysplasia, pigmentation of
the skin and nucous membrane near the midline, precocious
puberty, and other endocrinal manifestations (e.g. thyrotoxicosis,
acromegally and diabetes).
Clinical picture
1. Marked disfigurement with painless enlargement of the maxilla,
and headache.
2. The swelling is bony hard, diffuse, ill defined, not tender and with a
smooth surface. It is slowly growing and tends to stabilize at the
age of sexual maturity.
3. Nasal obstruction and proptosis may occur with further
enlargement.
 r
-204-

Investigations
1. Plain x-ray; shows dense heterogenous opacity (ground-glas
appearence). There is no bone erosion.
2. CT scan of the paranasal sinuses.
Treatment
Surgical removal; either total or partial removal through a sublabial
incision (if involving the maxilla). Generally, excision is better avoided
except for cosmetic reasons as it usually recurs.
///. Papilloma
A. Squamous cell papilloma (wart)
It arises from the skin of the vestibule and adjoining parts of the
septum. Microscopically, it is composed of a vascular core of
connective tissue, coverred by hyperplastic squamous epithelium. It
is seen as a small, single or multiple, pedunculated, warty growth
with a wide base.
Treatment
Surigcal exicision and cauterize the b^se.
B. Inverted papilloma (Transitional cell papilloma = Schniederian
papilloma
This is an intermediate (potentially malignant) tumour, which is
locally aggressive. It occurs at the age of 40-50 years with male
predominance. It arises from the lateral wall of the nose, but may
arise from the maxillary and ethmoid sinuses. Microscopically; it
arises from the schneiderian membrane of the epithelial lining of
the nose (which is derived from ectoderm, while the rest of
respiratory epithelium is derived from endoderm). There is gross
thickening and infolding of the epithelium producing deep
invaginations of the epithelium into the underlying stroma. The
epithelial covering consists of alternating layers of squamous,
columnar ciliated, and transitional epithelium.
Clinical picture
1, Unilateral progressive nasal obstruction, nasal discharge, and
recurrent epistaxis. There is epiphora and fullness of the nasal
fossa.
2. On examination : There is unilateral firm reddish grey mass
arising from the lateral wall of the nose. It usually presents as a
recurrent nasal mass after previous surgical excisions.
 -205-

Investigations
1. CT scan of the paranasal sinuses.
2. Biopsy and histopathological examination.
Treatment
1. Wide surgical excision through a lateral rhinotomy and medial
maxillectomy. This is needed especially in recurrent cases.
2. Endoscopic excision may be done for small localized lesions,
however, it carries a high incidence of recurrence.
- Recurrence is very common and each time it is more destructive.
Malignancy should be always suspected, as malignant
transformation occur in 5-10% of cases, which may be early or
as late as 20 years.
IV. Haenangioma
This is the commonest connective tissue tumour of the nose. There
are three types :
1. Capillary haemangioma
This is the most common and usually occurs after puberty. It occurs
on the anterior end of the septum (bleeding polypus of the septum),
where is appears as a sessile or pedunculated polyp, soft, red blue
or purple and bleeds easily on touch.
Treatment
Surgical excision and cauterize the base, or excision by laser.
2. Cavernous haemangiona
It affects children, and is located on the lateral wall of the nose. It
appears as a variable sized, vascular mass, that bleeds easily on
touch. There is usually frequent epistaxis. It may develope into a
cirsoid aneurysm to involve the whole tip of the nose.
Treatment
Excision by laser or cryosurgery.
3. Multiple telangectasia (see epistaxis)

Intermediate (locally malignant) tumours

/. Inverted papilloma; (mentioned before).
/ / . Adamantinoma; (Ameloblastoma).
It is a rare, locally invasive odontogenic tumour (but still the most
common adontogenic tumour). It usually occurs in the fourth and fifth
decades, and females are more commonly affected than females.
 -206-

- Origin : (odontogenic). It arises from the epithelium responsible for

tooth formation (residues of the dental lamina, or enamel organ).
- Site : Most commonly affects the mandible particularly the ramus
and the angle of mandible, less commonly it affects the maxilla.
- Microscopically, it resembles basal cell carcinoma where strands of
columnar epithelium are arranged in a pallisade manner with intact
basement membrane. Cut section shows shows cystic and solid
areas and the cysts contain brownish mucoid fluid.
Clinical picture
Slow expansion of the mandible or the upper jaw producing facial
deformity. The expansion is bony hard, but in advanced cases an egg
shell crackling sensation is apparent due to thinning of the cortical plate.
Later it ulcerates through the teeth socket and invades the soft tissues.
Other features are loose teeth, illfitting denture, and malocclusion of the
mandible.
Investigations
1. Plain x-ray; shows mukilocular radiolucent areas with well defined
borders.
2. CT scan of the paranasal sinues.
3. Biopsy and histopathological examination.
Treatment
Radical resection of the affected part of the mandible and then
reconstruction by a rib graft. If affects the maxilla, do partial
maxillectomy and reconstruction by a dental prosthesis,
///, Osteoclastoma
This is a locally malignant tumour of osseous origin. Plain x-ray
shows the characteristic soap-bubble or honeycoomb apperance. It is
treated by a wide surgical excision.

Malignant tumours of the nose and

paranasal sinuses
Cancer of the nasal cavities and paranasal sinuses constitutes about
1% of all malignancies and 3% of head and neck malignancies.
Age : Carcinomas affect old age group (50-70 years). Sarcomas affect
young age groups (20-30 years).
- Sex : males are more affected than females (2:1).
- Squamous cell carcinoma is the most common, representing about
7o of all cases.
 -207-

predisposing factors
1. Exposure to formaldehyde vapour, wood dust and nickel,
predisposes to squamous cell carcinoma.
2. Wood workers and leather workers are susceptible to
adenocarcinoma.
3. Hydrocarbons, chrome pigmants and radium paints.
4. Chronic rhinosinusitis (doubtful).
Pathology
Site; the maxillary sinus is the commonest (antroethmoidal angle)
(60%), followed by the nasal cavity (20%, from lateral wall or
floor), ethmoid sinus (10%). Sphenoidal and septal cancers are
very rare.
Microscopically
a. Squamous cell carcinoma with variable degrees of differentiation is
the commonest (80%).
b. Adenocarcinoma (5-10%), and adenoid cystic carcinoma (5-10%).
They arise from minor salivary glands.
c. Undifferentiated carcinoma, olfactory neuroblastoma and malignant
melanoma are rare.
Clinical picture
- The presentation depends upon the primary site the direction and the
extent of spread.
- Antral (maxillary) tumours are unlikely to present early and usually
they are diagnosed late after they have spread to the surrounding
structures. However, unilateral epistaxis or unilateral offensive
blood stained discharge in an elderly patient should be taken
seriously.
- Mostly, they are antroethmoidal tumours and present with the
following manifestations :
A. Manifestation of spread; (a late picture)
1. Downwards to the oral cavity and palate leading to :
a. Unilateral dull aching, persistent dental pain of the upper molars
and premolars. Pain that presists after extraction of a loose tooth
is common.
b. Unilateral loosening of the teeth.
c. Persistent oroantral fistula with offensive blood stained discharge
after tooth extraction.
 -208-

d. Swelling and later ulcertain of the palate, alveolar ridge and

gingivobuccal sulcus.
- These are the earliest manifestations of antroalveolar tumours
(infrastracture location).
2. Upwards to the orbit leading to unilateral:
a. Proptosis, diplopia, and pain felt over the eyes.
b. Opthalmoplegia due to invasion of the orbital muscles and
nerves.
c. Diminution of vision, and finally blindness may occur.
- These are the earliest manifestations of antroethmoidal
(suprastructure) tumours.
3. Posterior spread to the pterygopalatine and infratemporal fossa
leading to:
a. Trismus due to involvement of pterygoid muscles.
b. Numbness, parasthesia and anaesthesia over the cheek due to
involvement of the maxillary nerve.
c. Absent corneal reflex due to involvement of the sphenopalatine
ganglion.
d. Palatal numbness and loss of sensation over one side of the
palate due to involvement of the maxillary nerve or the greater
palatine nerve.
4. Medially to the nasal cavity leading to :
a. Unilateral nasal obstruction which is progressive.
b. Unilateral offensive blood stained discharge and may be
epistaxis.
c. Unilateral epiphora due to infiltration of the nasolacrimal duct.
d. Anterior rhinoscopy, may show a unilateral nasal mass arising
from the lateral wall of the nose which is soft, friable, polypoid,
with surface ulceration and haemorrhage. It bleeds easily on
touch with a probe. There may be displacement or erosion of the
septum with extension to other side.
5. Anterolateral spread; to the soft tissues of the face producesing
facial swelling with fullness of the nasolabial fold and blunting
of the infraorbital margin. There is also unilateral facial pain,
and in advanced cases there is ulceration of the skin over the
cheek.
 •^^IP

-209-

- Tumours arising primarily in the :

a. Ethmoid sinuses; there will be early nasal, and orbital
manifestations. Unilteral CSF rhinorrhea and anosmia may
occur due to erosion of the roof of the nose (floor of the anterior
cranial fossa, and this occurs particulalry in olfactory
neuroblastoma which arises from the olfactory epithelium in the
superior part of the nose. Swelling in the region of the inner
canthus and broadening of the nasal bridge may occur.
b. Nasal cavity; Presents early with nasal symptoms of obstruction
and epistaxis. Then it invads the sinuses.
c. Sphenoid sinus tumours; generally present late with
neurological symptoms. There will be headache, diplopia and
vision loss due to invasion of the optic nerve and the optic
chiasma. Invasion of the skull base exists in 50% of cases.
A. Metastatic manifestations
1. Lymphatic spread
- It is rare in maxillary tumours except if the soft tissues and skin
are infiltrated.
- Anterior group of sinuses (maxillary and anterior ethmoids)
produce metastasis to the submandibular and upper deep cervical
lymph nodes.
- Spread to the retropharyngeal nodes may occur and this may give
rise to 9th, 10th, and 11th cranial nerve palsies and Horner's
syndrome (due to invasion of cervical sympathetic chain).
However, they are not clinically palpable.
- Palpable cervical nodes are present in about 15% of patients on
there fost presentation.
2. Blood spread; (rare and late)
a. Lung; chest pain, dysponea, cough, haemoptysis, and malignant
pleural effusion.
b. Liver; pain in the right hypochondrium, jaundice.
c. Bones; bony aches, bony swellings and pathological fractures.
3. Cachexia and weight loss
Investigations
1. Plain x-ray; shows a soft tissue mass, with expansion of the sinus
and bone erosion particularly the lateral wall of the maxilla.
2. CT scan of the paranasal sinuses; This is very important to locate
the site and extensions of the tumour, bone erosion, intracranial
extension and non palpable node metastasis.
 -210-

3. MRI; useful particularly to detect soft tissued invasion (e.g. orbit,

pterygopalatine fossa, and intracranial extension).
4. Biopsy and histopathological examination; this is essential to
confirm the diagnosis. It is obtained from any apparent nasal mass
or palatal mass. Biopsy from antral tumours can be taken either by
nasoendoscopy or sublabial antroscopy.
Classification
Two systems were
adopted for planning
management and
prognosis.
A. Ohngren's classifi-
cation; (The older
one), where two re-
gions were delinated
by a line passing
across the inner can-
thus and the angle of
the meandible, to
seperate the anterio-
ferior (Fig.45)
Rq-4^
(infrastructure) from
the posterosuperior
(suprastructure):
B. Lederman classification; (the recent one), where three regions
were delineated; the suprastructure, mesostructure and
infrastructure.
The most important to be taken is that lesions involving the
infrastructure present as palatal lesions and carries a better prognosis as
regard complete eradication by partial maxillectomy, on the contrary,
lesions involving the suprastructure carries a less favourable prognosis,
because they involve mostly the ethmoid region which is composed of
many bony cells and is difficult to eradicate radically with an adequate
safety margin.
Treatment
Combined surgery and postoperative radiotherapy is the treatment of
choice. It could be curative if resecton is complete.
Operations performed
• Total maxillectomy or partial maxillectomy according to the
extent of the tumour, including exenteration of the ethmoid
cells, orbital exenteradon is done if the orbit is involved.
 -211-

a. Parial maxillectomy includes :

- Medial maxillectomy by a lateral rhinotomy approach,
- Palatal resection (inferior maxillectomy) through a sublabial
approach.
b. Total maxillectomy (Fig.46); it entails total removal of the
maxilla as a bony box (including the hard palate and the jaw).
It is approached by a weber-fergusson incision. The maxilla
is freed by osteotomies at the frontal process of the maxilla,
body of the zygoma and midline of the palate. After resection
of the maxilla, the ethmoid cells are exenterated, and the
sphenoid and frontal sinuses are opened widely.
• A pack is left for 48-72 hours.
• Reconstruction is done immediately by a temporary dental
prosthesis to support the pack, allows feeding and speech, and
two protect the area from being soaked by infected saliva. After
healing, it is changed to a permanent prosthesis.
• Orbital exenteration is done if the orbit is involved clinically,
radiologically, or invasion of the orbital periosteum as detected
intraoperatively.
• Radical neck dissection is done if there are palpable cervical
lymph nodes, although rare.
• Craniofacial resection entails extension of resection to involve the
roof of ethmoids and the cribriform plate if involved. This is
needed especially in olfactory neuroblastoma as it arises from
the olfactory epithelium situated in the roof of the nose.
* Postoperative radiotherapy is given as it improves the locoregional
control.
Chemotherapy; may be used although not effective as a single
modality. It is given either systemically or locally intra-arterial (no
longer used). Cytotoxic drugs used include endoxan, Nitrogen
mustarde, and methotrexate.
Palliative treatment
- Indicated in inoperable cases :
a. Bilateral involvement of the nasal cavities orbits, or sinuses.
b. Extension to the retromolar trigone, pterygopalatine fossa, or
intracranially beyond the optic chiasma.
c. Paralysis of the 9th, 10th, and 11th cranial nerves, and the
cervical sympathedc by enlarged retropharyngeal nodes.
 Il

-212-

d. Distant metastasis.
e. Enlarged fixed cervical lymph nodes.
Methods:
a. Chemotherapy and/or radiotherapy.
b. Adequate alimentation.
c. Pain killers.

Fig 46, Total

maxillectomy

Cysts of the nose and paranasal sinuses

/. Congenital
Dermoid cyst
Commonly, it occurs in the midline at the bridge of the nose. It is
hemispherical and firm with a blackish small depressed spot at its
center (punctum). It is liable for recurrent infection. It is treated by
surgical exision (avoid opening the capsule during excision).
//. Odontogenic systs, (cysts related to the jaw and teeth)
1. Dentigerous cyst (follicular cyst)
- It is due to cystic degeneration of the follicle (crown) of an
unerupted tooth.
[ - It occurs in children.
"^ - There is swelling of the maxilla.
- Plain x-ray shows the cyst and inside it there is an unerupted
tooth.
- Treatment: excision by the sublabial route.
2. Dental cyst
- It arises in relation to a septic tooth.
' - It occurs in adults.
- Plain x-ray shows the cyst.
- Treatment: excision and removal of the carious tooth.
T" 3. Adamantinoma ; (mentioned before).

T
 -213-

///. Non odontogenic developmental cysts

1. Nasopalatine (incisive canal) cyst : It arises from the epithelial
remnants of the nasopalatine duct that connects the oral and the
nasal cavities in the embryo. It presents as a slowly enlarging
swelling in the anterior part of the palate just behind the incisors.
Secondary infecdon may occur. Plain x-ray is diagnostic.
Treatment: Exision using a palatal flap.
2. Nasolabial (Nasoalveolar cyst) : It arises in the upper lip just
below the alar margin of the nose. It appears as a slowly enlarging
swelling that fills the nasolabial fold and pushes the nostril. It
produces a bulge in the floor of the nose. It can be palapated as a
fluctuant swelling within the labial sulcus.
IV Other cysts
1. Solitary bone cyst.
2, Aneurysmal bone cyst.
V. Mucocele
Cystic expansion of the sinus (mentioned before).
 -214-

Symptoms and signs of nasal diseases

1. Nasal obstruction.
2. Nasal discharge.
3. Epistaxis.
4. Facial pain and headache.
5. Abnormalities of smell.
6. Proptosis.
Nasal obstruction
A. Bilateral nasal obstruction
1. Congenital; bilateral congenital choanal atresia.
2. Oevelopmental; S-shaped deviated septum.
3. Traumatic :
a. Fracture nose.
b. Septal haematoma.
4. Inflammadons :
a. Acute and crhonic rhinitis.
b. Acute and chronic sinusitis.
c. Septal abscess.
5. Allergic and vasomotor rhinitis.
6. Bilateral allergic nasal polypi.
7. Neoplastic : Extensive malignant tumours of the nose and sinuses.
8. Granulomas of the nose e.g. Rhinocleroma, lupus, syphilis, and
leprosy.
9. Nasopharyngeal swellings :
a. Adenoids.
b. Cysts.
c. Benign tumours eg. angiofibroma.
d. Malignant tumours e.g. carcinoma and lymphoma.
B. Unilateral nasal obstruction
1. Congenital; unilateral congenital choanal atresia.
2. Developmental; deviated septume.
3. Traumatic :
a. Fracture nose.
b. foreign body.
4. Inflammatory :
a. Unilateral sinusitis e.g. of dental origin.
 -215-

b. Nasal diphtheria.
5. Antrochoanal polyp.
6. Bengin and malignant tumours of the nose and sinuses limited to
one side.
Nasal discharge
A. Bilateral nasal discharge
1. Watery
a. allergic rhinitis.
b. Ischaemic stage of acute rhinitis.
c. vasomotor rfiinitis.
d. Excessive lacrimation.
2. Bloody; all causes of epistaxis.
3. Fluids and food (Nasal regurge)
a. Perforadon of the hard palate e.g. syphilis.
b. Cleft palate.
c. Paralysed soft palate (e.g. diphtheria, bulbar palsy).
d. Shortening of the soft palate due to trauma or fibrosis.
4. Mucopurulent or purulent; all causes of nasal obstruction.
5. Crusty
a. Atrophic rhinitis.
b. Granulomas of the nose.
B. Causes of unilateral nasal discharge
1. Unilateral choanal atresia.
2. Unilateral sinusitis.
3. CSFrhinorrhea.
4. Oroantral fistula.
5. Bloody; epistaxis due to local causes.
6. Mucopurulent; causes of unilateral nasal obstruction.
7. Tumours.
N.B. : Nasal discharge is either nasal or postnasal. Postnasal discharge
may cause irritative cough, pharyngitis, laryngitis and gastric
troubles.
 T^

-216-

Epistaxis
• Epistaxis means bleeding from the nose. It is regarded as a symptom.
Aetiology
/. Local causes
1. Idiopathic; bleeding from
little's area is the commonest
cause and represents 90% of
cases. It usually occurs in
children and adolescents. It may
be precipitated by slight trauma,
and hot dry atmosphere. At the
little's area (kiesselbach's
plexus) (Fig.47), anastomoisis
takes place between the spetal
branch of sphenopalatine artery,
anterior ethmoidal artery,
greater palatine artery, and
superior labial branch of facial
artery. Frg.47 Little's area

2. Traumatic
a. Foreign body.
b. Blow to the nose,
c. Fracture nasal bones, septum, and sinuses, if it involves the nasal
mucosa the bleeding is mild and transient. If the anterior
ethmoidal artery is the source, bleeding is severe.
d. Fracture base of skull (anterior cranial fossa).
e. Surgical trauma; postoperative after nasal operations eg.
turbinectomy, F.E.S.S, and cauterizauon. Bleeding is usually
secondary (after 1 week).
3. Inflammatory
a. Acute nonspecific rhinitis.
b. Acute specific rhinitis, e.g. nasal diphtheria (mostly unilateral
blood stained discharge).
c. Chronic rhinitis (specific and nonspecific).
d. Acute and chronic sinusitis.
e. Fungal infections of the nose and sinuses.
 -217-

4. Neoplastic
a. Tumours of the nose and sinuses :
- Bengin e.g. haemangioma and inverted papilloma.
- Malignant tumours.
b. Tumours of the nasopharynx :
- Bengin e.g. Angiofibroma,
- Malignant e.g. carcinoma, and sarcoma.
5. Deviated septum; this is a very important and common cause. It is
due to angulation and kinking of the blood vessels and associated
mucosal dryness.
6. Septal perforation
7. Hereditary haemorrhagic telangectasia : (osier's - Rendu disease)
This is a congenital vascular malformation involving the lips, nose,
mouth, pharynx and may be larynx. It may be associated with
subcutaneous and intracranial haemangioma. In the nose, it is
usually located anteriorly on the septum.
8. Aneurysm of the internal carotid artery :
Bleeding is due to continuous leakage, and it is uaually fatal, it may
be;
a. Non traumatic (rare).
b. Posttraumatic (delayed after injury).
9. Sinus barotrauma.
IL General causes
1. Candiovascular causes
a. High arterial pressure (hypertension) as in chronic renal failure,
atherosclerosis, pregnancy and essential hypertension. This is
the commonest cause in the elderly. Bleeding is mostly from the
posterior part of the nose (sphenopalatine artery). It is usually
misunderstood that hypertension iniates epistaxis, but the
problem is once epistaxis starts for any cause, the high arterial
tension manitains bleeding and doesn't allow clotting to seal the
vessel.
b. High venous pressure as in :
- Cardiac causes; Mitral stenosis, and heart failure.
- Pulmonary; emphysema, whooping cough, and pneumonia.
- Chest; mediastinal masses.
 -218-

2. Haematologic diseases
a. Purpura due to thrombocytopenia, or thrombocytopathy.
b. Coagulopathy e.g. haemophilia.
c. Leukaemia and Hodgkin's disease.
d. Anticoagulant therapy e.g. hepain, and oral anticoagulants.
e. Antiplatelet drugs e.g. aspirin, quinine, methyldopa and
nonsteroidal anti-inflammatory drugs (NSAIDs).
3. Hepatic causes
a. Liver cirrhosis.
b. Liver failure.
Leading to hypoprothrombinaemia and vitamin k deficiency.
4. Fevers
a. Rheumatice fever and infective endocarditis, there is an
associated vasculitis.
b. Fevers e.g. exanthemata, typhoid, and diptheria.
Management of epistaxis
Epistaxis is an ENT emergency and it varies from mild to severe. It
may be anterior or postnasal. Postnasal bleeding is spitted or swallowed
and is vomited to be misdiagnosed as haematemesis.
L General measures (Hrst aid) and assessment
1. The padent is managed in the seated position with the head slightly
flexed and leaning forward (unless shocked).
2. The nose is pinched between the thumb and index fingers.
3. Apply cold compresses to the nose.
4. The patient is asked to spit blood in a container and not to swallow
it.
5. Insert a piece of cotton soaked with a vasconstrictor solution
(epinepherin 1/100,000 solu.) into both nostriles, and it is kept for
5-10 minutes, this may stop the bleeding if mild. Ademaline should
not be used in cardiac and hypertensive patients.
6. Assessment
Concise history and physical examination are obtained while
preparations are made to control bleeding.
A. History
It should include previous bleeding episodes, side of bleeding,
whether it is mainly anterior or posterior, duration and frequency
of bleeding, history of diabetes, hypertension, liver and cardiac
 -219-

l.:::o^.i.^u ;i • x i S ^ ,\

B. Physical examination
- This is performed to :
1. Detect site of bleeding; being either;
a. Unilateral or bilateral.
b. Anterior or posterior.
c. Above or below the middle turbinate.
- The sites of bleeding are either;
a. Little's area, on the anteroinferior portion of the septum. This
is the commonest site (90% of cases),
b. Upper pat of the nasal cavity above the middle turbinate due
to bleeding from anterior or posterior ethmoidal arteries
(from the ICA).
c. From the posterior part of the nasal cavity below the middle
turbinate, due to bleeding from the sphenopalatine artery
(from the ECA).
- If the site of bleeding is abscure, the nasal mucosa should be
constricted and anaesthetized by 4% cocaine, or 4% lidocain in
1/100000 epinephrin solution applied on cottonoid strip as a
pack for 5 minutes. This allows bleeding to lessen or stops, then
the nose is inspected to identify the bleeding site.
- A rigid endoscope can be used to identify the site of bleeding.
2. Detect severity of bleeding; which is either;
a. Mild to moderate.
b. Severe; and in this case, the patient may be shocked, and
there is no time for examination and nasal packing should be
done urgently.
3. To detect hypovolaemic shock ;
In cases of severe bleeding. It is manifested by :
a. Weak rapid pulse.
b. Hypotension,
c. Tochypnoea.
d. Pallor, and cold sweating.
e. Restlesness and irritability.
f. Decreased urine output.
4. To detect the cause; See later.
 r"
-220-

/ / . Control of bleeding
A. Mild epistaxis
a. General measures and assessment (as before). This may arrest
bleeding, and allows accurate identification of its site, particularly
if it is from little's area.
B. Cauterization; is done when the
bleeding stops or diminishes,
under local anasthesia (4%
cocain or 4% xylocain in
1/100000 epinephrine solution),
it is done either by;
1. Chemical cautery : by silver
nitrate or chromic acid
crystals. (Fig.48)
2. Electrocatery : under local
anaesthesia in adults or
general anaesthesia in Fig.48 Cauterization
children. It is more effective of Little's area
than chemical cautery.
- The bleeding site with a ring of
surrounding mucosa are caute-
rized.
- Post cauterization instructions :
a. Avoid manipulations of the nose as blowing and straining, hot
food or drink, alcohol, smoking and aspirin.
b. local humidification for 1 week.
c. Elevation of the head of the bed for 1 week.
d. Lubricant nasal drops for 1 week.
- N.B. : endoscopic cauterization of the bleeding point may be
performed if the site of bleeding is more posterior.
C. Nasal packing; is done if bleeding doesnot stop after cauterization,
//. Severe epistaxis
Stoppage of bleeding by (nasal packing or surgery) and control of
shock, if present) should be carried out simultaneously.
1. Nasal packing
a. Anterior nasal pack (Fig.49)
- Using a strip of ribbon gauze (50 cm long x 2.5 cm breadth)
impregnated with vaseline, lignocain (surface anaesthetic and
 -221-

an antibiotic ointment, It
is introduced in layers
from below upwards in
both sides of the nose.
The nose should be
sprayed with a surface
anasthetic (e.g. 10%
cocaine or xlocain),
before packing.
- The pack is left for 24-48
hours, with frequent
checking of the postnasal Fig.49. anterior nasal pack
space to detect any
postnasal bleeding.
Antibiotics should be given meanwhile to avoid secondary
infeciton.
- Alternatively, an inflatable rubber tampoon, or a mirocell
(artificial sponge like material) pack can be used, they are
easy to insert and effective.
b. Posterior nasal pack (Fig. 50)
- It is done if the anterior nasal pack failed to control bleeding. It
is done under general anaesthesia.
- A piece of gauze impregnated with an antiseptic ointment and
with 2 threads attached to it, and using two rubber catheters
that are introduced through the nose and withdrawn from the
mouth, and the end of each thread is tied to the oral end ot the
catheters, which are then withdrawn, till the pack is lodged
firmly into the pharynx, this can be helped by manipulating
the pack with the index finger under the soft palate. Then the
two ends of the threads are tied over a peice of rubber over
the columella.
- The pack is left 24-48 hours, and meanwhile antibiotics should
be given to avoid sedondary infection.
- Alternatively a foly's catheter can be used as a postnasal pack.
The catheter is introduced through the nose till its tip is seen
behind the uvula, then the balloon is inflated and the catheter
is pulled from the nose till the balloon lodges firmly in the
nasopharynx.
- The pack is more efficient in controlling postnasal bleeding
than rubber ballooning.
 T

-222-

Fig.50. posterior nasal pack

2. General measures; for control of shock if present and to restore

vital signs.
1. Bed rest, in the supine position with lowering of the head.
2. Sedatives e.g. diazepam (valium), avoid morphia as it causes
depression of the respiratory center.
3.1.V. fluids (saline, Ringer's).
4. Fresh blood transfusion in severe cases.
5. Warmth.
6. Other lines to aid in stoppage of bleeding,
a. Fresh frozen plasma or plasma extracts in haemophilia and
purpura.
b. Vitamin k. I.M.
The patients should be monitored frequendy for :
a. Vital signs.
b. Hb% and haematocritc.
c. Blood gases.
d. Urine out put.
3. Surgery (Arterial ligation);
It is needed if all the previously mentioned measures fail to stop
bleeding or in recurrent epistaxis despite repeated packing.
a. Ethmoidal arteries ligation; in bleeding from the superior part
of the nose above the middle tubinate. It is done through an
external frontocthmoidectomy approach, then ligation of the
 -223-

anterior ethmoidal artery and/or clipping of the posterior

ethmoidal artery in the medial wall of the orbit.
b. Maxillay artery ligation; in bleeding from the posterior part of
the nasal cavity. (Fig.51)
- It is done through a transantral
appraoch after removal of
the anterior and posterior
walls of the maxillary sinus,
then the maxillary artery and
if possible its branches are
clipped.
- It is more efficient than
external carotid artery
ligation due to cross
anastomosis between the two
external carotids of both Fig 51 Maxillary artery
ligatton
sides.
c. Diathermy; of the anterior ethmoidal artery or sphenopalatine
artery can be done, if bleeding is not so severe and the condition
allows.
5. Arterial embolization
This can be done after doing angiography to locate the bleeding
vessel. Then it is selectively embolized using polyvinyl alcohol
particles or gelfoam. This is particularly useful in recurrent
bleeding not amenable to routine measures.
///. Identification and treatment of the cause
The cause must be treated after stoppage of bleeding to prevent
recurrence of epistaxis.
A, Investigations
1. Complete coagulation profile; Bleeding time, clotting time,
prothrombin time and concentration, partial thromboplastine
time.
2. Complete blood picture; may show leukaemia or purpura.
3. C.T scan of the paranasal sinuses.
4. Biopsy from a nasal mass.
B. Treatment
1. Antihypertensive drugs in case of hypertension.
2. Treatment of blood diseases.
 -224-

3. Deviated septum : SMR.

4. Telangectasia : septodermoplasty or laser photocoagulation,
5. Tumours : surgical excision.

Headache and facial pain

Headache is pain felt in the head. It may be produced by a
multiplicity of conditions both intracranial and extracranial.
Mechanisms involved in headache
1. Traction on veins, middle meningeal arteries, and large arteries at
the base of the skull.
2. Dilatation of intracranial arteries.
3. Inflammation in or about pain sensitive structures.
4. Pressure by tumours on cranial or cervical nerves.
5. Psychogenic.
Pain sensitive structures in the head
1. Blood vessels and scalp.
2. Large venous sinuses and their tributaries.
3. Dural arteries, and cerebral arteries at the base of the brain.
4. 5th, 7th, 9th, and 10th cranial nerves, and 2nd and 3rd cervical
nerves.
Causes of headache and facial pain
/. Extracranial
A. Rhinological
1. Acute and chronic sinusitis : They represent 5-10% of cases, it is
called sinus headache and is characterized by :
- Periodicity; the headache starts early in the morning, reaches
it's peak at noon and tiien subsides gradually.
- related to posture; increasing on bending and walking.
- Sustained, deep aching and not pulsatile.
- My be associated with lacrimation and photophobia.
- More severe in acute cases.
- Site varies according to the affected sinus.
2. Malignant tumours of the nose and paranasal sinuses.
3. Inflammations; Acute rhinitis and vestibulitis.
4. Contact headache : e.g. in deviated septum and concha bullosa,
due to contact of the mucosa and pressure on nerve endings.
 -225-

5. Nasopharyngeal carcinoma : due to involvement of the

trigeminal nerve or intracranial extension,
B. Otological
1. Acute suppurative otitis media.
2. Complications of suppurative otitis media.
3. Otitis externa.
4. Tumours e.g. glomus tumours, and carcinoma.
The ear itself is a relatively uncommon source of headache.
C. Occular
1. Acute glaucoma.
2. Errors of refraction.
3. Tumours.
Pain is deep seated behined the eyes, so often at the end of the day.
D. Dental
L Dental caries.
2. Infections; periapical abscess, and periodontitis.
3. Post extraction neurajgia.
pain is localized and constant. It is dull aching or burning. It is felt
first over the diseased tooth, then spreads along the division of the
maxillary or mandibular nerves. The teeth are sensitive to thermal
stimulation and percussion. There may associated swelling in the
cheek, and local signs of infection.
£. Temporomandibular joint; as in :
1. Arthritis, and dislocation.
2. Malocclusion of the mandible (Costen's syndrome).
F, Cervical
1. Spondylosis.
2. Contractions of muscles of the head and neck. It is felt as a
sensation of tightness, felt mostly occipital.
G. Fatigue (tension) headache; It is localized chiefly to the back of
the neck.
H. Neuralgias
1. Trigeminal neuralgia (Tic doloureux)
- This consists of paroxysmal attacks of intense unilateral facial
pain of brief duration lasting for seconds to minutes. It is felt
along the divisions of the trigeminal nerve (usually the 2nd
and 3rd divisions). It has a sudden onset, and is often
 -226-

precipitated by stimulation of certain trigger areas (e.g.

shaving, washing the face and tooth brushing). Lacrimation
and rhinorrhea may occur,
- It usually occurs in old females above 50 years.
- The cause is unknown, but it may be due to a vascular loop
compressing the sensory root.
- Treatment
1. Medical
a. Tegretol (carbamazepine) : the major side effect is
irreversible bone marrow depression and aplastic
anaemia.
b. Phenytoin.
2. Surgical; in cases unresponsive to medical treatment:
a. Alcohol injection or rhizotomy of the sensory root.
b. Trigeninal neurectomy (division of the sensory root) it
carries the risk of corneal ulceration.
c. Decompression of a vascular loop compressing the
sensory root.
2. Glossophrayngeal neuralgia
A stabbing pain is felt in the tonsillar region and referred to the
ipsilateral car, Rarely, it is felt at the base of the tongue and the
angle of the jaw. The cause is unknown, it may be due to a long
styloid process irritating the glossopharyngeal nerve.
Treatment
1. Tegretol.
2. Glossopharyngeal neurectomy, through the tonsillar bed in
resistant cases.
3. Sphenopalatine neuralgia (Sluder's neuralgia)
Paroxysmal pain felt over the forehead, between the eye brows
and over the nasal bones. Touching the middle turbinate induces
pain. There is associated rhinorrhea, conjunctival congestion,
lacrimation, and face flushing. The cause is thought to be
vascular in origin.
4. Post herpetic neuralgia
There is intense, persistent lancinating pain, felt along the
distribution of the affected nerves.
 -227-

I. Vascular headache
1. Migraine
- It is a disorder, characterized by paroxysmal attacks of unilateral
headache (frontal, and temporoparietal) and hemifacial pain.
Headache is throbbing and occurs in attacks lasting several
hours, and the patient is free in between. Nausea, vomiting and
photophobia are usually present. The classic attack is preceeded
by a prodroma (aura) of blurring of vision, scotomas, flashes of
light and paraesthesia. A positive family history is usually
present.
- It is due to spasm of the intracranial arteries (responsible for the
aura, followed by dilatation of the intra and extracranial arteries
(responsible for the attack).
Treatment
1. Analgesics e.g. paracetamol.
2. Ergotamine tariarate plus caffeine (cafergot) is given to
patients who fail to respond to pain killers.
2. Temporal arteritis
This is an acute inflammauon of the temporal arteries in the form
of focal necrosis of the media of the vessel wall. The suprficial
temporal arteries are tender, cord-like, and the overlying skin is
red, hot and tender. It is usually seen in older age groups, and is
bilateral. The cause is thought to be autoimmune. Involvement of
the ophthalmic artery may result in blindness.
Treatment
a. Steroids,
b. Surgical excision of the offending artery may be needed.
J. General causes
1. Systemic infections.
2. Toxic causes:
a. renal and hepatic disorders.
b. Hypoxia.
c. Carbon monoxide poisoning.
3. GIT disturbances e.g. constipation.
//. Intracranial
1. Space occupying lesions e.g. tumours, abscess, aneurysm.
2. Inflammations; meningitis, encephalitis.

^
 -228-

3. After lumbar puncture.

4. Hydrocephalus.
5. Hypertension.

Smell disorders
For normal perception of odours, three factors are essential:
1. Odoriferous particles should come in contact with the olfactory
mucosa,
2. The mucous membrane must be moist and healthy.
3. The olfactory terminals and their nerve tracts must be normal.
A. Anosmia
It means loss of the sense of smell. Hyposmia is diminshed sense of
smell.
Causes
/. Intranasal
a. Misdirection of the air current e.g.-destruction of the alae nasi
by lupus, syphilis or malignant ulcers.
b. Pi"evention of access to the olfactory area in all cases of nasal
obstruction e.g. deviated septum, polypi, tumours, foreign
body, and infections.
c. Atrophy of the mucous membrane (atrophic rhinitis).
d. Peripheral neuritis e.g. diabetes, influenza, and lead
poisoning.
2. Intracranial
a. Congenital abscence of the olfactory bulbs and nerves.
b. Compression of the cortical centers or their association fibres
by tumours, abscess or granuloma.
c. Basal meningitis.
d. Fracture base of the skull involving the anterior cranial fossa.
3, Psychogenic.
B. Cacosmia
This is perception of bad odour. It is either due to the presence of
foreign body, local disease especially maxillary sinustitis of dental
origin and atrophic rhinitis.
 -229-

C. Parosmia
This is preversion of the sense of smell (abnormal smell which is
perceived only by the patient).
It is due to neuritis especially postinfluenzal, hysteria, epilepsy and
insanity.
D. Hyperosmia:
This means increased hypersensitiveness to odours. It is sometimes
met with in hysteria and mania. It may result from any lesion
irritating the olfactory bulbs.

Proptosis
This is forward displacement of the eye ball in relation to the skull.
Detection of the direction of proptosis is of great importance in the
diagnosis of the cause.
Causes of proptosis
I. Causes in the paranasal sinuses
1. Frontal sinus; e.g. mucocele, osteoma. Proptosis is downwards
and lateral.
2. Ethmoid sinus; e.g. mucocele, osteoma, malignant tumours.
Proptosis is lateral.
3. Maxillary sinus; e.g. malignant tumours. Proptosis is upwards.
n. Causes in the lacrimal gland
This leads to downwards and medial displacement.
IIL Causes in the orbit e.g. haematoma, cellulitis, abscess or tumour.
This causes forward displacement.
IV. Causes in the nasopharynx e.g. nasopharyngeal fibroma,
chordoma, or carcinoma.
V, Cavernous sinus thrombosis.
VI. Endocrinal causes ; toxic goitre.
 -230-

Nasal Operations
Antral puncture and lavage; (Maxillary sinus washout)
Indications
/. Diagnostic; (Proof puncture, when the plain x-ray shows sinus
opacity).
a. to know the contents of the sinus.
b. Culture and sensitivity of the pus obtained.
c. To inject lipiodol for contrast x-ray in cases of oroantral fistula,
and also to delineate thickened mucosa or polypi or masses
within the sinus lumen that appear as a filling defects.
2. Therapeutic;
a. Subacute and chronic sinustitis that failed to respond to medical
treatment.
b. Fungal infections e.g. mucormycosis for injection of an
antifungal drug e.g. amphotericin B within the sinus lumen.
N.B.: Antral puncture and lavage is not widely used nowadays.
Contra indications
1. Acute maxillary sinusitis for the fear of spreading infection.
2. Traumatic fracture of the maxilla.
3. Children and patients with hypoplastic maxillary sinus, due to
proximity of the orbital floor.
Anaesthesia; Local surface anaesthesia.
Technique (Fig.52)
- A trocar and cannula is introduced beneath the inferior turbinate
in the inferior meatus, one inch behind the anterior end of the
inferior turbinate. Then, the medial wall of the maxillary sinus is
pierced with the trocar directed upwards and laterally towards
the outer canthus, and the trocar is then removed.
- The sinus is then washed by warm sterile saline solution,
(antibiotics solution can be used). In cases of fungal infections
we can wash with amphotericin B. solution.
Complicatons
1. Injury of anterior wall of the sinus, with swelling of the cheek.
2. Injury of the orbital floor.
3. Mild haemorrhage.
4. Air embolism (rare).
 -231-

Fig.52. antral puncture

Intranasal (inferior meatal) antrostomy

Indication
This operation has been traditionally used in the treatment of
recurrent and chronic maxillary sinusitis which failed to respond to
conservative treatment, including repeated antral puncture and
lavage. It is not done nowadays being replaced by endoscopic
middle meatal antrostomy which is more physiological.
Principle (Fig.53)
The principle of the operation is
creation of a permanent opening
in the inferior part of the medial
wall of the maxillary sinus in
the inferior meatus which is
more dependent and lower than
the natural ostium. It relies upon
gravitational drainage which
improves the state of the sinus
mucosa, but this is proved to be
wrong because the mucociliary
clearance wave always beats Fig 53 inferior meatal antrostomy
towards the natural osdum.
Radical antrum operation (Caldwell - Luc*s procedure).
This entails total removal of the irreversibly damaged mucosa of
the maxillary sinus, with facilitation gravitational drainage an
areauon via and inferior meatal antrostomy.
 r
-232-

Indications
It has predominantly been used for persistent chronic maxillary
sinusitis, when medical treatment, antral puncture lavage and
inferior meatal antrostomy are ineffective. This is obsolete now but
is indicated in special situations :
1. Removal of recurrent antrochoanal polyp.
2. Removal of a foreign body within the sinus e.g. retained dental
root.
3. As as step in closure of oroantral fistula.
4. Dental and dentigerous cysts of the maxillary sinus.
5. Removal of bengin tumours.
6. Elevation and stabilizaton of orbital floor fractures.
7. A route for taking biopsy in antral malignancies.
8. Access to the pterygopalatine fossa as in ligation of the maxillary
artery in severe epistaxis.
Contraindications
1. Children as it can affect secondary dentition.
2. Hypoplastic maxillary sinus.
Anaesthesia : Local or general.
Technique (Fig.54)
- Through a sublabial incision
3mm above and parrallel to the
gingivo labial fold, the
mucoperiosteal flap over the
anterior wall of the maxillary
sinus, is elevated.
- A rounded opening is made in the
anterior wall of the maxillary
sinus using a gouge and
hammer.
- The mucosa of the sinus is
removed by a currette. Fig.54 Caldwell-luc's
operation
- Intranasal inferior meatal
antrostomy is performed.
- The sinus is packed with vaseline
gauze impergnated with
garamycin ointement to be
removed from the nose, after 48
hours.
 -233-

External frontoethmoidectomy
Indications
1. Chronic sinustits unresponsive to medical treatment. It is now
replaced by functional endoscopic sinus surgery.
2. Complications of acute ethmoiditis as orbital cellulitis for
decompression and drainage (replaced by endoscopic procedures).
3. Extensive recurrent nasal polyposis when previous nasal surgery
has destroyed useful landmarks.
4. Fomtoethmoidal mucoceles.
5. An access to ligate the ethmoidal arteries in epistaxis.
6. Dacryocystorhinostomy operation, repair of CSF leaks, and
decompression of the orbit for malignant exophthalnos.
Anaesthesia; general
Technique (Fig.55)
- An incision is made slightly cuvred,
medial and convcave towards the
medial canthus of the eye. It may be
extended under the eyebrow to
facilitate access to the frontal sinus.
- Tne periosteum is elevated and the
lacrinal sac is elevated and displaced
laterally.
Fig.55. Incision for external
- The thick medial wall of the orbit is ethmoidectomy
perforated and all the ethmoidal cells
are exenterated under direct vision
with removal of all diseased mucosa.
- The floor of the frontal sinus is opened and the sinus is cleared.
- A tube drain is placed to maintain drainage of the frontoethmoid
cavity for a month at least.
- The wound is then closed.

Nasal endoscopy
It is a recent mcdality which has been introduced to rhinology after
the invention of the Hopkin's rod lens system.
/. Diagnostic endoscopy of the nose and sinuses
It allows a detailed examination of the nose and sinuses.
Endoscopes used are 0" and 30" Hopkin's rigid endoscopes, 2.7 mm in
diameter is preferred.
 -234-

Technique
- The nose is sprayed with a surface anaesthetic and vasoconstrictor
(e.g. 4% xylocain in 1/100000 epinephrine) or it may be applied as
a soaked cotton pledget,
- Then the endoscope in introduced to examine the following areas :
a. Vestibule of the nose.
b. Floor of the nose, inferior meatus, the nasopharynx and the
pharyngeal orifice of the E.T.
c. The endoscope is then passed medial to the middle turbinate to
visualize the superior meatus and the sphenoethmoidal recess.
d. Inspect the middle turbinate itself.
e. The endoscope is the passed lateral to the middle turbinate to
examine the middle meatus.
Indications
1. Persistent nasal obstruction.
2. Chronic sinusitis.
3. Recurrent epistaxis.
4. Nasal polypi and adhesions.
5. Foreign body in a hidden area.
6. E.T. dysfunction.
7. Neoplasms of the nose, sinuses, and nasopharynx for
examination and biopsy.
8. Fungal sinusitis.
9. CSF rhinorrhea.
10. Postoperative assessment and care.
N.B.: Maxillary sinus endoscopy (antroscopy) is done via the anterior
wall of the sinus. After making s hole in the canine Fossa using
a trocar, and the endoscope (4mm) is introduced through this
hole to visualize the sinus.
Diagnostic nasal endoscopy can be used routinely as a part of nasal
examination, for accurate detailed examination and also for
documentation.
//. Endoscopic sinus surgery
Indications
1. Chronic and recurrent acute sinusitis, not responding to adequate
trails of medical treatment The operation done in this case is called
functional endoscopic sinus surgery (mentioned before).
 -235-

2. Nasal polyposis (endoscopic ethmoidectomy).

3. Antrochomal polyp.
4. Allergic fungal sinusitis and mycetoma.
5. Frontoethmoidal mucoceles.
6. Repair of CSF leaks.
7. Orbital and optic nerve decompression in selected cases of trauma.
8. Repair of blowout fractures.
9. Dacryocystorhinostomy.
10. Trans-sphenoidal pituitary hypophysectomy.
11. Choanal atresia-
12. Control of epistaxis in recurrent cases,
13. Septal and turbinate surgery.
14. Drainage of periorbital abscess.
15. Excision of limited nasal and sinus benign tumours.
Contraindications
1. Malignant tumours.
2. Fungal infecdons (except allergic fungal sinusitis).
3. Complicated sinusitis (e.g. meningitis, cavernous sinus thrombosis,
and brain abscess).
Complications
/. Major complications
1. CSF leakage and brain trauma.
2. Meningitis, brain abscess, carotid artery injury or intracranial
haemorrhage.
3. Severe haemorrhage that may need transfusion.
4. Orbital haematoma.
5. Diplopia and loss of vision.
6. Anaesthetic complications.
//. Minor complications
1. Recurrent sinus infections.
2. Postoperative epistaxis.
3. Periorbital oedema and ecchymosis.
4. Intranasal adhesions.
5. Anosmia due to injury of the medial wall of the middle turbinate
or the cribriform plate.
 71

-236-

THE LARYNX
Anatomy of the Larynx
The larynx is derived embryologically from the branchial arch
system. The hyoid bone is derived from the second and third arches, the
thyroid and epiglottis cartilages are derived from the fourth arch, and the
cricoid cartilages is derived from the sixth arch.
Structure and position
The larynx is the upper expanded part of the air passage. The
highest part of the larynx is the tip of the epiglottis at the level of 3rd
cervical vertebral, and its lower border is the lower edge of the cricoid
cartilage at the level of lower border of 6th cervical vertebra. It lies in the
midline of the neck just below the hyoid bone. It lies anterior to the
hypopharynx, and opens into its anterior wall by a long almost vertical
orifice, with a gutter on each side called the pyriform fossa. The larynx is
continuous below with the trachea.
Framework of the larynx (Fig.56)
It is formed of several cartilages connected by ligaments and
muscles. These laryngeal cartilages are :

EpigloKis

Hyoid bone

e-epiglottic >• Supra glottic

space
A ryepi glottic
fold

Ventricte Ventricular fold

Ar^enoid
Thyroidcartiiage Glottic
Cricoid Cricoid V p . , ^.
cartilage cartilage fSubglottK:

Anterior Posterior

Fig.56. anatomy of the larynx

 -237-

A. Single cartilages
1. Thyroid cartilage
It is formed of two quadrangular laminae that meet together
anteriorly in the midline to form the laryngeal prominence, which is
prominent in males and is called Adam's apple. The posterior edges
of the laminae are free apart and they are elongated superiorly and
inferiorly to form the superior and inferior comu respectively. The
lateral surface of each lamina shows a prominent raised line
passing downwards and forwards called the oblique line.
2. Cricoid cartilage
It resembles a signet ring, and is formed of a posterior quadrangular
lamina and a narrow anterior arch. The upper border of each lamina
shows a facet for articulation with the arytenoid cartilage
(cricoarytenoid joint), and another facet for articulation with he
inferior comu of the thyroid cartilage (cricothyroid joint). These
two joints are synovial joints.
3. Epiglottis
A single thin sheet-like clastic fibrocartilagc, with an upper free
end projecting upwards behined the base of the tongue and the
hyoid bone. It has two surfaces, an anterior (lingual) surface, and a
posterior (laryngeal) surface. Its lower end is attached to the inner
surface of the middle of the thyroid angle (i.e. at the junction of the
thyroid alae). Numerous seromucinous glands lie within pits
(fenestrae) in the cartilage, which are significant in the spread of
supraglottic carcinoma to the preepiglottic space.
6. Paired catilages
L Arytenoid cartilages
They resemble a three-sided pyramid, the base of each articulates
with superior border of the cricoid lamina. It has two processes, an
anterior (vocal process) for attachement of the vocal ligament, and
a lateral (muscular) process for attachement of the intrinsic muscles'
of the larynx.
2. Corniculate cartilages; two small cartilages lying on the superior
surface of the arytenoid cartilages.
3, Cuneiform cartilages; small nodules on the aryepiglottic folds.
Laryngeal ligaments and membranes :
7. Cricothyroid membrane; attaches between the lower border of each
thyroid lamina and upper border of the cricoid arch.
 -238-

2. Thyrohyoid membrane; attaches between the upper border of thyroid

cartilage and the lower border of the hyoid bone. It is pierced by the
internal laryngeal nerve and the superior laryngeal vessels.
J. Thyroepiglottic ligament; a short ligament that attaches the petiole of
the epiglottis to the middle of the inner surface of the thyroid angle.
4. Hyoepiglottic ligament; attaches the epiglottis to the hyoid bone.
5. Cricotracheal ligament; attaches the cricoid cartilage to the first
tracheal ring.
6. Two important intrinsic ligaments; They form a broad sheet of
fibroelastic tissue beneath the lining mucous membrane, that give
additional support to the laryngeal framework, and these are :
a. Superiorly; the quadrangular ligament attached between the lateral
border of the epiglottis and the arytenoid cartilage, which separates
the larynx from the pyriform fossa.
b. Inferiorly; the conus elasticus which is strong, and extends
upwards and medially from the arch of the cricoid cartilage, to join
the vocal ligament (cord) on each side, thus it lies beneath the
mucosa of the undersurface of the true vocal cords.
Laryngeal folds
1. The vocal folds (cords); (True vocal cords)
These are two ligamentous structures attached on both sides from the
vocal process of the arytenoid cartilage posteriorly to the middle of
the inner surface of the thyroid angle anteriorly. They are the upper
boundary of the conus elasticus.
2. The ventricular folds (bands); (False vocal cords).
These are two mucosal bands situated above the level of the vocal
folds.
3. Aryepiglottic folds; attached from the lateral border of the epiglottis
to the arytenoid cartilage. It is the upper boundary of the quadrangular
ligament.
4. Glossoepiglottic folds; two lateral and one median glossoepiglottic
folds, attached between the lingual surface of the epiglottis and the
base of the tongue. A fossa is located on each side of the medial
ligament which is called the vallecula.
The laryngeal inlet
It lies obliquely, directed slightly posteriorly. It is bounded by the
free border of the epiglottis anteriorly, the two aryepiglottic folds
on each side and the arytenoid cartilages posteriorly.
 -239-

Cavity of the larynx

The true vocal cords divide the cavity of the larynx into three
areas:
1. The glottis; the space between the vocal cords, that extends to
about 1 cm below the free border of the vocal cords.
2. The supraglottis; the area above the level of vocal cords, extending
to the tip of the epiglottis.
3. The subglottis; extends from the lower boundary of the glottis, to
the lower border of the cricoid cartilage.
Laryngeal muscles
A. Intrinsic muscles
These move various cartilages of the larynx and are responsible for
vocal cord mobility and tension, and these are :
1. Abductor; the posteior cricoarytenoid muscle (the posticus
muscle), which extends from the posterior surface of the cricoid
lamina, and gets inserted into the muscular process of arytenoid
cartilage. It rotates the arytenoid carilage outwards, and thus
abducts the vocal cords and open the glottis. It is a small but a very
important muscle (the muscle of life as it is the opener of the
laryngeal glottis).
2. Adductors
a. Lateral cricoarytenoid; originates on the lateral cricoid arch &
insets into the muscular process of arytenoid.
b. Thyroarytenoid muscle & the vocalis muscle; they make up the
bulk of the vocal cords and are barely seperable.
c. Interarytenoid muscle; extends from one aryteroid to the other.
d. Cricothyroid muscle; this muscle adducts the vocal cord and
closes the glottis during phonation.
3. Tensors
a. Vocalis muscle (internal part of the thyroarytenoid muscle).
b. Cricothyroid muscle.
Cricothyroid muscle; this is the only intrinsic muscle which lies
outside the larynx. It is a broad fan-shaped muscle that
originates anteriorly from the cricoid arch, and inserts on the
broad lateral surface of the thyroid ala. Contraction of this
muscle pulls the thyroid cartilage forwards, thus streching &
tensing the vocal cord. Furthermore, it rotates the arytenoid
medially and thus adducting the vocal cords.
 -240-

B. Extrinsic muscles
They attach the larynx to neighbouring structures, and they move the
larynx as a whole. They are categorized according to function into :
1. depressors (strap muscles); omohyoid, sternothyroid, and
sterenohyoid. They originate inferiorly.
2. Elevators; mylohyoid, geniohyoid, geniogiossus, hyoglossus,
digastric, stylohyoid and thyrohyoid. The thyrohyoid although
considered as a strap muscle it functions mainly as an elevator.
3. Inferior constrictor muscle of the pharynx; which acts during
swallowing, and is attached to the posterior border of the thyroid
ala.
Two spaces of paramount importance
1. Preepiglottic space; it lies infront of the infrahyoid portion of the
epiglottis. It is bounded superiorly by the hyoepiglottic ligament,
arteriorly by the thyrohyoid membrane and posteriorly by the
epiglottis. It contains fat and lymph nodes. It is an important route
in the spread of supraglottic carcinoma.
2, Paraglottic space; it lies between muscles of the true and false
cords medially and the thyroid cartilage laterally and thus it
surrounds the glottis, it is very important in the spread and
management of laryngeal carcinoma.
The laryngeal mucosa
- The larynx is lined by respiratory epithelium (pseudostratified
columnar ciliated epithelium with goblet cells and seromucinous
glands), except at the true vocal cords, superior part of the
epiglottis and the aryepiglottic folds, that are lined by
nonkeratinizing stratified squamous epithelium.
- Mucous glands are distributed throughout the mucous membrane,
and are particularly numerous on the posterior surface of the
epiglottis forming indentations and fenestrations, and such
fenestrae are significant in spread of carcinoma to the preepiglottic
space.
Nerve supply
The vagus nerve (lOth carnial nerve) gives motor and sensory
supply to the larynx through its superior laryngeal and recurrent
laryngeal branches.
1. Motor
All intrinsic muscles of the larynx are supplied by the recurrent
 •fW™!^^

-241-

laryngeal nerve except the cricothyroid muscle, which is supplied

by the external branch of the superior laryngeal nerve.
2. Sensory
a. Above the level of the vocal cords, the mucosa is supplied by the
internal branch of the superior laryngeal nerve.
b. Below the level of the vocal cords, the mucosa is supplied by the
recurrent laryngeal nerve.
Blood supply
The arterial supply and venous drainage of the larynx are closely
parallel to the nerve supply, and they are :
a. The superior laryngeal artery and vein, which are branches of the
superior thyroid artery and vein. They join the internal branch of
the superior laryngeal nerve to form the neurovascular pedicle that
pierces the thyrohyoid membrane.
b. The inferior laryngeal artery and vein from the inferior thyroid
vessels, they enter the larynx alongside the recurrent laryngeal
nerve.
Lymphatic drainage
Knowledge of the lymphatic drainage of the larynx is important in
cancer therapy. There are two separate drainage systems :
a. Superiorly; the supraglottis, which has a very rich lymphatic
supply drains into the upper deep cervical lymph nodes.
b. Inferiorly, the subglottis, which has also a rich lymphatic supply,
but it is more diverse, going to the pretracheal nodes (one in
particular is just anterior to the cricoid and is called the delphian
node), then to the lower deep cervical nodes, the supraclavicular
nodes, and even the superior mediastinal nodes.
- The vocal cord (glottis) has no lymphatics as the Rinek's space
contains no lymph vessels. The Rinek's space is a potential
space beneath the epithelium of the vocal cords. So do not
expect nodal metastasis in early glottic carcinoma.
Functions of the larynx
A. Protection of the air way
The larynx serves as a sphincter for protection of the lower respiratory
passages, from aspiration of fluids, saliva, and food, during
swallowing. This is achieved by :
a. Closure of the three sphincters :
- Aryepiglottic folds by contraction of the thyroarytenoid to close
the laryngeal inlet.
 -242-

- Ventricular (false vocal) fold.

- Vocal cords adduction.
If the patient is having one half of his larynx removed he can still
swallow without aspiration, due to the compensatory mechanism of
the other half.
b. Elevation of the larynx under the base of the tongue so that the
epiglottis and aryepiglottic folds close the laryngeal inlet, and
directs the food laterally on both slides of the larynx.
c. Reflex cough if any foreign material enters the larynx,
d. Reflex inhibition of respiration during swallowing mediated by
receptors in the mucosa of the supraglottic area.
B. Respiration
During respiration the intrathoracic pressure is controlled by variable
degrees of closure of the glottis. In addition, the vocal folds act as a
pressure valve, when closed they allow build up of the intrathoracic
pressure necessary for straining acts such as lifting or defecation.
C. Phonation
Voice production is carried out by vibrations of the true vocal folds.

Examination of the larynx

History
Any symptom is analysed regarding onset, course and duration.
The following laryngeal symptoms should be analysed :
1. Change of voice (Hoarsenss and dysphonia).
2. Stridor I noisy respiration, and whether (inspiratory, expiratory or
biphasic).
3. Dyspnoea : difficult respiration.
4. Cough, expectoration and haemoptysis.
5. Pain in the larynx, and if referred to ear.
6. Dysphagia, and repeated chocking attacks.
Examination
A. External examination
1. Position and movement of the larynx during swallowing.
2. Contour : swelling and broadening occurs in laryngeal tumours.
3. Laryngeal click : by moving the larynx from side to side over the
vertebral column. Normally, a click is felt (Moure's sign negative),
if lost (Moure's sign positive). This indicates that there is a mass
 -243-

occupying the space between the larynx and the vertebral column,
particularly postcricoid carcinoma.
4. External swelling and tenderness as in perichondritis.
5. Crepitus and deformity in fracture of the laryngeal framework, and
surgical emphysema.
B. Indirect laryngoscopy (mirror examination of the larynx) (Fig.57)
This is the office examination
which stood the test of time.
Visualization of the larynx is carried
out using a laryngeal mirror while the
patient is sitting and slightly leaning
forwards. The tongue is protruded and
held firmly by a piece of gauze, and
the mirror is introduced by the other
hand just abuts the soft plalate. If
there is severe gag reflex, a topical Fig,57 indirect
anaesthetic spray can facilitate laryngoscopy

examination. Ask the patient to

phonate the vowel "a" to elevate the
epiglottis and expose the laryngeal
inlet, then the vowel "e" to assess mobility and adduction of the vocal
cords. Remember, that the chair of the examiner must be lower than the
chair of the patient.
C. Flexible fiberoptic laryngoscopy
In cases where direct laryngoscopy is difficult due to severe gag
reflex or folded epiglottis that obscures the view, a flexible fiberoptic
laryngoscope can be used. It is introduced through the nose (after
spraying it with a surface anaesthetic), down to the pharynx, till it
reaches the larynx. Photographic documentation can be also done.
D. Direct laryngoscopy under general anaesthesia
This is direct visualization of the larynx by introducing a rigid
laryngoscope through the mouth. It allows detailed examination of the
larynx. An operating microscope can be used for further magnification
especially when performing microlaryngosurgery, laser surgery, or
taking a biopsy.
 TSTTi

-244-

Congenital diseases of the larynx

/. Congenital web
This is a fibrous band which connects the two vocal cords together
anteriorly (Fig.58). It is due to arrest during development with failure of
the larynx to establish its lumen at the lOth week of intraauterine foetal
life. Heredity plays a role.
Site : The commonest site is the glottis at the level of the vocal cords,
and lies anteriorly (anterior 1/2 or 2/3). Rarely, it is subglottic or
supraglottic. It varies from a small web confined to the anterior part
of the glottis to a large imperforate fibrous ring.
Clinical picture
A. Small web
- It may be asymptomatic.
- There may be hoarseness
during crying, with mild
inspiratory stridor which
is exaggerated by upper
respiratory tract infection Fig.58, glottic web

due to superimposed
oedema.
B. Large web
- There is evident inspiratory stridor soon after birth and the child
has a weak hoarse cry.
C. Imperforate type
- The child becomes deeply cyanosed after birth with no cry. It may
be fatal and cause neontal death if not urgendy managed.
- On examination; (Flexible laryngoscopy or direct laryngoscopy) :
The web is seen as a symmetrical* greyish white thick membrane,
sometimes it appears as a scmitranslucent triangular band, between
the anterior 2/3 of the vocal cords, with a sharp posterior border.
Treatment
/. Mild cases; are left without treatment, if not symptomatizing.
2. Servere cases
a. Tracheostomy may be necessary if there is severe respiratory
obstruction.
b. The web is excised by microlaryngosurgery using either laser,
cautery or microlaryngosurgical cold instruments (ordinary
surgical instruments; scissors, forceps etc.).
 IP

-245-

c. Laryngofissure operation with excision or division of the web

and insertion of a skin graft is preferred in very thick webs,
3. Imperforate web; urgent tracheostomy, or introducing a rigid
bronchoscope to rupture the web can save the neonate.
//. Laryngomalacia (congenital laryngeal stridor)
This is stridor occuring due
to a weak flaccid larynx. The
cartilagenous framework of the
larynx is abnormally soft and
flaccid and gets collapsed during
inspiration especially the
supraglottic structures (epiglottis
and aryepiglottic folds). (Fig. 59)
Clinical picture
1. Inspiratory stridor starting sometimes after birth. It is aggravated
when the child lies in the supine position and improves on lying in
the prone position (as the epiglottis falls away from the laryngeal
inlet). It varies in severity, but usually it is mild. The condition is
exaggerated by vitamin D deficiency, postnasal drip especially in
case of infected adenoids, and upper respiratory tract infection.
2. No hoarse cry.
3. The child looks healthy without significant respiratory distress.
4. On examination (Flexible l^yngoscopy or direct laryngoscoy), the
epiglottis looks elongated, narrow, and sharply folded (omega
shaped epiglottis). The two aryepiglotdc folds are approximated,
shortened, and flaccid. The flaccid epiglottis and aryepiglottic folds
are sucked in during inspiration, and the laryngeal aperture is
reduced and looks like a cruciate.
- Laryngomalacia is considered an exaggerated type of an infantile
larynx.
Treatment
1. No treatment is usually required as the condition improves
spontaneously by the age of 12-18 months when the laryngeal
framework becomes strong and firm. Only vitamin D, and
calcium supplements may be given.
2. Removal of excess mucosal fold using laser microlaryngosur-
gery may be beneficial in severe recurrent cases.
3. Rarely, tracheostomy or endotracheal intubation is needed in
severe respiratory distress.
 -246-

///. Congenital subglottic stenosis

- It presents with biphasic stridor since birth with no change of voice
(no hoarse cry).
- Direct or fiberoptic laryngoscopy shows narrowed subglottic area
which may be membranous or cartilagenous.
- It is associated with laryngomalacia in 10% of cases, and there may
be other associated congenital anomalies.
Treatment
1- Observation in mild cases.
2- In severe cases, tracheostomy may be needed.
3. Laryngofissure or endoscopic laser surgery may be done.
/ v . Subglottic haemangioma
1. It presents in infants less than 6 months and enlarges during the first
year of life, then it starts to regress spontaneously.
- The child may be asymptomatic at birth, and then stridor starts to
appear at the age of 3-6 months, which increases with crying and
straining due to vascular engorgement. There is no hoarse cry or
bleeding. It is associated with cutaneous haemangioma in 50% of
cases.
- Direct or flexible laryngoscopy shows a reddish or purpulish
subglottic soft mass, situated posteriorly or laterally.
Treatment
1. No treatment is usually required as it regresses spontaneously.
2. If symptomatizing with respiratory obstruction :
a. Tracheostomy and wait for spontaneous regression.
b. Endoscopic laser excision, cryosurgery, or injection of
sclerosing material may be tried but with no much success.
V. Congenital cysts
- These present with episodes of stridor and cyanosis, but without
hoarseness of voice.
- Direct laryngoscopy shows the cyst usually at the base of the tongue,
on the aryepiglottic flods, or the ventricular folds.
- Treatment
Microlaryngosurgery and excision by laser or cold instruments. If
this is not possible aspiration or marsupiulization of the cyst may
be done. In large cysts, tracheostomy and external laryngeal
surgery may be needed.
 -247-

Laryngocele
This is a special type of congenital cyst, that develops from the
laryngeal saccule (anterior portion of the ventricle between the tnie
and false cords). It may present at any age.
Clinical picture
1. Bulging of the false vocal fold and the ventricle on one side.
2. As it enlarges, it dissects its way through the thyrohyoid membrane
along the superior laryngeal nerve to present as a soft compressible
mass on the lateral side of the neck.
3. Stridor and airway obstruction as it enlarges and encroaches upon
the airway. Straining and coughing aggravate the stridor,
4. There is hoarseness of voice.
5. Sudden severe stridor, localized neck pain and tenderness occur if it
is infected.
6. X-ray lateral view shows air fluid level in the cyst. CT scan is
diagnostic.
7. Aspiration of the cyst with a fine needle may be done to establish
the diagnosis.
Treatment
Surgical excision using either, an endoscopic laser or microsurgery,
or an external approach in large extemal laryngocele. Temporary
tracheostomy may be rarely needed.
VI. Laryngotracheo-oesophageal cleft
- This is a rare congenital anomaly, which is due to failure of fusion of
the dorsal portion of the cricoid cartilage and the
tracheo-oesophageal septum creating a communication between the
larynx and trachea with the hypopharynx and oesophagus.
- It presents with hoarse cry, inspiratory stridor, and severe respiratory
distress. Coughing, chocking and cyanosis occur during feeding
due to aspiration, and this may lead to recurrent pneumonia.
VII. Congenital vocal cord paralysis
It is usually due to birth trauma, but it may be due to a congenital
CNS disorder (e.g. meningocele) or chest disease (e.g. mediastinal mass).
It may be unilateral or bilateral.
Treatment
Endotracheal intubation should be done in severe cases, followed
by tracheostomy, in bilateral cases.
 -248-

Trauma to the larynx

Types of trauma
/. Mechanical trauma
1. Penetrating wounds e.g. gunshots, bullets, stab wound, and cut
throat. This is usually associated with haemorrhage due to injury of
vessels in the neck.
2. Blunt injuries e.g. blow to the larynx, strangulation, and motor car
accidents. These may lead to fracture of the laryngeal cartilages,
dislocation of laryngeal joints or even cricotracheal separation
which is fatal.
3. Inhaled foreign body (mentioned later).
4. Surgical trauma;
a. Rough endoscopy (direct laryngoscopy, hypopharyngscopy, and
bronchoscopy), which may cause avulsion of the vocal cords,
and cricothyroid or cricoarytenoid joints dislocation.
b. High tracheostomy or cricothyroidotomy which may cause
perichondritis of the cricoid cartilage with subsequent subglottic
stenosis (mentioned later).
5. Intubation injury;
a. Rough endotracheal intubation may cause avulsion of a vocal
cord or intubation granuloma later.
b. Prolonged intubation may lead to subglottic stenosis later.
//. Chemical injury
1. Ingestion of corrosive material e.g. caustic potash.
2. Inhaled irritant gases, and steam.
///. Irradiation Injury; this may cause severe oedema, perichondritis of
the laryngeal cartilages and cartilage necrosis.
Clinical picture
Symptoms
1. History of external trauma or surgery.
2. Dyspnoea and stridor due to :
a. Displacement of the fractured cartilages.
b. Haemorrhage with blood trickiing down to the trachea.
c. Severe laryngeal oedema.
d. LaryngcEil stenosis, later on.
3. Severe local pain and dysphagia. Dysphagia may be due to
 249-

severe pain in the larynx during deglutition, oedema of the

arytenoids, associated pharyngeal or oesophageal injury.
4. Haemoptysis may occur due to tear of the mucous membrane.
5. Haemorrhage in cases of penetrating wounds.
6. External swelling due to oedema, haematoma, or surgical
emphysema.
7. Hoarseness of voice due to injury of the vocal cords (e.g.
avulsion), or vocal cord paralysis. Vocal cord paralysis may be
due to dislocation of the cricothyroid joint.
8. Shock : due to severe pain (neurogenic shock), or severe
haemorrhage (hypovolaemic shock), that particularly occurs
with penetrating wounds.
Signs
1. External swelling due to surgical emphysema, oedema, or
haematoma.
2. Deformity as blunting of the thyroid prominence and depressed
cartilages due to facture of the cartilagenous framework.
3. An evident external wound is seen in penetrating wounds.
4. Localized tenderness and crepitus due to fracture of the
cartilages or the hyoid bone which may be accompanied by
surgical enphysena.
5. Shock due to severe pain or haemorrhage.
Treatment
1. Ensure a patent airway by endotracheal intubation or tracheostomy
if there is severe stridor, or haemorrhage (to avoid aspiration of
blood).
2. Control the shock if present.
3. Management according to the pathology present:
a. Reduction of fractured cartilages or dislocated joints,
b. Ligature of bleeding vessels.
4. Steroids in cases of oedema particularly due to chemical or
irradiation injury.
5. Systemic antibiotics to guard against secondary infection.
 -250-

Inhaled foreign body

It is usually seen in children and mentally retarded adults, but may
occur also in normal adults.
Types of inhaled foreign bodies
1. Vegetable F.B. : seeds, beans, peanuts.
2. Non vegetable F.B.: pins, glass beads, plastic pieces, buttons, e t c .
3. Endogenous F.B. : vomitus, blood, etc ....
Sites of impaction
1, F.B. impaction in the larynx is rare to occur, because any F.B.
passing through the aerodigestive enterance (mouth or nose)
either passes down to the oesophagus, or through the glottis into
the bronchi. A large bolus of food or a sharp F.B. may rarely
impact in the larynx.
2. In the bronchi. : The F.B. usually impacts in the right main
bronchus being wider and more in line with the trachea.
However, it may remain in the trachea or passes down into
smaller bronchi.
Clinical picture
It occurs usually in children who may have the F.B. inhaled
during laughing, crying, or coughing.
A. Initial stage
A sudden onset of severe paroxysmal cough, chocking, dyspnoea,
cyanosis, and sometimes expectoration of blood stained secretions.
This occurs at the time of inhalation of the F.B. This history is usually
given by the parents of the child, but it may pass unnoticed if the child
was not supervised,
B. Latent stage
A variable free interval during which there may be mild paroxysmal
cough and expectoration. The length of this duration varies depending
on the size and the type of the foreign body. An organic F.B. gives
rise to inflammatory changes and secondary infections early,
C. Manifest stage
1. Mechanical obstruction may be either
a. Complete obstruction of a bronchus or bronchiole, which leads to
collapse of a lobe or segment of the lung (absorption collapse).
It manifests b y :
- Dyspnoea, cough and expectoration.
 -251 -

- Tactile vocal fremitus decreased.

- Shift of the mediastinum to the same side of the collapse.
- Localized dullness on percussion.
- No air entery on the affected side on auscultation, and no
wheezes.
b. Partial obstruction of a bronchus, which leads to obstructive
emphysema. The F.B. acts as a one way valve allowing air
entery into the lung during inspiration (as the bronchi dilate), but
preventing air out during expiration. There will be :
- Dyspnoea, cough and expectoration.
- Tactile vocal fremitus increased.
- Shift of the mediastium to the opposite side.
- Localized hyperesonance on percussion.
- Unilateral localized wheezes, and diminshed air entery on
auscultation.
2. Inflammatory changes
An organic F.B. exites severe irritation and inflammatory reaction
leading to bronchitis, bronchopneumonia, atelectasis, and lung
abscess, while a non organic F.B. produces a little inflammatory
reaction.
D. A large F.B. impacted in tiie larynx causes suffocation and death if not
urgently tracheostomized, and a shaip F.B. impacted in the larynx
may cause haemoptysis and pain on deglutition.
Investigations
1. Plain x-ray of the neck and chest: may show a radiopaque F.B., and
the secondary effects (i.e. collapse or emphysema).
2. Laryngoscopy and bronchoscopy.
Treatment
1. Urgent tracheostomy in cases of a large F.B. impacted in the.
larynx,
2. Removal of tiie F.B. by:
a. Direct laryngoscopy, if impacted in the larynx.
b. Bronchoscopy, if impacted in a bronchus, or trachea. The
procedure of bronchoscopy is a critical one, that needs a good
experience of the endoscopist, and the anasthesis, because it is a
shared airway between both of them. Here, aneasthetist is going
to be introduced through die bronchoscope itself. The setup of
 -252-

instruments must be equipped with different kind of forceps,

which can cope with different foreign bodies. One of the most
difficult foreign bodies that one can meet is an open small safety
pin in an infant.

Laryngeal stenosis
- This is cicatricial narrowing of the endolarynx, leading to respiratory
distress.
- Chronic laryngeal stenosis may be glottic, supraglotdc, subglottic, or
involving more than one region. The most common, and the most
difficult to treat is the subglottic stenosis.
Aetiology
A. Congenital stenosis
It is due to inadequate recanalization of the laryngeal lumen.
According to the degree of canalization, it may be :
1. Congenital laryngeal atresia.
2. Congenital laryngeal web.
3. Congenital subglottic stenosis.
B. Trauma
Laryngeal trauma is the most common cause of acquired laryngeal
stenosis. It may be :
1. External laryngeal trauma e.g. penetrating wounds or blunt
injury. Blunt trauma is more prone to produce stenosis due to a
fractured cricoid cartilage or inadequately managed case in the
early stages.
2. Internal laryngeal trauma
a. Prolonged endotracheal intubation is the most common cause
of subglottic stenosis (about 90% of cases). It occurs more
with rubber tubes than with silastic ones.
b. Laryngeal surgery :
- Cricothyroidotomy and high tracheostomy can lead to
subglottic stenosis especially in children.
- Partial laryngectomies.
- Excision of bilateral vocal cord nodules or multiple
papillomata can lead to an anterior glottic web particularly
if both vocal cords are denuded simultaneously.
b. Over dose of radiation therapy to the larynx may lead to
cartilage necrosis and subsequent stenosis.
 1 ^

-253-

d. Intralaryngeal burns due to thermal injury (e.g. fumes), or

chemical injury (e.g. corrosives ingestion).
C. Chronic inflammation
- The most important is laryngoscleroma which causes subglottic
stenosis.
- Others include, T.B., syphilis, leprosy, sarcoidosis, amyloidosis,
and diphtheria.
D. Laryngeal neoplasms
- Chondroma, fibroma, haemangioma and carcinoma.
- It may be due to tumour infiltration associated, infective
perichondritis, postirradiation perichondritis or post surgical
scarring.
Types of laryngeal stenosis (Fig.60)
1. Subglottic stenosis is the most
common.
2. Supraglottic stenosis.
3. Glottic stenosis, which.may be.
a. anterior glottic stenosis,
which usually follows
Fig.60. subglottic
microlaryngosuregy. stenosis
b. posterior glottic stenosis due
to endotracheal intubation.
c. complete glottic stenosis which is usually associated with
supraglottic or subglottic stenosis.
Clinical picture of subglottic stenosis
A. Mild to moderate stenosis may be asymptomatic. Stridor may
manifest on exertion, or during an upper respiratory tract infection.
B. More severe stenosis:
1. Biphasic stridor and dyspnoea.
2. Vigorous effort during respiration.
- Symptoms appear 2-4 weeks after the laryngeal insult, but may be
longer. In congenital laryngeal stenosis it appears shortly after
birth.
- Examination : Indirect laryngoscopy and fiberoptic laryngoscopy
show the stenosis, and the degree of narrowing of the airway.
 -254-

Investigations
1. Plain x-ray soft tissue lateral view :
2. CT scan of the neck : to show the length, site and degree of the
stenotic segment.
3. Direct laryngoscopy and bronchoscopy.
4. Pulmonary function tests to compare the preoperative with the
postoperative values.
Treatment
A. Tracheostomy should be done if there is moderate or severe stridor.
B. Endoscopic procedures:
1. Endoscopic laser excision of the stenosis.
2. Repeated dilatation with or without intralesional steroid injecton.
C. External laryngeal surgery (laryngoplasty), it includes submucosal
excision of the stenosis, with insertion of a skin graft or stent to
maintain the lumen.
 - 255 -

Inflammations of the larynx

/. Acute non-specific laryngitis
This is an acute catarrhal inflammation of the mucosal lining of the
larynx.
Aetiology
- It usually follows upper respiratory tract infections e.g. common
cold, influenza, and exanthemata.
- Organisms : It is almost always a viral infection, or it starts as
viral to be followed later by secondary bacterial infection,
a. The common virses include; influenza, parainfluenza,
rhinovirus, coxackivirus, respiratory syncytial viruses,
myxovirus and adenovirus.
b. The secondary bactrerial invaders include : streptococcus
pneumonia, Beta haemolytic streptococci, and
staphylococci.
- Predisposing factors :
a. Improper use of'voice.
b. Tobacco smoking.
c. Postnasal discharge as in sinusitis.
d. Irritant fumes e.g. chloride, bromide, ammonia.
e. Dusty occupation or environment,
f. Trauma e.g. F.B. inhalation, endoscopy and intubation.
Clinical picture
1. Headache, fatigue, malaise, and occasionally fever.
2. Hoarseness of voice.
3. Sensation of discomfort in the larynx and pain on phonation.
4. Dry cough, but later on, there may be viscid yellowish sputum'
due to secondary bacterial infection.
5. Indirect laryngoscopy (or flexible laryngoscopy) reveals;
a. Diffuse bilateral symmetrical congestion and oedema of the
mucosa of the larynx.
b. Congested oedematous mobile vocal cords. Sometimes, the
cords fail to approximate completely during phonation.
c. Encrusted mucoid secretion may be detected, and occasionally
there may be submucosal haemorrhage.
 -256-

Treatment
1. Voice rest.
2. Adequate fluids and light diet.
3. Humidification : steam inhalation medicated by tincture
benzoine.
4. Systemic antibiotics to avoid secondary bacterial infection.
5. Mucolytics.
6. Avoid antihistaminics as they render secretions more viscid and
difficult to expectorate
Acute non specific laryngitis in children
Acute laryngitis in children is more critical, and differs from that in
adults because of:
1. Anatomical factors :
a. The lumen of the larynx is relatively smaller in proportion to
other regions, therefore minimal oedema may cause marked
airway obstruction.
b. The mucosa is less closely adherent to the submucosa, and the
submucosal areolar tissue is loose, therefore oedema when
occurs is more extensive.
c. The lumen of the larynx is funnel shaped with the subglottic
region being the narrowest part.
d. The lymphatic supply of the mucosa is more abundant.
2. The immune system of the child is not well developed and more
unstable.
3. The nervous regulation of the larynx in infants is still immature,
therefore any irritation by infection or secretions causes glottic
.spasm.
- Because of the above mentioned factors, acute laryngitis is a serious
affection in childhood, that should be taken seriously and handled
promptly.
Aetiology
' It usually starts by viral infection, that is followed by secondary
bacterial infection.
' It usually follows viral upper respiratory tract infections e.g.
common cold, influenza, and viral exanthemata.
 -257-

Clinical picture
1. Dry cough with metallic rough tone.
2. Inspiratory stridor, dyspnoea and rapidly developing cyanosis
may occur due to oedema or laryngeal spasm.
3. Hoarseness of voice.
4. Examination by flexible laryngoscopy reveals; bilateral diffuse
erythema, congestion, and oedema of the mucosa of the larynx
and vocal cords. Subglottic oedema with narrowing of the
airway is alwr^ys evident. There may be viscid mucoid
secretions.
Differential diagnosis
Acute stridor in children with special concern to :
1. Laryngeal diphtheria.
2. Laryngomalacia,
3. Inhaled F.B.
Treatment
1. Hospitalization, bed rest, and adequate fluids.
2. Parenteral antibiotics e.g. penicillin, ampicillin, and third
generation cephalosporins.
3. Steroids e.g. dexamethazone I.V. to decrease oedema.
4. Antispasmodics.
5. Oxygen inhalation.
6. Humidification.
- The child should be carefully observed for signs of respiratory
obstruction, and other vital signs. If there is severe respiratory
distress from the start, or the condition is deteriorating, do not
hesitate to ensure a patent airway by endotracheal intubation or
tracheostomy..
N.B. : Nasotracheal intubation is better tolerated than oral intubation. •
//. Acute epiglottitis
Aetiology
- It is usually caused by Haemophilus influenza type B.
- It is more common among infants and children than in adults.
Clinical picture
1. It usually starts by sorethroat, and manifestation of viral upper
respiratory tract infection. This is followed by severe
odynophagia and drooling of salvia.
 -258-

2. There is high fever, and sometimes the temperature exceeds

40''C, associated with signs of severe illness (malaise, headache,
and anorexia).
3. The patient has a muffled voice (hot potato voice).
4. There is often a rapidly progressive and potentially fatal increase
of stridor, that may occur suddenly and may be life threatening,
especially in children.
Examination
1. Indirect or flexible laryngoscopy show marked oedema of the
epiglottis, aryepiglottic folds and the whole supraglottic area.
2. The epiglottis is often directly visible on inspection of the
oropharynx, as a red swollen mass. Care should be taken when
derpressing the tongue as this can cause fatal glottic spasm.
3. Pharyngeal congestion and oedema.
4. Enlarged tender upper deep cervical lymph nodes.
N.B. : Examination should be carried out in a room with facilities to
do urgent tracheostomy, or intubation.
Treatment
Acute epiglottitis is considered as an emergency situation and the
patient should be hospitalized.
1. If there is airway obstruction, maintain the airway by peforming
tracheostomy or endotracheal intubation.
2. Parenteral antibiotics.
3. Steroids.
4. Oxygen inhalation and humidification.
///. Acute laryngotracheobronchitis
Aetiology
In children, an acute respiratory infection may run a fulminant
course spreading to the entire respiratory tract. The organisms are-
those commonly involved in respiratory infection, but the
haemolytic streptococci are the predominant.
Clinical picture
1. It usually starts by manifestations of coryza in the form of mild
fever, rhinorrhea, and nasal obstruction. This is followed by
marked rise of temperature and toxaemia, with malaise,
anorexia, and generalized fatigue.
2. Slowly pregressive stridor and respiratory distress with croupy
 -259-

cough, and expectoration of thick viscid tenacious sputum. This

is the usual presentation in children.
3. In adults, it presents more with hoarseness of voice rather than
stridor, as the larynx is wider and larger in size.
4. Examination reveals subglottic oedema.
Treatment
1. Hospitalization as it requires vigorous treatment.
2. Broad spectrum antibiotics.
3. Systemic corticosteroids to reduce the inflammatory reaction and
oedema.
4. Mucolytics and aerosols inhalation.
5. Tracheostomy or endotracheal intubation should be performed if
there is severe respiratory obstruction, however, it is rare to
occur.
IV, Acute specific laryngitis (laryngeal diphtheria)
It usually occurs secondary to faucial diphtheria, rarely it is
primarily laryngeal.
Clinical picture
1. Manifestation of toxaemia (mentioned before).
2. Hoarseness of voice and brassy cough.
3. Stridor due to obstruction by the diphtheritic membrane.
4. Dyspnoea, may be due to heart failure.
5. Examination (indirect or flexible laryngoscopy) shows the
greyish white, dirty, diphtheritic membrane.
Treatment
1. Antitoxic serum (see faucial diphtheria).
2. Tracheostomy in severe airway obstruciton.

Chronic laryngitis
/. Chronic nonspecific laryngitis
1. Chronic diffuse hypertrophic laryngitis.
2. Chronic localized hypertrophic laryngitis.
3. Chronic atrophic laryngitis.
//. Chronic specific laryngitis
1. Laryngoscleroma.
2. T.B. and lupus vulgaris.
 -260-

3. Syphilis.
4. Leprosy.
5. Mycosis of the larynx (fungal infections).
Chronic difTuse hypertrophic laryngitis
Aetiology
1. Repeated acute laiyngitis.
2. Excessive smoking.
3. Abuse of voice e.g. shouting and screaming.
4. Dusty environment, and exposure to fumes.
5. Postnasal discharge due to chronic sinusitis, nasal allergy and
adenoids.
Clinical picture
1. Hoarseness of voice is the main symptom.
2. Irritative cough and expectoration.
3. Sensation of dryness in the throat, with desire for frequent
clearing of the throat (hemming).
4. Examination (indirect laryngoscopy) reveals :
a. Diffuse congestion of the mucosa of the larynx.
b. Bilateral symmetrical congestion and thickening of the vocal
cords. The edges of the vocal cords appear rounded instead of
being flat, with free mobility, but incomplete approximation
during phonation.
c. Dilated vessels may be seen on the vocal cords, or on the
ventricular bands.
5. It may be complicated by contact ulcer on the vocal cords, and
arthritis of the cricoarytenoid joint.
Treatment
1. Elimination of predisposing factors. This is the most important
measure.
2. Adequate voice rest.
3. Steam inhalation of tincture benzoine.
4. A moist warm climate is beneficial.
Chronic localized hypertrophic laryngitis (Fig.61)
A. Vocal cord nodules (singer's nodules).
This is a localized area of hyperplasia of the epithelium on the free
edge of the vocal cord or cords, or it may be an organized
subepithelial haematoma. It is more common in females.
 ^m

-261-

Aetiology
1. The chief cause is voice
misuse, that's why it is more
common in professional
voice users e.g. singers, and
teachers.
2. Now, there is a relation
between reflux oesophagitis,
and the development of vocal Fig,61. vocal cord
nodules
cord nodules.
3. It may be periciptated by
viral laryngitis.
Clinical picture
1. Hoarseness of voice, with weakness and change in the timbre of
voice.
2. Examination (indirect and flexible laryngoscopy) reveals;
bilateral small tiny nodules, that are pinkish or pearly white in
colour. They appear as raised projections on the free margins of
the vocal cords, usually at the junction of the anterior and
middle thirds of the vocal cord (this is the most active segment
of the cord, and it is the site of maximum traumatization).
Treatment
1. Voice rest, and avoid voice abuse.
2. Speech therapy to teach the patient the correct way of
vocalization. This may be effective in early recent nodules.
3. Topical steroid spray may be recently developed nodules.
4. Removal by microlaryngosurgery using microlaryngosuregical
instruments, or laser. It is indicated in persistent nodules, and
should be followed by voice therapy, as they have the tendency
to recur after excision.
B. Vocal cord polyp (Fig.62)
This varies from localized subepithelial oedema (oedeinatous
polyp), to vascular engorgement (vascular polyp), which is followed by
fibrosis (fibrotic polyp). It is more common in males.
Aetiology
Voice abuse is the cause. It is due to vacolization in a loud harsh
manner. This causes injury of the subepithelial connective tissue. It may
develop after a single voice strain. Allergy may play a role.
 -262-

Clinical picture
1. Hoarseness of voice.
2. Intermittent aphonia (voice breaks)
may occur if the polyp becomes
wedged between the vocal cords
during phonation.
3. Chocking may occur with large
polyps.
Fig.62. right vocal
4. Examination (indirect or flexible cord polyp
laryngoscopy) reveals, a sessile or
pedunculated single polyp, which
arises mostly from the undersurface
of the free margin of the vocal cord usually at the junction of its
anterior and middle thirds. It is variable in size, it may be uni or
bilobed, or even multilobed. The colour of the polyp is usually
translucent. Pale grey (oedematous polyp), whitish (fibrotic
polyp) or red congested (haemangiomatous polyp).
Treatment
1. Voice rest, humidification, and topical steroid spray.
2. Avoid voice abuse.
3. Excision by microlaryngosurgery is always needed in addition to
the above measures. It is done either using laser or
microlaryngosurgical instruments. This should be followed by
speech therapy to teach the patient the healthy way of
vocalization.
C. Leukoplakia
This is localized hyperplasia and hyperkeratinization of the
epithelial lining of the vocal cords. The epithelial cells show marked
degree of dysplasia. It presents with persistent hoarseness of voice. On
examination, it appears as a whitish plaque or patch, at the level of the
vocal cord, or slighdy raised above the surface. It may appear as a diffuse
villous or verrucous lesion. The vocal cords are freely mobile.
Treatment; Excision by microlaryngosurgery using laser or cold
instruments. Removal should be followed by careful prolonged
follow up as the condition is precancerous.
Chronic specific laryngitis (Granulomas of the larynx)
A. Laryngoscleroma
- This is a chronic specific inflammation of the upper respiratory tract
 -263-

caused by klebsiella rhinoscleromatis (Frisch bacillus). It is

endemic in Egypt, It is alway secondary to and associated with
rhinoscleroma (rhinolaryngoscleroma), but it may be primarily
laryngeal.
- It most commonly affects the subglottic region, but it may occur in
any part of the larynx.
Clinical picture
1. Diphasic stridor and dyspnoea due to subglottic stenosis or
webbing.
2. Hoarsness of voice may be present,
3. Irritating cough with expectoration of greenish crusts.
4. Examination (indirect or flexible laryngoscopy) reveals, a pale
pinkish smooth swelling on both sides of the subglottic region,
which is covered by greenish crusts. Later, in the fibrotic stage,
there will be subglottic webbing or stenosis.
Investigations
1. Direct laryngoscopy and biopsy.
2. Plain x-ray of the larynx, soft tissue lateral view.
3. CT scan of the larynx to show the degree and the length of the
subglottic stenosis.
Treatment:
1. Medical treatment (mentioned in rhinoscleroma).
2. Voice rest and humidification.
3. Tracheostomy may be needed if there is significant respiratory
obstruction.
4. Endoscopic laser excision of the subglottic web.
B. T,B, of the larynx
Aetiology
It is almost always secondary to pulmonary T.B. Primary T,B. of
the larynx is extremely rare.
Clinical picture
1. Hoarseness of voice, which is at first mild, but later becomes
progressive. There is phonosthenia (weak voice which tires
easily), which is due to tuberculous myositis of the laryngeal
muscles. There may be periods of aphonia.
2. Odynophagia (pain on swallowing), which is a marked symptom.
It prevents the patient from swallowing, and this is cridcal as the
tuberculous padent needs adequate nutridon.
 -264-

3. Localized pain referred to the ear, secondary to mucosal

ulcerations.
4. Tendemess may be detected due to perichondritis.
5. Stridor and dyspnoea are not common.
6. Examination (indirect and flexible laryngoscopy) reveals;
a. Pallor of the pharyngeal and laryngeal mucosa.
b. T.B. granulation tissue on the arytenoids, and the
interarytenoid region.
c. Pseudooedema of the arytenoids, epiglottis and aryepiglottic
folds.
d. T.B. ulcers on the interarytenoid region, arytenoids, or the
posterior parts pf the vocal cords. The ulcers are superficial,
irregular with thin ragged undermined edges, cyanotic bluish
margins, and yellow caseous floor,
e. Rarely, a tuberculoma is seen as a small tumour like mass of
T.B. granulations at the base of the epiglottis.
f. Impaired cord mobility due to myositis, affection of the
cricoarytenoid joint, or involvement of the recurrent
laryngeal nerve by an apical pulmonary T.B.
N.B.: T.B. cheifly affects the posterior half of the larynx, mainly the
interarytenoid region, arytenoids, and posterior parts of the
cords. It may also affect the venticular folds or the laryngeal
surface of the epiglottis.
7. Manifestations of T.B. toxaemia : night fever, night sweating,
anorexia, loss of weight and wasting.
8. Manifestations of pulmonary T.B. : chest pain, productive cough
and haemoptysis.
Complications
1. Stenosis and excessive fibrosis.
2. Cartilage necrosis and perichondritis.
Investigations
1. Sputum analysis for T.B. bacilli.
2. Chest x-ray may show pulmonary T.B.
3. High ESR.
4. Tuberculin test: This is a good test when negative.
5. Direct laryngoscopy and biopsy.
 -265-

Treatment
1. Antituberculous drugs e.g. PAS A, streptomycin, rifampicin, and
pyrazinaniide. They are given in various combinations for a long
period of time (9-18 months).
2. Tracheostomy is done if needed.
3. Local anaesthetic spray before meals, as the ulcers are severly
painful.
C. Lupus of the larynx
It is rare and is mostly secondary to nasal lupus. It affects young
age. The site of predilection is the epiglottis, then the aryepiglotdc folds.
Gross pathology; pale reddish (apple jelly nodules) are seen on a pale
mucosa. Areas of ulceration occur on one side of the lesion with a
healed scarred edge on the other side. The epiglotus looks notched and
later on scarred.
Clinical picture
, - May be symptomless.
- Vague discomfort in the throat.
- No hoareseness of voice, only in very late cases.
- No dyspnoea.
Investigation
- X-ray chest,
- Biopsy from the lesion reveals the pathologic picture (see nasal
lupus).
Treatment
- Antituberculous treatment.
- Calciferol (vitamin D2).
D, Syphilis of the larynx
- It is very rare.
- It affects mainly the anterior half of the larynx, mainly the epiglottis.
Stages
1. Primary sypivlis : Chancre of the epiglotds, which is very rare.
2. Secondary syphilis: mucous patches, which are also very rare.
3. Tertiary syphilis : Gumma is the commonest form of syphilis in
the larynx.
Clinical picture
1. Hoarseness of voice is the main symptom (Harsh strong voice).
 — ^ - -'

-266-

2. Stridor due to oedema and fibrosis (uncommon).

3. Sensation of discomfort in the throat and irritative cough, but
there is no pain.
4. Examination reveals affection of the anterior half of the larynx,
most commonly the epiglottis. It takes one of two forms :
a. Localized gumma of the epiglottis, where the epiglottis
appears swollen with ulcerated necrotic surface.
b. Diffuse asymmetrical gummatous infiltration without
ulceration.
5. Vocal cord paralysis may occur due to tabes dorsalis.
Complications
1. Healing by dense fibrous tissue and stenosis.
2. Perichondritis.
3. Vocal cord paralysis.
Investigations
1. Direct laryngoscopy and biopsy.
2. Serological tests for syphilis.
Treatment
1. General antisyphilitic treatment: Penicillin 100,000.0 units/day
I.M., 10-14 days, which may be repeated.
2. Tracheostomy if necessary.
D. Leprosy of the larynx
- Two forms of leprosy can occur in the larynx either lepromatous or
tuberculoid leprosy.
- The epiglottis and the aryepiglottic folds are most often affected.
There is granulatomatous swelling and often ulceration and
destruction, primarily in the supraglottic region. The epiglottis may
be curled, and the mucosa may^be studded with tiny nodules.
- It is treated by Dapson, clofazimine, and rifampicin. The treatment
should be prolonged for years.
E, Fungal infections (Mycosis) of the larynx
Aetiology
1. Prolonged use of antibiotics.
2. Generalized disease, as diabetes, hypovitaminosis, malnutrition,
hepatic diseases, and disseminated malignant disease.
3. Cytotoxic chemotherapy.
 -267-

Isolated infection of the larynx is rare, but usually it is a part of a

fungal infection of the aerodigestive tract, or a systemic fungal
infection.
Types :
1. Candidiasis (moniliasis):
It is caused by Candida albicans, and is usually secondary to
candidiasis of the oropharynx. There is oedema and erythema of
the mucosa, with whitish grey adherent fibrinous pseudomembrane
and superficial ulceration. Treatment is primarily directed to treat
the underlying cause, and drugs containing nystatine or miconazale
are given topically as lozenges or as aerosol.
2. Coccidioidomycosis :
It presents as a granulomatous lesion. Amphotericin B is the
treatment of choice.
3. Histoplasmosis : Similar to coccidioidomy cosis.
4. Actinomycosi.
5. Blastomycosis.
6. Cryptococcosis,
7. Aspergillosis.
 -268-

Vocal cord paralysis

Vocal cord paralysis is due to affection of the nerve supply of the
larynx, either the vagus nerve or the recurrent laryngeal nerve (RLN).
The left recurrent laryngeal nerve is more commonly affected than the
right due to its longer course.
/. UnliUUeral vocal cord paralysis
Ateiology
A. Peripheral lesions
These are the commonest causes accounting for about 90% of
cases.
1. Surgical trauma (20%)
a. Oesophageal and lung surgery especially for carcinoma.
b. Cardiovascular surgery.
c. Thyroidectomy (the right recurrent laryngeal nerve is more
liable to injury, because it runs from lateral to medial, and not
lengthwise with the trachea.
d. Radical neck dissection.
e. Removal of a pharyngeal pouch.
f. Surgery of the skull base.
2. Neoplastic (25%)
a. Bronchogenic carcinoma.
b. Oesophageal carcinoma.
c. Thyroid malignancy especially anaplastic carcinoma.
d. Nasopharyngeal carcinoma and middle ear carcinoma eroding
the skull base. Here the 9th, 10th, 11th, and 12th cranial
nerves may be involved and not the vagus alone.
c. Malignant tumours of the hypopharynx,
f. Malignant cervical lymph nodes (metastasis or lymphoma).
g. Hilar lymphoma and mediastinal tumours.
h. Meningioma, and acoustic neuroma (skull base tumours).
3. Non surgical trauma (20%)
a. Neck injuries e.g. circumferential neck trauma, strangulation,
and open injuries.
b. Dislocation of the cricothyroid joint.
c. Fracture base of skull ,
d. Pressure on the left RLN by enlarged left atrium or an aortic
aneurysm.
 -269-

4. Inflammatory (5%)
a. Apical pulmonary tuberculosis.
b. Basal meningitis, and skull base osteomyelitis.
c. Syphilis.
5. Preipheral neuritis
a. infections; herpes, influenza, typhoid, diphtheria and
infectious mononucleosis.
b. Chemicals: alcohol, lead, mercury.
c. Diabetic neuritis.
d. Beri Beri.
e. Ascending polyneuritis (Guillian - Barre syndrome).
f. Radiation neuritis.
6. Congenital
a. Platybasia.
b. Hydrocephalus.
c. Amold-chiari syndrome.
7. Miscellaneous
a. Myasthenia gravis.
b. Rheumatoid arthritis, polyarteritis nodosa, systemic lupus.
c. Sarcoidosis.
d. Thrombosis of the subclavian artery.
8. Idiopathic (15-30%)
It is clained to be a viral neuritis. The right vocal cord is more
common to be affected.
B. Central lesions
1. Cerebral : trauma e.g. lacerations, thrombosis, embolism,
haemorrhage, meningitis, encephalitis, abscess and tumours.
2. Bulbar : due to affection of the nucleus ambiguous of the vagus
in the medulla (true bulbar palsy) by thrombosis, embolism or
haemorrhage of the posterior inferior cerebellar artery, head
trauma, encephalitis, poliomyelitis and diphtheria, and
medullary tumours.
Positions of the vocal cords (Fig.63)
1. Median postition : both cords are in the midline.
2. Paramedian position : 3-5 mm width of the glottis.
3. Cadaveric (intermediate) position : 7 mm width of the glottis.
 -270-

4. Slight abduction : 14 mm width of the glottis.

5. Full abduction position of respiration : 18-19 mm width of the
glottis.

paramedian cadaveric

full abduction
Fig.63. unilateral vocal cord paralysis

Explanation of difTerent positions of the vocal cords

in cord paralysis:
A. Semon's law : It is proposed that the motor fibres innervating the
adductor and the abductor muscles lay in separate bundles in the
recurrent laryngeal nerve, so that a progressive RLN injury will
lead first to abductor paralysis with the vocal cord in the median or
paramedian position. Secondly, adductor paralysis will occur with
the vocal cord in the cadaveric position.
B. Wegener - Grossman theory : It is proposed that a paralysed
vocal cord in the paramedian position is a purely RLN paralysis
(continued adducting action of cricothyroid), while a paralysed
cord in the cadaveric position is due to combined SLN and RLN
paralysis (the adducting action of cricothyroid muscle is lost).
C. Adductors are more powerful than abductors allover the body,
because of their natural protective functions, so when the RLN is
injured, the adductors take tiie upper hand.
Clinical picture
There is affection either of the recurrent laryngeal nerve or both
recurrent and superior laryngeal nerves (SLN) (i.e. vagal injury). In
the latter the adducting action of the cricothyroid muscle is lost.
 -271-

Symptoms
1. It may be asymptomatic due to compensation by the other cord.
2. Hoarseness of voice which appears early and recovers
spontaneously because the mobile vocal cord compensates by
crossing the midline to meet the paralysed cord during
phonation.
3. There is no stridor or respiratory distress because the space
between the two vocal cords (Laryngeal shink) is sufficient to
cope with the respiratory needs, as the healthy cord can fully
abduct,
4. Aspiration may occur as the laryngeal sphincteric mechanism is
incompetent and part of the larynx is insenistive, this improves
later.
5. Lack of build up of the intrathoracic pressure, leading to inability
to strain and to perform heavy manual work. It is due to
inadequate closure of the glottis.
Signs
1. Indirect (or flexible) laryngoscopy reveals :
a. median or paramedian position of the vocal cord in RLN
inujury.
b. Cadaveric position of the vocal cord in both RLN and SLN
injury (paralysis of the cricothyroid muscle). In addition there
will be bowing of the vocal cord due to lost tension.
c. The vocal cord is paralysed (no motion) and appears shorter,
thinner and at a lower level than the opposite cord. The
arytenoid is leaning forwards, and the aryepiglottic fold is
leaning inwards.
d. Compensation by the other cord may be seen during
phonation.
2. Full head, neck and chest examination to detect a cause
especially bronchogenic carcinoma (remember that vocal cord
paralysis is a sign of an underlying disease).
Investigations
A. To detect the cause
1, Plain x-ray chest, nasopharynx, and neck.
2, Barium swallow.
3, Thyroid scan.
 Wgf

-272-

4. C.T scan from the skull base to the midthorax.

5. C.T scan and MRI brain may be done.
6. Haematological; full blood count, ESR, viral studies, and
blood sugar.
7. Panendoscopy; This includes, nasopharyngoscopy, direct
laryngoscopy, hypopharyngoscopy, oesophagoscopy, and
bronchoscopy. Biopsy should be taken from any suspicious
lesion, howerver, a biopsy from the fossa of rosenmuller on
the side of the paralysed cord, and from the bronchial carina
should be performed even if there is no evident growth. At
the end of endoscopy, palpate the arytenoid by an instrument
to distinguish between vocal cord paralysis and arytenoid
fixation in cricoarytenoid joint arthritis.
Panendoscopy is done if the clinical and radiological evaluations
did not reveal a cause.
B, Respriratory function test; to assess the results of surgery.
Treatment
1. Treatment of the cause if possible. If the patient has
bronchogenic carcinoma of the left lung with a paralysed left
cord, it is considered inoperable.
2. Most cases require no treatment as compensation by the other
cord usually occurs, and also spontaneous recovery of the
paralysed cord may occur especially in post-traumatic cases. It
requires only observation or speech therapy if there is marked
dysphonia.
3. Surgical Treatment Before embraking on restorative procedures,
6-12 months interval should elapse to allow time for
compensation,
- // is indicated in :
a. Persistent marked dysphonia after maximum compensation
especially in professional voice users, or if compensation
did not occur.
b. Persistent serious aspiration.
- Operations performed:
The aim is medialization of the paralysed vocal cord. This
can be achieved by one of the following procedures :
a. Teflon injection lateral to the true vocal fold in order to
increase its bulk and move it medially, to ensure adequate
 -273-

glottic closure. The amount of injected teflone paste is

critical and should be accuratly determined to avoid
hazards of over injection, mainly respiratory obstruction.
b. Collagen injection is more preferred nowadays, but its
drawback is that it is absorbed after several years.
c. Medializauon of the vocal cord (Thyroplasty type I)) : It
consists of medial displacement of a small rectangular
musclocartilagenous flap of the thyroid cartilage with the
attached perichondrium with the help of a fashioned
silastic block, at the level of the vocal cord in order to
displace it medially.
d. Nerve muscle pedicle reinnervation is tried with doubtful
results.
//. Bilateral vocal cord paralysis (Bilateral abductor
paralysis).
Aetiology
The lesion is peripheral affecting the two recurrent laryngeal nerves
1. Surgical trauma:
d. During thyroidectomy (the commonest cause),
b. Oesophageal resection.
2. Peripheral neuritis (mentioned before).
3. Neoplastic :
e.g. Anaplastic corcinoma of the thyroid gland.
Clinical picture
Symptoms
1. The voice is fairly good, monotonus, but tires easily.
2. There is stridor which may be severe as the glottic shink in not
enough. Stridor increases on exertion or if there is upper
respiratory tract infection and during pregnancy.
Signs
1. Indirect laryngoscopy reveals:
Both vocal cords are in the median or
paramedian positions with inability of
abduction, so that the glottic shink is
very narrow. (Fig.64)
Fig.64, bilateral
2. Head and neck examination may abductor paralysis
reveal a cause.
 •w

-274-

Investigations
1. Thyroid scan and fine needle aspiration from any thyroid nodule
if malignancy is suspected.
2. CT scan of the neck.
3. Haematological investigations.
4. Respiratory function tests to compare the preoperative and
postoperative respiratory functions, to assess the results of
surgery.
Treatment
1. Tracheostomy should be done if there is severe stridor.
2. If it is discovered soon after thyroidectomy which is the
commonest cause, immediate nreexploration of the neck is
performed to remove a ligature possibly entangling the nerve.
However, reanastomosis of a sectioned nerve is not beneficial.
3. In established paralysis :
a. Surgical treatment for widening of the glottis is carried out, if
the cords don't show spontaneous recovery in a period of 3-6
months. It is done by one of the following procedures ;
1. Endoscopic arytenoidectomy with posterior cordectomy
preferably done by CO2 laser or by microlaryngosurgical
instruments. Removal of the anterior two thirds of one
arytenoid, and the posterior part of the cord is usually
sufficient. This is the procedure of choice nowadays.
2. Woodman's operation : It is done by an external approach,
and it entails displacement and fixation of one arytenoid
cartilage downwards and laterally.
3. Other procedures of doubtful results include ;
- Cutting the superior laryngeal nerve to paralyse the
cricothyroid muscle.
- Reinnervation procedures for the posterior cricoaryte-
noid muscle or RLN reinnervation are tried but with
poor results.
N.B.: when considering treatment, it is important to remember that
the patient has a good voice but a poor airway, and any
operative procedure to improve the airway will decrease
the quality of voice, and on occasions it fails to improve
the airway, furthermore, some degree of aspiration may
occur after the surgery. Therefore, sometimes a permanent
tracheostomy with a speaking valve may be another good
option.
 -275-

Tumours of the larynx

Benign tumours of the larynx
A. Epithelial
1. Papilloma.
2. Neurofibroma (occurs in the aryepiglottic fold).
3. Schwannoma.
4. Chemodectoma (paraganglioma) occurs in relation to the superior
or recurrent laryngeal nerves.
5. Granular cell tumour (occurs in the posterior third of the vocal
cord.
6. Adenoma, is the mostly in supraglottic region.
B. Mesenchymal
1. Haemangioma : —> a. Infantile : subglottic.
—> b. Adult: supraglottic.
2. Chondroma.
3. Fibroma.
4. Lipoma, myxoma, myoma.
/. Papilloma (The commonest bengin laryngeal tumour)
A. Single papiiloma
It affects mainly adults (30-50 years), and males are more
commonly affected than females 2:1.
Pathology
Site : The free edge of the vocal cord is the commonest site.
However, it may arise in the subglottic region, ventricular
folds, or the anterior commissure.
Microscopically : A cord of vascular C.T., covered by hyperplastic
stratified squamous epithelium.
Clinical picture
Symptoms
1. Hoarseness of voice is the main symptom,
2. Stridor may occur if it reaches a large size.
Signs : (Indirect laryngoscopy)
Shows a solitary, unilateral, whitish or pinkish warty like verrucoid
growth usually on the vocal cords. It is sessile or pedunculated and
of variale size.
 -276-

Treatment
Surgical excision either by:
1. Microlaryngosurgery using laser or cold instruments if small.
2. Laryngofissure if large.
It may recur after removal, and may turn malignant in 3-4% of cases.
B. Multiple papillomatosis (Recurrent respiratory papillomatosis or
juveinl multiple papillomatosis).
It affects children. 5-15 years.
Aetiology
It is not a true neoplasm, but it may be due to :
1. Viral infection with Human papilloma virus especially types 6
and 11. (most accepted)
2. Autoimmune disturbance or hormonal imbalance.
Pathology : resembles squamous cell papilloma of adult but it is
sessile, smaller, multiple and never turns malignant.
Site : It commonly affects the vocal cords, but it may occur
anywhere in the larynx, and may extend to the trachea, bronchi,
or even the tracheostomy orifice.
Clinical picture
Symptoms
1. Stridor and respiratory
obstruction are the main
symptoms.
2. Hoarseness of voice.
Signs : (indirect laryngoscopy
or flexible laryngoscopy)
Show multiple, sessile,
whitish or pinkish warty Fig.65. multiple
growths affecting any papillomatosis
portion of the larynx, and
may extend to the trachea.
(Fig.65)
Treatment
1. Tracheostomy is almost indicated as there is always marked
respiratory obstruction, but it carries the risk of implantation of
the papillomata at the orifice of the tracheostomy with extension
to the lower respiratory mucosa, so, it should always be a low
trachestomy.
 - 277 -

2. Repeated endoscopic surgical excision by laser micivlan ngosiu

gery or by cold instruments. Laser is prefera\l because of its
excellent haemostasis, minimal fibrosis and lesser incidence of
recurrence.
3. Inteferon therapy following laser excision is claimed to reduce
the incidence of recurrence.
- There is a high incidence of recurrence after excision, but it tends to
regress at puberty. It never turns malignant.
- Radiotherapy was previously used as a treatment modality, but it was
abandoned used because it interferes with normal development of
the larynx, induces perichondritis, and is carcinogenic after a latent
period.
//. Chondroma
- It occurs in old ages (40-60 years), and is more in males.
- Site : The commonest site is the cricoid cartilage where it arises from
the internal aspect of the posterior lamina (70%). It may arise from
the thyroid cartilage (20%), or from the arytenoid cartilage (10%).
Clinical picture
1. It presents mainly with stridor and airway obstruction as it is
commonly subglottic. Hoarseness of voice occurs later when it
reaches a large size. There may be dysphagia and sense of
fullness in the throat.
2. Examination reveals a subglottic mass usually bulging from the
posterior aspect, which is smooth, covered by intact mucosa,
firm and fixed. It is faint blue grey in colour with a hyaline
apearance.
Investigations
1. Plain x-ray soft tissue lateral view.
2. C.T. scan of the neck.
3. Flixable laryngoscopy and it is difficult to take a biopsy for"
histopathological examination as the mass is hard and slippery.
N.B. : Chondroma arising from the cricoid cartilage is benign in
contradistinction to those arising from the base of the skull, as
they are mostly low grade chondrosarcomas, difficult to
distinguish histoloigcally from chondromas.
Treatment
Preoperative tracheostomy, then surgical excision through an
external approach e.g. laryngofissure.
 -278-

Malignant tumours of the larynx

(Laryngeal carcinoma)
Incidence
Laryngeal carcinoma is a common neoplasm representing about 1%
of all malignancies diagnosed annually, and about 35% of all head and
neck malignancies.
Age : It usually occurs in old age (60-70 years). However, it may
affect younger age groups, particularly smokers.
Sex : It is more common in males than females of a ratio of 8:1.
Predisoposing factors
1.^ Tobacco smoking is the most important factor. It was found that
less than 5% are nonsmokers.
2) Alcohol consumption, which particularly predisposes to
supraglottic carcinoma. Smoking and alcohol have a synergistic
action in the development of laryngeal carcinoma.
3) Expsourc to irradiation.
4y Industrial exposure to asbestos and nickel. It is also more common
/•—\j
in wood workers.
5y Oesophageal reflux is claimed to be a predisposing factor.
Precancerous lesions
1. Leukoplakia precipitated by smoking and oral sepsis.
2. Laryngeal keratosis with severe dysplasia.
3. Single papilloma in adults.
According to the site of the lesion^ laryngeal carcinoma is classified
into: (Fig.66)
7. Supraglottic carcinoma
It represents about 20-40% of
laryngeal carcinomas. It carries
a very high incidence of early
cervical lymph node metastasis.
2. Glottic carcinoma
It is the most common,
representing about 50-70% of
laryngeal carcinomas. It usually
presents early with hoarseness
of voice, and rarely gives rise to
lymph node metastasis. 'fig 66
 flB??T

-279-

5. Subglottic carcinoma
It is rare, representing about 1-8% of all laryngeal carcinomas. It
often presents early with stridor and airway obstruction. Most of
subglottic carcinomas are extensions of glottic ones, and rarely they
are primarily subglottic.
4, Transglottic carcinoma
These represent tumours, that crossed the laryngeal ventricieln a
vertical plane, involving the supraglottis and the glottis, with
possible involvement of the subglottis. They are highly aggressive,
with a very high incidence of cartilage invasion, extralaryngeal
spread, and cervical lymph nodes metastasis. They mostly start in
the laryngeal ventricle and extend up and down the laryngeal
lumen.
Microscopic picture
- Squamous cell carcinoma is the commonest histopathological
diagnosis representing about 95-97% of all cases. The malignant
squamous cells are arranged as cell nest with central keratin.
- Sqamous cell carcinoma shows variable degrees of differentiation,
either well, moderatly, or poorly differentiated. The most common
are moderatly differentiated tumours. Differentiation is important
in management, becuase well differentiated tumours are less
responsive to radiotherapy than poorly differendated ones.
- Border's calssification :
Grade I : 75-100% well differentiated.
Grade II : 50-75% well differentiated.
Grade HI: 25-50% well differentiated.
Grade IV : 0-25% well differentiated.
Spread
I. Direct spread of the primary tumour
A, Glottic tumours
1. They initially spread along the length of the vocal cord and reach
to the anterior commissure, then to the opposite cord.
2. Vertical spread, upwards to the supraglottis and downwards to
the subglottis.
3. Deep spread invading the piu-aglottic space, to cause fixaiton of
the vocal cord.
4. Thyroid cartilage invasion occurs early in anterior commissure
lesions, since the mucous membrane is separated from the
 -280-

carilage by the anterior commissure tendon, and there is no

cndochondrium at the site of insertion of the tendom. It is less
common in cordal tumours.
5. Posterior extension to the arytenoids, and the posterior
commissure.
B, Supraglotiic tumours
These include tumours of the epiglottis (suprahyoid and infrahyoid
portions), aryepiglottic folds, arytenoids, ventricles, and ventricular
folds.
1. Anteriorly, it extends to the preepiglottic space through fenestrae in
the epiglottic cartilage. This is seen more in tumours of the
infrahyoid portion of the epiglottis, and the ventricles.
2. Posteriorly, to the arytenoids, and postcricoid area.
3. Laterally to the paraglottic space epecially with ventricular
tumours, and to the medial wall of the pyriform fossa.
4. Upwards, to the vallecula, and base of the tongue.
5. Downwards, to the vocal cords, and the anterior commissure.
C, Subglottic tumours
1. Upwards to the vocal cords.
2. Downwards to the trachea.
3. Circumferentially, to the opposite side.
4. Subglottic tumours have a very high incidence of cricoid cartilage
invasion, and extralaryngeal spread to the thyroid gland, and the
hypopharynx.
D, Transglottic tumours; (those arising in the ventricle) are aggressive
with early invasion of the paraglottic space, and thyroid cartilage,
and early extralaryngeal spread.
II. Lymph node metastasis
- Cervical lymph node metastasis occurs in the upper, middle and
lower deep cervical lymph nodes. The lower deep cervical group is
particularly involved in subglottic tumours. It occurs either by
lymphatic permeation or embolization.
There are several factors that determine cervical lymph node
metastasis:
1. Site of the tumour
i. Glottic tumours : Nodal metastasis is very rare (1-8%), as there
are no lymph vessels in the Rinek's space, so, nodal metastasis
doesnot occur in early glottic tumours (i.e. T, & T2). Nodal
 -281 -

metastasis occurs when the paraglottic space, supraglottis,

subglottis, or the thyoid cartilage are invaded by the glottic
tumour.
2. Supraglottic tumours : Nodal metastasis is common and early
(30-50%) to the upper deep cervical nodes, because the
supraglottis has a very rich lymphatic drainage. Furthermore,
there is a very high incidence of occult nodal metastasis (non
palpable nodes) and bilateral nodal metastasis.
3. Subglottic tumours : nodal metastasis is common (10-20%), first
to the prelaryngeal, pretracheal and paratracheal nodes, then to
the middle and lower deep cervical nodes. Bilateral nodal
metastases is also cmmon.
4. Transglottic tumours : frequent and early nodal metastasis.
2. Size of the tumour : The incidence of nodal metastasis increases,
with increased size of the tumour.
3. Stage : nodal metastasis is more in advanced (T3 & T4) lesions,
than in early (Tl & T2) lesions.
4. Tumour differentiation : It is more with poorly, than with well
differentiated tumours (according to Broders classification).
5. TTie incidence of nodal metastasis increases with cartilage invasion,
extralaryngeal spread, and neural infiltration.
II. Blood spread; (rare and late)
To lungs (commonest site), bone, and liver.
N.B. : Laryngeal carcinoma is associated with a high incidence to
develop a second primary in the areodigestive tract especially
bronchogenic carcinoma. It occurs either synchronously (at the
same time) in 0.5-1%, or metasynchronously in 5-10% of cases.
Therefore, proper assessment and prolonged follow up of
laiyngeal carcinoma is essential.
Clinical picture
Symptoms
L Hoarseness of voice which is progressive and unremitting. It is
the earliest symptom in glottic tumours, and may presist as the
only symptom for several months. An important consideration is
the cancer which develops in one who sufferes from chronic
laryngitis, as they are at risk from delay in diagnosis, because
they already have hoarseness of voice. Any patient presenting
with hoarseness of voice for more than two weeks should be
examined and investigated properly.
» .'
 -282-

2. Supraglottic tumours, produce a muffled voice rather than

hoarseness.
3. Sensation of discomfort in the throat on swallowing may be an
early symptom of supraglottic tumours.
4. Referred otalgia to the ipsilateral ear along the Ar-nold's branch
of vagus.
5. Dyspnoea and stridor due to airway obstruction. It occurs early
in supraglottic tumours. It is due to enchroachement upon the
airway by a large tumour, or fixation of the arytenoid or vocal
cord.
6. Localized pain is rare, it may occur with supraglottic tumour, or
may be due to perichondritis.
7. Cough and irritation in the throat may be the early symptoms.
8. Swelling in the neck or larynx mainly due to lymph node
metastasis in the upper, or middle cervical groups. It may be due
to direct penetration of the thyroid cartilage and extralaryngeal
spread. Perichondritis and abscess formation may give rise to
painful, tender, ©edematous swelling.'
9. late symptoms:
a. Foetid breath.
b. Dysphagia due to invasion of the hypopharynx.
c. Haemoptysis especially in epiglottic tumours.
d. Anorexia and cachexia.
Signs
A. Examination of the larynx
- by indirect laryngoscopy, flexible laryngoscopy or direct
laryngoscopy under general anaesthesia in difficult cases (severe
gag reflex or excessive froth of saliva).
- Examination should include appearance of the mucosa, condition
of the airway, and mobility of the vocal cords. Full description
of the lesion regarding shape, size, site and extension should be
noted, and documented on a chart.
1. Glottic tumours, typically appear as a hyperkeratotic warty or
papillary growth, but it may appear as a localized thickening or a
raised nodule.
2. Supraglottic tumours apears as a focal swelling, redness or
ulceration.
 -283-

3. Difficult areas for examination (where you can miss a lesion)

iire:
a. The posterior surface of the epiglottis, the lesion may be
hidden by the backward curve of the tip of the epiglottis.
b. Subglottic area, where lesion often appear as an asymmetrical
swelling, usually masked by mucoid debris.
c. The laryngeal ventricle, where the intial presentation may be a
slight fullness.
4. Assessment of extension to the hypopharynx and tongue
infiltration which is better palpated with the finger (it is rather
felt than seen).
5. Assessment of cord mobility :
a. Limited mobility without fixaton, may be due to the weight of
a bulky tumour or moderate invasion of the thyroarytenoid
muscle.
b. Fixation of the cord is due to invasion of the thyroarytenoid
muscle (more than 3/4), invasion of cricoarytenoid joint or
the thyroid cartilage.
B. Examination of the neck to detect;
1. Enlarged deep cervical lymph nodes, usually the upper and
middle groups. They are firm and mobile, later, hard and fixed.
Report on their number, side (ipsilateral or bilateral), size, and
mobility.
2. Swelling and broadening of the larynx due to extralaryngeal
spread and perichondritis.
3. Tenderness due to perichondritis,
4. Examination of the thyroid gland.
C. General examination
1. Teeth for sepsis and oral hygiene.
2. Distant metastasis.
3. Chest examination.
TNM classificaiton
This calssification applies only to carcinoma. It is important to
decide the line of treatment and to predict prognosis.
A. T for the primary tumour
- Tjg : carcinoma in situ (preinvasive carcinoma).
- Glottic tumours
 •284-

• Ti : Tumour limited to the vocal cords with normal mobility of

the vocal cords.
* T l a : limited to one vocal cord.
* Tib : involves both vocal cords.
• T2 : Tumour extends to the supraglottis and/or the subglottis widi
normal mobility of the vocal cord (T2a) or impaired cord
mobiUty (T2b).
• T3 : Tumour confined to the larynx, with fixed cord.
• T4 : Tumour invading the thyroid cartilage and/or extralaryngeal
spread, e.g. pharynx, soft tissues of the neck and tongue.
- Supraglottic tumours
Tj : Tumour involving the supraglottis with normal cord mobility.
T2 : Tumour extends to the glotds with normal cord mobility.
T3 : Tumour confined to the larynx with fixed cord.
T4 : Tumour invading the thyroid cartilage and/or extralaryngeal
spread.
- Subglottic tumours
T l : Tumour limited to the subglottis with normal cord mobility.
T2 : Tumour extends to the glottis with normal cord mobility.
T3 ; Tumour confined to the larynx with fixed cord.
T4 : Cartilage invasion and/or extralaryngeal spread.
B) N : Regional nodal metastasis
NO : No clinically palpable nodes.
Nl : Single ipsilateral node 3 cm or less in diameter.
N2a : Single ipsilateral node 3-6 cm in diameter.
N2b : Single ipsilateral node none more than 6 cm in diamter.
N3a : Single ipsilateral node one more than 6 cm in diameter.
N3b: Bilateral nodes.
N3c: Contralateral nodes only.
C) M : Distant metastatis :
MO : No clinical or radiological evidence of distant metastasis.
M l : Present clinical or radiological evidence of distant metastasis.
Investigations
1. Plain x-ray soft tissue lateral view : shows the tumour, and its upper
and lower limits. It is of little value.
2. CT. scan of the neck : This is the most important radiological
 -285-

investigation. It shows the site and extent of the tumour,

particularly the lower limit of the subglottic extension. It also
shows, cartilage invasion, extralaryngeal spread, and non palpable
cerivcal nodal metastasis. It is very important to detect invasion of
the paraglottic and preepiglottic spaces, which is important, in
order not to leave residues of the tumour during surgery. CT scan
should be done before direct laryngoscopy examination, as oedema
from that procedure might interfere with the radiological findings.
Thus, CT scan is important for accurate staging.
3. Direct laryngoscopy and biopsy :
- It is important to report on the site, and extent of the tumour, and
to take a biopsy for histopathological examination to confirm the
diagnosis.
- Repeatedly negative biopsies in a highly suspicious lesion may
occur in verrucous carcinoma (The tumour lacks the usual
histological criteria of malignancy). It is often diagnosed as
keratosis, so deep biopsy is alway recommended.
- It is always difficult to assess cases that received previous
radiotherapy because of the postirradiation oedema.
4. Metastatic work-up : chest x-ray, abdominal ultrasound, and bone
scan.
5. Routine preoperative investigations : complete blood count, liver
and kidney functions, ECG & coagulation profile.
6. Nasopharyngoscopy, oesophagoscopy and bronchoscopy for
synchronous tumours.
Treatment
* Laryngeal carcinoma is a highly curable disease, and has a generally
favourable prognosis, with an overall 5-year survival rate of about
67%. Early diagnosis and proper assessment is the key for good
survival and cure rates.
* Treatment modalities may fall into the following categories :
1- Curative (radical).
a. Surgery alone.
b. Radiotherapy alone.
c. Combination of surgery and radiotherapy.
d. Chemoradiotherapy.
2. Palliative for inoperable cases.
a. pain relief
 '-t

- 286 -

b. Palliative surgery, and tracheostomy.

c. Palliative radiotherapy and/or chemotherapy.
* Tracheostomy should be done if the patient is in stridor, it should be
a low tracheostomy in subglottic tumours. One should always try to
avoid doing a tracheostomy prior to surgery, as it increases the
incidence of tumour recurrence at the orifice of the tracheostomy
(stomal recurrence).
* Factors that determine selection of the treatment modality :
a. Site and size of the tumour.
b. Stage of the tumour, according to the TNM classification.
c. Age and general health of the patient.
d. Quality of voice desired.
e. Cost of treatment and patients attitude.
The results of each treatment modality is expressed in terms of
5-year survival rate (i.e. if the patient does not develop a recurrence
within 5 years, he is considered totally cured for life).
Treatment according to the site and the stage of the tumour.
A. Glottic tumours
T is (carcinoma in situ); (95-100% 5-year survival)
a. Surgery in the form of repeated vocal cord stripping by
conventional microlaryngosurgery or CO2 laser excision.
b. Radiotherapy, however, surgery is preferred because of the long
time spent during treatment with radiotherapy, and post irradiation
oedema which makes follow up by direct laryngoscopy difficult.
Furthermore, radiotherapy may fail and the preinvasive carcinoma,
changes into frank invasive carcinoma.
- Prolonged follow up is essential after treatment of carcinoma in situ.
Tj glottic lesion (i.e, the vocal cords are freely mobile); (85-96%
5-years survival)
a. Surgery either in the form of:
- Endoscopic laser excision by microlaryngosurgery (transoral laser
cordectomy), if the lesion is limited to the midthird of the vocal
cord.
OR.
- Laryngofissure and cordectomy if the lesion is limited to the
midthird of the vocal cord.
- Partial vertical laryngectomy (vertical hemilaryngectomy):
 "287-

i. Vertical hemilaryngectomy if the lesion limited to one vocal

cord and not reaching to the anterior commissure or the vocal
process of the arytenoid catilage posteriorly.
ii. Frontolateral hemilaryngectomy, if the tumour extends to the
anterior commissure, and up to the anterior third of the
opposite vocal cord.
iii. Frontal partial laryngectomy (anterior commissure resection)
in tumours limited to the anterior commissure, or the anterior
third of one or both vocal cords.
b. Radiotherapy, possibly gives equal results to surgery, but with the
same disadvantages as mentioned before.
T^ glottic lesion (70-85% 5-years survival)
a. Surgery in the form of:
' Partial vertical hemilaryngectomy in T2a (i.e. the cord is freely
mobile).
- Cricohyoidoepiglottopexy (supracricoid laryngectomy or near
total laryngectomy). The cricoid cartilage and at least one
arytenoid are left for better vocalization and voice production in
T2b (i.e impaired vocal cord mobility).
b. Radiotherapy gives more inferior results than surgery particulariy in
T2b lesions (i.e. impaired cord mobility).
N.B. ; T2b lesions with impaired cord mobility may be regarded as T3
lesions, because in such lesions there is invasion of the
paraglottic space, that might necessitate total laryngectomy for
radical removal of the tumour.
Ts glottic lesion (50-70% 5-years survival)
a. Total laryngectomy with or without postoperative radiotherapy.
Postoperative radiotherapy has certain indications (mentioned
later), however, in some centers it is given routinely in T3 lesions
as it improves the locoregional control and survival rates.
b. Near total laryngectomy (cricohyoidoepiglottopexy) can be done in
selected cases, if the tumour is not extending to the subglottic
region for more than one cm.
T, glottic lesion (40-55% 5-years survival)
a. A trial of chemoradiotherapy (organ preservation therapy). Where
tliree cycles of chemotherapy (5-flurourdciI and cisplatinum) are given
and the larynx is examined to evaluate the response.
- if there is 50% or more reduction in the size of the tumour (i.e.
responsive), then radical dose of radiotherapy is given.
 -288-

- if there is no response to chemotherapy, resort to total

laryngectomy.
b. Total laryngectomy and postoperative radiotherapy is also a
treatment option, however, the recent trend now in many cancer
institutes is organ preservation by chemoirradiation following the
above mentioned protocol, as both modalities give the same poor
survival rate.
Management of cervical metastasis in glottic tumours
Radical neck dissection is done if there are cervical nodal
enlargment Do not expect nodal metastasis in early (Tl and T2) glottic
lesions; and prophylactic neck dissection is not required.
B. Supraglottic tumours
Tj and Tj lesions (70-80% 5-years survival)
a. Horizontal supraglottic partial laryngectomy with lesions limited to
the supraglottis and witii no involvement of the preepiglottic space
and both vocal cords are freely mobile. It is contraindicated if the
tumour extends to the vocal cords, anterior commissure or
arytenoid cartilage.
b. Transoral endoscopic supraglottic excision can be done in selected
cases of supraglottic cancer, without involvement of the
preepiglottic space.
c. Supracricoid laryngectomy with cricohyoidopexy may be done in
more larger tumours, extending to the anterior commissure or the
vocal cords.
d. Total laryngectomy in T2 lesions, if partial laryngectomy cannot be
done as in old age with bad pulmonary functions for fear of
aspiration.
e. Radiotherapy; is the preferred treatment in some centers in case ofo
Tl and T2 lesions.
Tj and T^ supraglottic lesions (50-60% 5-years survival)
Total laryngectomy and postoperative radiotherapy is the treatment
of choice.
N.B.: In some centers, they start by radiotherapy as a definitive treatment
for all stages of supraglottic carcinoma, provided that there are no
palpable neck nodes, and resort to salvage total laryngectomy if
radiotherapy fails.
 -289-

Management of cervical nodal metastasis in supraglottic tumours.

1. If there are palpable neck nodes, radicaJ neck dissection should be
done.
2. If there are no palpable neck nodes, bilateral prophylactic neck
dissection should be done (Selective neck dissection) due to the
high incidence of occult (hidden) metastasis.
C. Subglottic tumours
- Tl lesions : either radiotherapy or total laryngectomy.
- T2, T3 and T4 la ion : Total laryngectomy with or without
postoperative radiotherapy.
- Total thyroidectomy is perfomed with total laryngectomy in all
subglottic tumours.
- Radical neck dissection is done if there are palable neck nodes, with
dissection of the superior mediastinal nodes.
D. Transglottic tumours : Total laryngectomy with enblock radical neck
dissection and postoperative radiotherapy.
Indications of total laryngectomy in laryngeal carcinoma.
1. T3 and T4 glottic and supraglottic tumours.
2. All subglottic and transglottic tumours.
3. Cartilage invasion and extralaryngeal spread.
4. Posterior commissure involvement or extension to both
arytenoids.
5. Recurrence or failure of conservative surgery.
6. Recurrence after radiotherapy.
7. Radioecrosis and perichondritis after radiotherapy.
8. Contraindication to radiotherapy or conservative surgery.
9. Certain histological types eg. adenocarcinoma, and spindle cell
carcinoma.
10. Thyroid and hypopharyngeal tumours invading the larynx.
N.B. : Total laryngectomy entails removal of the whole larynx
includine the cricoid and arytenoid cartilages.
Contraindications of total laryngectomy.
1. Poor general condition e.g. recent myocardial infarction or
patient in heart failure.
2. Refusal by the patient.
3. Distant metastasis,
4. Involvement of important unresectable structures eg, carotid
artery.
 -290-

Disadvantages of total laryngectomy:

1. Loss of voice.
2. Permanent tracheostomy.
3. Loss of nasal functions as humidification, filtration and
airconditioning.
4. Inability to increase the intrathoracic pressure.
5. Limitation of certain activities eg. heavy manual work and
swimming.
Regarding conservative (partial laryngectomy), good pulmonary
functions prior to surgery is essential, so as tolerate the postoperative
aspiration.
Radiotherapy
Usually, 6000-8000 rads is given in fractionated doses over 6-8
weeks. The field of irradiation includes the primary tumour and the neck
in supraglottic, transglottic and subglottic tumours, due to the high
incidence of occult nodal metastasis.
Indications of radiotherapy
1. T is , Tl and T2 glottic carcinoma as alternative to partial
laryngectomy.
2. Tl and T2 supraglottic carcinoma.
3. In combination with chemotherapy in advanced lesions (organ
preservation).
4. Palliative in inoperable cases.
5. Postoperative radiotherapy is indicated in :
a. Invaded resection margins.
b. Histopathologically positive nodal metastasis.
c. Invasion of adipose tissue.
d. Preoperative tracheostomy.
e. Prophylactic to the neck in supraglottic and transglottic
tumours.
6. Preoperative radiotherapy is indicated if tiiere are fixed cervical
lymph nodes.
Contraindications of radiotherapy
1. Fixed vocal cord.
2. Perichondritis and cartilage invasion.
3. Palpable nodes.
4. Previous radiotherapy.
5. Radioresistant tumours e.g. adenocarcinoma.
 -291 -

Complications of radiotherapy
1. Anorexia, nausea.
2. Xerostomia.
3. Osteoradionecrosis of the mandible.
4. Perichondritis of the laryngeal cartilages.
5. Laryngeal oedema.
6. Skin burns and discolouration.
7. Increased incidence of pharyngocutaneous fistula if salvage total
laryngectomy is done.
Important points concerning radiotherapy
1. It is a prolonged treatment and needs regular follow up.
2. Follow up for a residual or recurrence is often difficult due to
prolonged postradiotherapy oedema.
3. It is more effective in poorly, than well differentiated tumours.
4. It gives better quality of voice than in partial laryngectomy.
5. Elderly patients cannot tolerate radiotherapy easily in contrast to
what is believed to be, and surgery is the preferable treaunenl.
N.B.: Surgery fails in the periphery of the tumour, (margins), while
radiotherapy fails in the center of the tumour (due to low 02
content). So a combination of both modalities is recommended
in specific situations as mentioned before.
Rehabilitation after surgery
1. Voice therapy after partial laryngectomy.
2. Learning oesophageal speech or the use of electronic larynx after
total laryngectomy.
Palliative Treatment
It is indicated in inoperable cases (see contraindications of total
laryngectomy). It includes:
1. Tracheostomy for airway obstruction.
2. Ryle tube feeding, or gastrostomy in severe dysphagia.
3. Palliative laser excision of a fungating mass.
4. Palliative radiotherapy and/or chemotherapy.
5. Antibiotics for infections.
6. Pain Killers.
 -292-

Stridor
Stridor means noisy respiration, which is a symptom of partial
airway obstruction in the larynx and/or the trachea.
Stridor may be either;
a. Inspiratory : laryngeal obstruction at or above the level of the
glottis.
b. Inspiratory and expiratory : subglottic or tracheal obstruction,
(Biphasic stridor).
c. Expiratory : in bronchial obstruction (Bronchial asthma).
1. Congenital
a. Congenital web.
b. Laiyngomalacia,
c. Subglottic haemangionia.
d. Congenital subglottic stenosis.
e. Congenital cysts.
2. Traumatic
a. Inhaled foreign body.
b. Mechanical trauma e.g. penetrating wounds, blunt injury, or
endotracheal intubation.
c. Laryngeal bums e.g. thermal injury or corrosives.
d. Postradiotherapy oedema,
3. Inflammatory
a. Acute laryngitis:
- Acute nonspecific laryngitis in children.
- Acute epiglottitis.
- Laryngeal diphtheria.
b. Chronic laryngitis:
- Laryngoscleroma.
-T.B.
- Syphilis.
4. Neoplastic
a. Benign tumours e.g. multiple papillomatosis, subglottic
chondroma.
b. Malignant tumour (laryngeal carcinoma).
5. Neurological: Bilateral abductor paralysis.
 -293-

6. Laryngeal cysts eg. congenital cysts or retention cysts.

7, Laryngeal spasm e.g. tetany.
9. Subglottic stenosis.
Clinical picture of airway obstruction
L Stridor, (noisy respiration).
1. dyspnoea (difficult breathing).
3. Irritability, restlesness, fatigue and sweating.
4. Tachycardia (rising pulse).
5. Working alae nasi.
6. Retraction of the suprasternal, supraclavicular, intercostal, and
subcostal spaces during inspiration.
7. Overworking accessory muscles of respiration (pectoralis, and
latissimus dorsi).
8. Congested neck veins during expiration.
9. Hoarseness of voice may be an associated feature.
10. Cyanosis, bradycardia are late sings denoting marked hypoxia.
Finally, coma and cardiac arrest.
N.B. : Tracheostomy should be done at ease whenever possible, and
do not wait for cyanosis and bradycardia to appear as they are
very late signs, and by that time the padent may not be saved.
Causes of stridor in children
1. Congenital causes (mentioned before).
2. Inflammatory :
a. Acute nonspecific laryngitis.
b. Acute epiglotdtis.
c. Laryngotracheobronchids.
d. Laryngeal diphtheria,
3. Traumauc :
a. Foreign body inhalation.
b. Ingestion of corrosives.
4. Neoplastic : multiple papillomatosis.
5. Angioneurotic oedema.
6. Retropharyngeal abscess and angina.
 -294-

Hoarseness of voice
Hoarseness of voice means, changes in the quality and timbre of
voice so that it becomes rough, harsh and of low pitch than normal for
the individual. It is a symptom and not a disease.
Setting the air column in vibration by the larynx is a purely
mechanical process. Anything that interfers with the perfect working of
this mechanism produces hoarseness.
Mechanical factors concerned are;
1. Approximation of the cords.
2. Tension of the cords.
3. Vibration of the cords.
Approximation may be impaired by;
1. Tumour or secretion between the two cords.
2. Fixation or limitation of movement of the cricoarytenoid joint.
3. Paralysis of the laryngeal muscles.
4. Cicatricial concavity of the cord edges.
B. Tensing of the cordal edges may be interfered with by;
1. Thickening of the cordal edges.
2. Paralysis or weakness of the laryngeal muscles.
3. Excessive approximation of the ventricular bands.
C. Vibration may be impaired by;
1. Inflammatory changes of the cord.
2. Tumour infiltration.
3. Paralysis of the laryngeal muscles.
4. Incomplete approximation.
Causes of hoarseness of voice
1. Congenital: web
2. Traumatic:
a. Foreign body.
b. Instrumentation.
c. Voice abuse.
3. Inflammatory : all acute and chronic inflammations.
4. Neoplastic : bengin and malignant tumours.
5. Unilateral vocal cord paralysis.
6. Arthritis of the cricoarytenoid joint.
7. Hysterical.
t
 "—V

-295-

Laryngeal Operations
Tracheostomy
This is the creation of a surgical opening in the anterior wall of the
trachea.
Indications of tracheostomy
I. Upper respiratory tract obstruction
1. Congenital
a. Congenital web.
b. Laryngomalacia.
c. Subglottic haemangioma and stenosis.
d. Congenital cysts.
2. Traumatic
a. Inhaled RB.
b. Penetrating or blunt injury.
c. Severe oedema due to thermal bums or corrosives ingestion.
d. Postirradiation oedema.
3. Inflammatory
a. Acute :
- Acute nonspecific laryngitis in children.
- Acute epiglottitis.
- Laryngeal diphtheria.
b. Chronic specific laryngitis :
- Laryngoscleroma.
- T.B. of the larynx.
- Syphilis of the larynx.
- Mycosis of the larynx.
4. Neoplastic
a. Benign tumours e.g. multiple papillomatosis, subglottic
chondroma, haemangioma, and lymphangioma.
b. Malignant tumours (laryngeal carcinoma).
6. Laryngeal oedema e.g. angioneurotic oedema.
7. Laryngeal stenosis (mentioned before).
8. Extralaryngeal causes
a. Maxillofacial injury e.g. fracture mandible. This causes locai
oedema and aspiration of blood.
 —^

-296-

b. Severe tongue and neck oedema.

c. Deep neck spaces suppuration e.g. ludwig's angina, and
retropharyngeal abscess.
d. Tumours, particularly malignant tumours of the oral cavity,
tongue, and pharynx.
The value of tracheostomy in upper respiratory tract obstruction is
to by-pass the obstruction.
11. Lower respiratory tract obstruction
A. Respiratory difficulties due to retained secretions
The presence of accumulated secretions in the lower respiratory
tract, leads to impairment of gas diffusion in the alveoli with
inefficient ventilation (the patient may be drowned in his secretions).
- Laryngeal incompetence, causes frequent aspiration and
accumulation of secretions. In this case, a cuffed tracheostomy tube
is used to avoid aspiration of secretions, blood, saliva, or vomitus.
- Inability to expel secretions, may be due to a central or peripheral
cause inhibiting the cough reflex.
1. Central causes (coma)
a. Head injury e.g. cerebral contusion, lacerations, or brain oedema.
b. Cerebrovascular strokes e.g. haemorrhage, thrombosis, and
embolism.
c. Drug intoxication e.g. barbiturates.
d. Brain tumours and abscesses.
e. Coma due to uraemia or ketoacidosis.
f. Neurosurgical intracranial procedures.
2. Peripheral
a. Respiratory muscle paralysis and respiratory failure.
b. Severe chest injury e.g. multiple rib fractures and flail chest
(patient cannot cough due to severe pain).
c. Post surgical.
d. Pneumonia.
B. Respiratory failure (Mechanical respiratory insufficiency)
This may be due to;
1. Chronic obstructive airway disease e.g. emphysema.
2, Neurological disorders leading to respiratory muscles paralysis
e.g. motor neurone disease, myasthenia gravis, poliomyelitis and
diphtheria.
 - 297 -

Tlie value of tracheostomy in lower respiratory obstruction is to :

a. Allow frequent acurate aspiration of secretions.
b. Elimination of tlie upper respiratory dead space by fifty percent.
c. Allow inicmiittent or continuous positive pressure ventilation.
d. Prevent aspiration by the use of a cuffed tracheostomy tube.
e. Avoid complications of prolonged intubation especially
subglottic stenosis.
III. Elective
There is no airway obstruction, and tracheostomy is done when the
airway is at risk as in :
A. Before major operations on the mouth, pharynx, mandible ami
maxilla to avoid aspiration of blood, and laryngeal oedema, as in :
1. Excision of nasopharyngeal angiofibroma.
2. Maxillectomy.
3. Commando operation for tumours of the oral cavity.
B. Before laryngeal surgery :
1. Laryngofissure.
2. Partial laryngectomy.
3. When difficult endotracheal intubation is expected as in
laryngeal carcinoma and subglottic stenosis.
C. Permanent tracheostomy is done at the end of total laryngectomy.
Types of tracheostomy (Fig.67)
A. High tracheostomy : It is done in the 1st and 2nd trachea! rings,
above tlie isthmus of tlie thyroid gland. It is easy, rapid, and can be
performed in emergency. Its major disadvantage is the iiigli
incidence of cricoid and upper tracheal stenosis. It is not generally
preferred.
B. Low tracheostomy : It is done in the 5th and 6th tracheal rings,
below tlie istlimus of the thyroid gland.
- It is indicated in :
1. Recurrent multiple papillomatosis.
2. Laryngea carcinoma with subglottic extension.
3. Subglottic and upper tracheal stenosis.
- Its disavdantages arc :
1. difficult as the trachea is liecply seated.
2. higher risk of pleural injury,
 -298-

3. higher risk of injury of big vessels at the root of the neck e.g.
innominate vein.
4. The tube slips easily from the trachea.
C. Mid tracheostomy:
It is done in the 3rd and 4th tracheal rings behind the isthmus of the
thyroid gland. It is the selected procedure, as it avoids the
disadvantages of high and low tracheostomy.

high
mid
low

Fig.67 types of tracheostomy

Technique of the operation

1. anaesthesia
a. Local anaesthesia by infiltration of 2% xylocaine in adrenaline.
b. General anaesthesia is better in children or if there is time for
possible endotracheal intubation. It is used also in elective cases.
c. Under no anaesthesia is urgent tracheostomy in order to save the
patient's life if there are late sings of airway obstruction
(bradycardia, cynosis and coma).
Tracheostomy should be done at ease whenever possible, and one
should not wait for the late signs of airway obstruction. If in a
hurry, make an incision in the cricothyroid membrane, and not in
the trachea, although this is not preferred because of the latent
cricoid stenosis.
2. Position of the patient
The patient should lie supine with a sand bag under his
shoulders, but if the operation is done under local anaesthesia
and the patient is markedly obstructed, it may be performed in
the siting or the semistting position as extension of the neck
causes strech of the trachea with further narrowing of the
airway.
 - 299 -

3. Skin incision
a. A midline vertical incision from the upper border of the cricoid
cartilage down to the suprasternal notch. It is done in urgent
cases, as it is easier. (Fig.68)
b. A transverse incision midway between the lower border of the
cricoid cardlage and the suprasternal notch. It is done in a skin
crease, so it is more cosmetic. It should be done in elective
cases.
4. The incision is deepened through the subcutaneous fat, superficial
fascia, and deep fascia. The pretracheal muscles are separated and
retracted laterally by two retractors. (Fig.69)
5. The thyroid isthmus is dissected from the trachea, and incised
between two kochers, and then transfixed. (Fig.70)
6. Opening of the trachea
- Before opening the trachea, few drops of a local anasthetic are
injected into its lumen to avoid reflex coughing on opening the
trachea.
- The cricoid cartilage is held by a hook in order to bring the
trachea superficial in the wound, and to stabilize it.
- The tracheal wall (3rd & 4th ring) is opened as a flap, based
inferiorly. (Fig,71)
7. The tracheostomy tube is then inserted into the stoma The
diameter of the tube should cope with the diameter of the stoma to
avoid air leakage and tube slippage.
8. Adequate haemostasis is then performed. Haemostasis should be
done before opening the trachea to avoid entery of blood into the
trachea.
9. The wound is closed by suturing the upper part of the incision to
avoid tight closure, air trapping and surgical emphysema. The tube*
is fixed to the skin by sutures to avoid its slippage.
N.B.: A slit in the trachea may be done, without making a hole in tlic
anterior wall, particularly in children to avoid tracheal stenosis,
Types of tracheostomy tubes
1. It may be made up of metal or sialastic.
2. Cuffed (inflatable cuft^ or non cuffed tubes.
3. Tubes with expiratory speaking valve for voice production.
 -300-

Fig.68, midline Fig.69. pretracheal

vertical incision muscles

" Fig.71. opening of the

trachea
Fig.70.

Complications of tracheostomy
1. Complications of general anaesthesia, or anaphylaxis from local
anaesthesia.
2. Haemorrhage
a. Primary haemorrhage, usually arises from the anterior jugular
vein or the thyroid gland. Severe bleeding may occur if the
innominate vein is injured, which may be fatal and carries the
risk of air embolism.
b. Reactionary, due to slipped ligature or from a collapsed vein (as
the veins are collapsed during surgery by the negative
intrathoracic pressure). Reexploration of the wound to secure
haemostasis by ligature or diathermy is needed.
c. Secondary haemorrhage due to infection is rare.
3. Apnoea
This is a period of cessation of respiration during opening the
trachea. It is due to rapid wash-out of CO2 with rapid drop of the
high CO2 tension which was the only stimulus of the respiratory
 -301 -

center during the period of hypoxia. It occurs only when the

operation is done under local anaesthesia. It is avoided by allowing
the patient to breath a mixture of 95% O2 in 5% CO2 during the
procedure. Also instillation of local anaesthetic into the trachea
before opening it, to avoid severe repeated coughing attacks which
causes rapid washout of CO2. If aponea occurs it is treated by
assisted ventilation.
4. Injury of important structures
a. The posterior wall of the trachea may be injured (transfixion of
the trachea), leading to tracheo-oesophageal fistula. It may occur
if you do not pull the cricoid with a hook in order to bring the
trachea more anterior, or if the tube is introduced forcibly. It is
treated by surgical repair, and ryle feeding is maintained until
the fistula heals.
b. Big vessels at the root of the neck particularly the innominate
vein. This is a surgical catastrophy that needs blood transfusion.
Saline should be poured on the wound in order to avoid air
embolism in such cases.
c. Thyroid gland injury leading to haemorrhage.
d. Apex of the pleura leading to pneumothorax.
e. Cricoid cartilage leading to subglottic stenosis later on.
5. Pneumothorax
It is due to injury of the apex of the pleura, particularly if the
patient is struggling or coughing vigorously. It is diagnosed by
persistent dyspnoea after tracheostomy, with diminished airentery
on auscultation. Plain x-ray chest is diagnostic. It is treated by
insertion of an intercostal tube connected to an underwater seal.
6. Pneumomediastinum
It is due to excessive inferior dissection opening planes for escape
of air into the mediastinum. It is usually mild and resolves
spontaneously. If massive, it may lead to fatal cardiac tamponade
and acute heart failure.
7. Air embolism
It is due to injury of large neck veins particularly the innominate
vein. Air is sucked in and passes rapidly to tlie right atrium. It may
lead to fatal cardiac tamponade and death. It is treated by pouring
saline into the wound, compression of the opened vein, elevation of
the foot of the bed, and blood n*ansfusion.
 -302-

8. Subcutaneous (surgical) emphysema

This is accumulation of air under the skin. It may be due to :
a. Delay in opening the trachea with the patient in severe stridor.
This causes leakage of air into the subcutaneous tissues.
b. Excessive lateral neck dissection.
c. Improperly fitting tube (too small tube or too large stoma), which
lead to air leakage from around the tube, and the skin being
sutured tightly.
It may be severe and reach the mediastinum, face or chest. It is
treated by removal of skin sutures and insert a more fitting tube.
9. Infection
a. Wound infection.
b. Chest infection especially in children.
10. Recurrent laryngeal nerve paralysis due to dissection off the
midline into the tracheo-oesophageal groove.
11. Tube complications
a. Slippage of the tube due to low tracheostomy, wide stoma, short
thick neck, or short tube.
b. Blocked tube by dried secretions :
- These conditions are diagnosed by recurrence of stridor and
respiratory distress, with the ability of the patient to speak
without closing the tracheostomy.
Treatment
1. Reposition of the slipped tube and suture it to the skin.
2. If the tube is blocked, remove it for cleaning with
NaHC03 and reinsert it again. To avoid blockage of the
tube by dried secretion, frequent suction with NaHC03 id
done.
c. Injury of the posterior wall of the trachea by a too long tube.
12. Scabs and crustations in the trachea, as the tracheostomy alters
the physiology of the inspired air from being filtered. Also, it
interferes with the capacity of mucociliary clearance of pulmonary
and bronchial secretions.
13. Dysphagia and aspiration due to oesophageal irritation, and loss
of laryngeal competence.
 -303-

14. Delayed complications

a. Tracheal stenosis due to erosion by the tube or infection.
b. Subglottic stenosis particularly in high tracheostomy due to
injury of the cricoid cartilage.
c. Tracheo-oesophagael fistula due to erosion of the posterior wall
of the trachea by the tube.
d. Difficult decanulation (extubation).
e. Persistent tracheocutaneous fistula.
Postoperative care
1. Patient should lie in the semisitting position.
2 Humidification by steam inhalation.
3. Antibiotics to avoid secondary infection.
4. Mucolytics to avoid dryness of secretions.
5. Observation for vital signs, bleeding, and respiratory distress.
6. Care for the tube :
a. Frequent suctioning at intervals by sterile catheters. NallCO^
may be be used to dissolve mucus.
b. Regular removal of the inner tube for cleaning.
7. Extubation, if the cause of respiratory obstruction is treated. The
tube is closed witii a cork during the day time, then day and night,
and then removed.

Direct laryngoscopy
This id direct visualization of the larynx under general anaesthesia.
CFig.73)
Indications
A. Diagnostic
1. Examination of the larynx in infants and children.
2. Examination of the larynx in adults with difficult indirect
laryngoscopy (miror examination) is difficult.
3. To assess extent & site of a lesion, as for staging of malignant
tumours.
4. To take a biopsy.
B. i'lionipcutic
1. Removal of a foreign body.
2. Microlaryngosocpic surgery e.g. to remove a polyp, nodules, oi
small localized tumours under magnillcation.
 -304-

Laryngoflssure
The larynx is entered through a midline incision in the thyroid
cartilage, an approach known as median thyrotomy. A tracheostomy
should be done at first.
Indications
1. Excision of large bengin tumours.
2. Cardectomy for Tl glottic carcinoma limited to the mid third of
a mobile vocal cord.
3. Submucosal resection of laryngeal stenosis.

Fig.73. Vocal cords seen by direct laryngoscopy

 -305-

THE PHARYNX
Anatomy of the pharynx
The pharynx is a fibromuscular tube which lies infront of the
vertebral column, extending from the nasal and oral cavities above (at the
level of the 1st cervical vertebra), to the oesophagus below (at the level
of the 6th cervical vertebra, opposite the lower border of the cricoid
cartilage).
The pharynx is divided into : (Fig.74)
a) Nasopharynx.
b) oropharynx.
c) Hypopharynx.
A. The Nasopharynx
It lies behind the nose, above the level of the soft palate, extending
to the base of the skull. It lies at the level of the 1st cervical vertebra.
It opens anteriorly into the nose via the posteior nasal apereture
(choana), and opens downwards into the oropharynx.
The pharyngeal orifice of the E.T. opens in the nasopharynx and
lies about 1 cm behind the posterior end of the inferior turbinate, and it is
surrounded above and behind by a prominent bulge called the torus
tubarius which is composed of cartilage covered by mucous membrane.
Above and behind the torus tubarius is a small recess called the fossa of
RosenmuUer, and its importance is that it is one of the commonest sites
to harbour nasopharyngeal carcinoma, and it is one of the silent areas.
The roof of the nasopharynx shows aggregations of lymphoid tissue
called the nasopharyngeal tonsil, which when hypertrophies especially in
children, it is is called adenoids.
B. The oropharynx
It extends from the level of the soft palate above till the level of the
free border of the epiglottis below. It lies infront of the 2nd and 3rd
cervical vertebrae. It communicates above with the nasopharynx, below
with the hypopharynx, and anteriorly with the oral cavity.
The fauces (pillars) separate the oropharynx from the oral cavity.
They consist of two pillars (flods of mucous membrane) extending from
the soft palate to the side of the tongue. They are called the anterior and
posterior pillars, and they enclose the faucial tonsil.
 -306-

C. The hypopharynx (laryngopharynx)

It lies behind the larynx extending from the upper edge of the
epiglottis above, to the beginning of the oesophagus below. It lies infront
of the 4th, 5th, and 6th cervical vertabrae. It communicates above with
the oropharynx.

1 NoMrof
•piphorynat

On-or
TT^sophory

Loryngon

Fig.74. Anatomy of the pharynx

Structure of the pharyngeal wall

The pharyngeal wall consists of a muscle coat covered by mucosal
layer. It is formed of the following four layers :
1. Mucous membrane; the pharynx is lined by stratified squamous
epithelium, except the roof and the lateral walls of the nasopharynx
that are lined by pscudostratified columnar ciliated epithelium with
goblet cells and seromucinous glands.
2. Subepithelial connective tissue (pharyngeal aponeurosis); which
covers the muscular coat.
3. Muscular layer, which consists of three main muscles; the superior,
middle and inferior constrictors of the pharynx. They are
responsible for the process of deglutition. Other small muscles
include, palatopharyngeus, salpingopharyngeus, and
stylopharyngeus muscles.
4. Buccopharyngeal fascia; that covers the pharyngeal muscles from
outside, and separates them from the prevertebral fascia. It is
 - 307 -

connected with the prevertebral fascia by the median raphe in the

midline posteriorly.
Waldeyer*s ring (Fig.75)
This is a ring of lymphoid tissue that surrounds the pharynx. It lies
in the subepithelial connective tissue and drains into the
retropharyngeal and the upper deep cervical lymph nodes. It
consists of :
1. Nasopharyngeal tonsil.
adenoids
2. Tubal tonsils, arround the
pharyngeal orifice of the
E.T.
3. Palatine (Faucial) tonsils.
These are the largest of all.
4. Lingual tonsils, at the base of
the tongue.
5. Discrete lymphoid nodules
on the lateral and posterior
pharyngeal walls.
N.B : In no place else in the body, except the Waldeyer's ring, and
peyer's patches of the intestines, the lymphoid tissue is in direct
contact with the surface mucosa.
Blood supply
A. Arterial supply -
1. Ascending pharyngeal artery from the external carotid artery,
2. Tonsillar and ascending palatine arteries from the facial artery.
3. Descending palatine artery from the maxillary artery.
4. Lingual artery.
B. Venous drainage
To the pharyngeal and pterygoid venous plexus, then to the
common facial veins and the internal jugular vein.
Nerve supply
A. Motor
All muscles of the pharynx and palate are supplied by the cranial
portion of the accessory (11th) cranial nerve, via the vagus nerve,
except, the tensor palati muscle which is supplied by the
mandibular nerve (from trigeminal), and stylopharyngeus muscle
which is the only muscle supplied by the glossopharyngeal nerve.
 -308-

B. Sensory
1, TTie nansopharynx, oropharynx, and the base of the tongue are
supplied by the pharyngeal plexus of the glossopharyngeal (9th
cranial) nverve.
2. The hypopharynx is supplied by the glossopharyngeal as well as
the vagus nerve via its superior laryngeal branch.
Lymphatic drainage
The pharynx drains into the retropharyngeal and lateral pharyngeal
lymph nodes then to the deep cervical nodes.
Functions of the pharynx
1. Respiratory channel.
2. Voice resonance.
3. Articulation of speech.
4. Deglutition:
• PcgutitJon may t?g divided into three stages:
- 1st stage : Movement of food from the mouth into the pharynx
(voluntary).
- 2nd Stage: Transport of food through the pharynx
(involuntary).
- 3rd stage : Passage of the bolus of food through the
oesophagus (involuntary).
- The steps of deglutition arc as follows :
a. Following mastication, food is positioned on the middle third
of the tongue. Elevation of the tongue and soft palate forces
the bolus of food into the oropharynx.
b. The suprahyoid muscles contract elevating the hyoid bone and
the larynx, thus opening the hypopharynx. The intrinisic
muscles of the larynx contract in a sphincter-like fashion to
prevent aspiraton,
c. A strong motion of the tongue posteriorly, pushes the bolus of
food inferiorly along the oropharynx, aided by contraction of
superior and middle constrictor muscles.
d. The thyropharyngeus part of the inferior constrictor muscle
contracts pushing the bolus of food down the oesophagus,
and at the same time the cricopharyngeus part of the inferior
constrictor relaxes.
e. Oesophageal peristalsis, assisted by gravity, move the food
down the oesophagus into the stomach.
 -309-
• ^

Anatomy of the palatine tonsils

These are two ovoid masses of lymphoid tissue lying in the
tonsillar fossa, one on each side of the lateral wall of the oropharynx. The
tonsillar fossa is traingular in shape and is enclosed between the anterior
and posterior pillars, and the posterolateral third of the tongue.
The tonsil has two surfaces; a lateral surface covered by the
tonsillar capsule which separates the tonsil from its bed (superior
constrictor muscle). The medial surface is free and is covered by
stratified squamous epithelium that invaginates into the tonsil forming
12-15 crypts. The largest crypt is called the crypta magna and is present
near the upper pole of the tonsil (vestige of the second pharyngeal
pouch).
Blood supply
Arterial
1. Tonsillar branch of the facial artery, that pierces the superior
constrictor muscle to enter the lower pole of the tonsil.
2. Descending palatine branch of the internal maxillary artery.
3. Ascending palatine branch of the facial artery.
4. Ascending pharyngeal artery.
Venous drainage
To the paratonsillar veins, and then into the pharyngeal plexus of
veins.
Functions of the tonsils
Protection of the upper airway from organisms found in food,
mouth, and pharynx. It plays a role in humoral and cell mediated
immunity, till the age of 4-5 years.
 ^&

-310-

Diseases of the nasopharynx

Adenoids
This is hypertrophy of the
nasopharyngeal tonsil sufHcient to
produce symptoms. The enlarged
mass is a subepithelial lymphoid
aggregate, and it has only efferent but
no afferent lymphatics.
TTie adenoid tissue arises at the
junction of the roof and the posteior
wall of the nasopharynx (Luska's
pouch), and is composed of vertical
ridges of lymphoid tissue. Adenoids Fig.76. Adenoids
is the commonest nasopharyngeal
swelling. (Fig.76)
Age
It is considered a disease of childhpod, and it is usually an
adenotonsillar hypertrophy. It occurs most commoly between the age of
2-12 years, then gradual involution and atrophy occurs at the age of
puberty. Occasionally, persistent adenoid or adenotonsillar hypertrophy
is deteced in adolescents and adults.
Aetiology
It is related to repeated upper respiratory tract infection. It occurs
more in debilitated children, and in nurseries where children are more
exposed to infection.
Clinical picture
/. Effects of hypertrophy
1. Bilateral nasal obstruction
a. There is mouth breathing, and the child has a noisy respiration
while awake, and snoring is present during sleep. In marked
adenotonsillar hypertrophy there may be sleep apnoea.
b. In infants, there is difficulty of feeding and suckling with loss of
weight.
C. The voice looses its tone and becomes nasal (Rhinolalia clausa).
d. Bilateral mucoid nasal discharge due to mechanical obstruction
of the posterior nares.
e. Foetor oris.
f. Huge adenoids may be a source of epistaxis.
 ^c«

-311-

2. Eustachian tube obstruction leading to;

a. Middle ear effusion (secretory otitis media) and conductive
deafness is very common.
b. Recurrent acute suppurative otitis media.
3. Adenoid facies
- Open dry mouth.
- Narrow pinched anterior nares.
- Prominent incisors.
- Elevated short thin upper lip.
- High arched (Gothic) palate : any newly bom has a high arched
palate and the continuous pushing of the tongue against the
palate, provided the mouth is closed results in flattening of the
arch.. In prolonged nasal obstruction, the opened mouth
abolishes adaptation by the tongue and exaggerates this tenting,
- Underslung lower jaw.
- Mucoid secretions over the upper lip.
- Apathetic expressionless look.
Adenoid facies develops in long standing cases due to chronic nasal
obstruction, and mouth breathing.
//. Recurrent infectoins
1. Recurrent rhinitis and sinusitis.
2. Recurrent acute suppurative otitis media with incomplete
resolution.
3. Postnasal discharge and irritative cough.
4. Recurrent pharyngitits and laryngotracheobronchitis.
5. Cervical adenitis.
///. General manifestations
1. Marked adenotonsillar hypertrophy with mouth breathing leads to
sleep apnoea and chronic hypoxia. There are night terrors and
nocturnal enuresis.
2. The child is shy and friendless.
3. Mental dulhiess and apathy due to chronic hypoxia, and deafness.
Examination :
1. Adenoid facies.
2. Examination of the ears :
a. Retracted T.M. is usually present.
 -312-

b. Secretory otitis media.

c. Various manifestations of infected middle ear (A.S.O.M.)
d. Tuning fork tests; show conductive deafness.
3. Anterior rhinoscopy:
a. Vertical slit apeature of the nose.
b. Narrowed nasal chambers.
c. Mucoid or mucopurulent nasal discharge.
4. Mouth and oral cavity:
a. Distorted, dry, decayed teeth. Abnormalities of dentition with
overcrowded teeth and prognathia which needs orthodontic
treatment later on.
b. Inflammed spongy gums.
c. Arching of the hard palate and the soft palate is often relaxed.
d. Enlarged faucial tonsils (i.e. adenotonsillar hypertrophy).
e. Discrete patches of lymphoid tissue on the posterior pharyngeal
wall.
f. Egg white postnasal discharge may be' seen.
g. In marked adenoid hypertrophy, it's lower edge may be seen
during examination of the oral cavity.
h. Foetororis.
5. Posterior rhinoscopy in older children; the growth may be seen as a
dark pinkish cushion.
6. Digital palpation of the nasopharynx : The adenoid tissue is felt as
if touching a punch of earth womis. It is very annoying to the child.
7. Flexible nasopharyngoscopy shows the adenoid tissue appearing as
a lobulatcd mass having the same colour as the surrounding
mucous membrane.
N.B : Manifestations of prolonged nasal obstruction and hypoxia are :
A. Adenoid facies.
B. Sleep apnoea syndrome (mentioned later).
C. Chest: Retracted lower costal margin, and prominent sternum
(pigeon chest).
Investigations
1. Plain x-ray soft tissue lateral view nasopharynx, shows a
radiopaque soft tissue shadow arising from the superior and
posterior walls of the nasopharynx with narrowing of the
nasopharyngeal air column..
2. Audiogram and tympanogram.
 -313-

Treatment
- Removal of the adenoid tissue (adenoidectomy). It is usually
combined with tonsillectomy (adenotonsillectomy) as there is
usually recurrent tonsillitis or associated tonsillar hypertrophy.
In certain cases especially in young children, it is preferred to
remove the bulk of the adenoid tissue and not to deprive the
child from the protective functions of the faucial tonsils.
Indications for adenoidectomy
1. Obstructive sleep apnoea.
2. Obligatory mouth breathing.
3. Chronic mucopurulent nasal discharge.
4. Recurrent or chronic middle ear disease. In associated
secretory otitis media, myringotomy and insertion of
ventilation tubes is performed.
5. Recurrent sinusitis.
6. Frequent cold catching.
7. Spasmodic cough.
8. Malformation of the chest and palate.
Preoperative preparations : (mentioned with tonsillectomy)
Antibiotics and decongestants should be given before surgery if
there is active infection.
Anaesthesia:
General intubation anaesthesia after good premedication (including
preoperative sedation e.g. phenergan or valium syrup to alleviate
anxiety).
Position of the patient
The patient lies on his back, with the head slightiy flexed, A pillow
should not be placed under his shoulders in order not to have the cervical
spine projecting, to avoid its injury.
Technique of the operation (Fig,77)
The anaesthetic is given untill the reflexes are abolished (i.e.
swallowing and cough reflexes). The mouth is opened with the
Boyel-Davis gag, a sharp adenoid curette is introduced behind the soft
palate until it touches the back of the septum. Then die curette is pressed
downwards, and the adenoid tissue is shaved forwards. A pack is then
insened into the nasopharynx to compress the adenoid bed for 10-15
minutes, until bleeding stops. Do not use electric suction as it does not
allow enough time for clot formation.
 B5—S-

-314-

If bleeding does not stop, the soft palate is retracted and

electrocoagulation of the adenoid bed using bipoplar diathermy is
performed, and this is usually sufficient to stop the bleeding. If bleeding
is still present or becomes severe, a postnasal pack is placed to be
removed after 24-48 hours.

Fig.77. Adenoidectomy

Postoperative care
1. Rest for 3-4 days.
2. Steam inhalation and iced water.
3. Analgesics and antipyretics e.g. paracetamol and novalgine.
Avoid salicylates and nonsteroidal anti-inflammatory drugs as
these may cause bleeding.
4. Decongestant nasal drops.
Complications of adenoidectomy
1. Complications and collapse from anaesthesia.
2. Incomplete removal of the adenoid tissue due to :
a. Wrinkling of the nasopharynx due to muscular contractions
due to superficial anaethesia.
b. Using a blunt curette.
Incomplete removal may cause postadenoidectomy bleeding and
may lead to hypertrophy of the residual lymphoid tissue, and in
such case readenoidectomy should be done.
3. Post adenoidectomy bleeding :
a. Primary haemorrhage due to :
- Incomplete removal.
 -315-

- Blood dyscrasia e.g. haemophilia.

- Over curettage with retropharyngeal muscle injury.
b. Reactionary haemorrhage : This occurs soon after the
operation or within the first 24 hours. It is usually due to a
defect in the coagulation mechanism.
c. Secondary haemorrhage : This occurs after 5-7 days, and is
due to secondary infeciton.
Treatment
a. Primary Haemorrhage : Reanaesthesia and complete removal
of adenoids if there are remanants, suture the prevertebral
muscles if teard. Fresh frozen plasma is given in cases of
haemophilia. If bleeding is severe and did not stop a
postnasal pack is inserted to be removed after 24-48 hours.
Blood transfusion may be needed.
b. Reactionary haemorrhage is treated as the primary one.
c. Secondary haemorrhage : antibiotics and conservative
treatment. Sometimes, blood transfusion is needed.
4. Injury of surrounding structures :
a. The soft palate may be injured. This may cause rhinolalia
aperta and nasal regurge.
b. The uvula may be bruised against the pharyngeal wall or even
detached.
c. Stripping of an excess mucous membrane.
d. Damage of the apoeneurosis and musculature of the pharynx
due to overcurettage.
e. The cartilagenous orifice of the E.T. may be injured, and this
will lead later to scarring and obstruction of the tubal orifice
with subsequent secretory O.M., and recurrent A.O.M.
f. A prominent atlas may catch over the curette.
g. Injury of the cervical spine, which may lead to torticollis.
5. Postoperative infection which may cause secondary
haemorrhage, local sepsis, postnasal discharge, and descending
infection.
6. Pulmonary complications e.g. lung collapse and lung.abscess. It
may e due to inhalation of a blood colt, a piece of adenoid tissue
or aspiration during anaesthesia.
 i = ^ .

-316-

Contraindications
1. Blood dyscrasia e.g. leukaemias, purura and haemophilia.
Von-Willebrand*s disease (deficiency of cofactor VIII) should
always be suspected as it is present in 1% of the population.
2. Uncontrolled systemic diseases e.g. Diabetes, and heart failure.
3. Acute infection.
4. Cleft palate either frank or submucosal to avoid velopharyngeal
incompetence and rhinolalia aperta. The problem comes when there
is a submucous cleft (the mucosa is intact, but the palatal muscles
are deficient underneath). In such a situation, adenoidectomy is id
modified to remove the lateral parts only and leave the central
portion.

Tumours of the nasopaharynx

/. Benign tumours
A. Epithelial: Papilloma, adenoma and bengin tumours from minor
salivary glands.
B. Mesenchymal: - Angiofibroma (the commonest one).
- Haemangioma, lymphangioma.
- Chondroma.
- Lipoma, myoma, myxoma.
- Chemodectoma (neuroectodermal tumours)
//. Intermediate (locally malignant) tumours
- Chordoma.
- Teratoma.
- Craniopharyngioma.
///. Malignant tumours
- Squamous cell carcinoma (the commonest one).
- Anaplastic carcinoma (previously named lymphocpithelioma).
- Rabdomyosarcoma, chondrosarcoma.
- Lymphomas, and extramedullary plasmacytoma.
N.B.: Cysts of the nasopharynx
1. Thornwaldt's cyst (congenital).
2. Retention mucus cyst
3. Branchial cyst (from the dorsal portion of the 2nd arch).
 -317-

Nasopharyngeal angioflbroma
This is the most common bengin tumour of the nasopharynx. It is
histologically benign, but locally aggressive.
Age : It affects only prepubertal and adolescent males (between 10-20
years), with a peak age at 13-16 years. It never occurs in
females.
Aetiology and pathogenesis
Several theories were postulated, and these include :
1. A true benign fibroma.
2. Hamartoma (vascular malformation), at the junction of the
viscerocranium with the neurocranium.
3. Chemodectoma. arising from the paraganglionic tissues in relation
to the terminal part of tiie maxillary artery.
4. Endocrinal hormonal imbalance.
Pathology
The site of origin is the superior margin of the sphenopalatine
foramen situated in the posterosuperior part of the lateral wall of the
nose. So it is considered a nasal tumour and not a nasopharyngeal one,
although traditionally it is termed nasopharyngeal angiofibroma.
Previously, it was thought that it arises from the periosteum of the vault
of the nasopharynx.
Microscopically
- The growth consists of two components, a vascular component
and fibrous tissue stroma. The vascular component is formed of
large, neumerous sinusoidal spaces that are devoid of muscular
coat, so they are incapable of contraction and bleed profusely.
- The stroma is composed of coarse parallel wavy or interlacing
bundles of collagen in which the stromal cells are seen to radiate
outwards from the vessels.
- With maturity of the tumour, the fibrous component increases,
with decrease in the vascular element.
Blood supply; the tumour receives its blood supply mainly from
the maxillary artery or one of its branches. If it extends
intracranially, it acquires blood supply from the internal carotid
artery.
Behaviour of the tumour
1. Spontaneous regression may occur at the age of sexual maturity
(about 25 years), although this is rare.
 -318-

2. Extension due to pressure necrosis and displacement of the

surrounding structures. Having filled the nasopharynx, the
tumour extends:
a. Forwards, to the nasal cavity, displacing the septum to one
side (type A).
b. Laterally, through the sphenopalatine foramen to the
pterygopalatine fossa (type B). It may reach the infratemporal
fossa through the pterygomaxillary fissure, and it may even
appear externally under the cheek, (type C)
c. Upwards; intracranially through the roof of the sphenoid
sinus, foramen lacerum or foramen ovale and may involve
the cavernous sinus (Type D).
d. Downwards to the oropharynx.
e. Through the inferior orbital fissure, it reaches the orbit and
causes proptosis.
Clinical picture
The patient is alway an adolescent male (10-20 years of age).
A. General manifestations; easy fatiguability, pallor, and palpitation
due to chronic anaemia. Anaemia is due to recurrent epistaxis.
B. Nasal manifestations
1. Gradual progressive nasal obstruction.
2. Intermittent epistaxis which is spontaneous, usually severe and
profuse. It usually stops spontaneously.
3. Nasal tone of voice (rhinolalia clausa).
4. Purulent, mucopurulent or blood stained foetid nasal discharge
due to stasis of secretions and infection.
5. Hyposmia or anosmia.
6. Examination:
- Anterior rhinoscopy shows abundant mucopurulent secretions
together with bowing of the septum to the uninvolved side. A
unilateral nasal mass may be seen, which bleeds profusely on
touch,
- Posterior rhinoscopy in a cooperative patient displays a pink or
red mass filling the nasopharynx. It is lobulated or nodular,
covered by intact mucosa with many tortuous vessels on its
surface.
- Digital palpation should be avoided as it may lead to profuse
uncontrollable bleeding.
 nHML.1

-319-

C. Aural manifestations; conductive deafness and middle ear

effusion may be detected. They are due to obstruction of the
pharyngeal orifice of the E.T. by the mass.
D. Oropharyngeal examination may show sagging of the soft palate.
Intraoral palpation in the space between the ramus of the mandible
and the side of the maxilla may reveal a fullness due to extension
of the tumour into the infratemporal fossa.
E. External examination may reveal;
- Proptosis due to extension to the orbit.
- Unilateral swelling of the cheek or the temple due to obstruction
of the pterygoid venous plexus or extension to the infratemporal
fossa.
- Frog-face deformity and manifestations of intracranial extension
in advanced cases.
Investigations
1. CT scan of the paranasal sinuses with contrast reveals an
enhancing nasopharyngeal soft tissue mass. It is very important
to study the extensions of the tumour to the pterygopalatine
fossa, infratemporal fossa and intracranially. Anterior bowing of
the posterior wall of the maxillary sinus with no invasion of its
cavity is a characteristic radiologic sign.
2. Bilateral carotid angiography is important to confirm the
diagnosis (it shows the characteristic tumour blush), and to
identify the feeding vessels for preoperative embolization.
3. MRI and MR angiography are very helpful if available.
4. Biopsy is usually not needed and is not recommended, as the
diagnosis is based on clinical and radiological evaluation.
However, if there is significant doubt, endoscopic intranasal
biopsy can be done in an operating theatre, under general
anaesthesia, with blood transfusion to be ready, as well as,
facilities to control bleeding.
Differential diagnosis
1. Antrochoanal polyp : it never bleeds, and CT scan is diagnostic.
2. Malignant tumours : common in old age, rapid progressive
course, cranial nerve palsies, and CT scan shows bone erosion.
Treatment
A. Surgical treatment
Surgical excision of the tumour by one or more (combination) of
 -320-

the following approaches:

1. Transpalatal approach if the tumour is confined to the
nasopharynx.
2. Lateral rhinotomy approach if the tumour extends to the
pterygopalatine fossa, or into the nasal cavity.
3. Transnasal / Transantral approach via a Weber-Fergusson
incision or a midfacial degloving approach, if the tumour
extends to the infratemporal fossa. Alternatively an
infiratemporal fossa approach may be performed.
4. If there is intracranial extension, a bifrontal craniotomy may
be needed to deliver the intracranial part.
- Preoperative embolization of the feeding vessels and the
tumour bed is done ^2-3 days prior to surgery in order to
minimize bleeding during operation.
- Preoperative tracheostomy should be done in extensive
cases to avoid aspiration of blood during surgery, and to
avoid respiratory obstruction due to the severe
postoperative oedema.
B. Hormonal therapy (controversial)
Testosterone, oestrogen or a combination of both was advocated.
It may induce maturation of collagen and reduction of the
vascularity of the tumour. Thus, it may be used preliminary to
surgery, however the results are doubtful.
C. Radiotherapy
- The effect of radiotherapy is to induce fibrosis, hardening and
shrinkage of the tumour with a resultant reduction of it's size and
vascularity. However, it is not used now because of its
carcinogenic effect, as it induces malignancy after a latent
period, most commonly in the skin and the thryroid gland,
(radiation induced malignancy).
N,B : Nasopharyngeal angiofibroma is a bengin tumour occuring in
youngesters with an expected long life span. The situation is
different in nasopharyngeal malignancy as here the condition is
lethal and thus radiotherapy is the treatment of choice.
- Radiotherapy may be used in selected cases of angiofibroma e.g.
those with inoperable intracranial extensions, or inoperable
recurrence after surgery.
 -321-

Nasopharyngeal carcinoma
Nasopharyngeal carcinoma is the commonest malignant tumour of
the nasopharynx where it constitutes about 80% of all nasopharyngeal
cancers.
Race; it is highest among Chinese and orientals.
Age; it occurs usually in old ages (40-60 years), although younger age
groups may be affected. Sarcomas are more common in young
ages. (15-25 years).
Sex; it is more common in males than in females (3 : 1).
Aetiology
A. Certain envu*onmental agents were linked to the development of
nasopharyngeal carcinoma, and they include :
1. Epstien-Barr virus (EBV) infection, and this is evidenced by
raised antibody titre to EBV in the patient's serum, also the
viral genome was detected in the tumour cells.
2. Nitrosamines, polycyclic hydrocarbones, formaldehyde, and
wood dust.
3. Cigarette smoking, and household smoke and fumes.
B. Genetic perdisposition : Certain major histocomptability genes
are thought to play a role in the development of nasopharyngeal
carcinoma.
Pathology
Site
1. Fossa of Rosenmuller, this is the commonest site.
2. Lateral and superolateral walls of the nasopharynx.
3. Posterior wall of the nasopharynx (less common).
4. Upper surface of the soft palate (rare).
N.B.: The tumour may be multicentric involving more than one site.
Microscopically
1. Squamous cell carcinoma is the commonest histopathological
type representing about 85% of all cases. It is either well,
moderately or poorly differentiated, but the commonest is
non-keratinizing poorly differentiated squamous cell carcinoma.
2. Anaplastic carcinoma (previously termed lymphoepithclioma) :
It is an undifferentiated nonkeratinizing squamous cell
carcinoma with infiltration of lymphocytes among the tumour
 -322-

cells, and that lymphoid tissue is not sharing in the malignant

process.
3. Others e.g. adenocarcinoma, and mixed salivary tumours arising
from minor salivay glands.
Spread
A. Direct spread of the primary tumour
1. Anteriorly; to the nose, maxillary sinus, pterygopalatine fossa. It
may reach the orbit through the inferior orbital fissure.
2. Posteriorly; to the retropharyngeal space, prevertebral muscles
and fasica and the 1st and 2nd cervical vertebrae.
3. Inferiorly; to the soft palate, hard palate and oropharynx.
4. Laterally; to the pterygoid plate and muscles, and the E.T. It may
extend to the parapharyngeal space to involve the mandibular
nerve, last four cranial nerves, cervical sympathetic chain, and
the deep lobe of the parotid gland.
5. Superiorly; intracranial extension through the foramen lacerum,
carotid canal and the foramen ovale.
B. Lymphatic spread
It is verly early and common. First, lymphatic metastasis to the
retropharyngeal lymph nodes (not clinically reachable to
palpation), then to the upper deep cervical lymph nodes. Bilateral
nodal metastases are common when there is a midline growth or
due to lymphatic crossover.
C. Blood spread; rare and late; to bones, lungs, and liver.
Clinical picture
It runs a gradual incidious onset and a progressive course.
A. Aural manifestations
1. Unilateral secretory otitis media with conductive deafness and
tinnitus. Middle ear effusion may be due to obstruction of the
E.T. orifice by a fungating mass, paralysis of the levator palati
muscle (due to involvement of its nerve supply), or it may be
due to infiltration of the peritubal lymphatics. Erosion of the
E.T. itself is rare, as cartilage is resistant to tumour infiltration.
2. Referred otalgia due to tumour infiltration of the mandibular
nerve, 7th or 10th cranial nerves.
B. Nodal manifestations
Enlarged upper deep cervical lymph nodes, particularly the
jugulodigastric node behind the angle of the mandible. Nodes
 -323-

are hard, painless, and not tender. They are first mobile and later
they become fixed. About 70% of patients with nasopharyngeal
carcinoma present with enlarged lymph nodes at the time of
diagnosis. An important point is that the nasopharynx is one of
the silent areas and metastatic cervical lymph node enlargement
may be the first presentation (40% of cases).
C. Rhinological manifestations
1. Unilateral or bilateral nasal obstruction.
2. Slight intermittent epistaxis.
3. Nasal tone of voice.
4. Foetid mucopurulent nasal discharge.
5. On examination (Posterior rhinoscopy, flexible or rigid
nasopharyngoscopy) the growth may appear as an :
a. Exophytic fungating mass.
b. Ulcerative lesion (less common).
c. Submucosal swelling which may be deceiving, as it looks
normal.
6. Anterior rhinoscopy may reveal a nasal mass if the tumour
extends to the nasal cavity.
D. Neurological manifestations
1. The vidian nerve (nerve of the pterygoid canal) is the first to be
affected, by intracranial extension through the foramen lacerum.
It presents as defective lacrimation and decreased nasal
secretion.
2. Cranial nerve palsies :
a. Trigeminal (5th nerve) is commonly and early affected,
particularly the maxillary division. There will be unilateral
facial pain and numbness* with decreased facial, palatal and
pharyngeal sensations.
b. 3rd, 4th, and 6th cranial nerves are affected by intracranial
extension of the tumour, leading to ophthalmoplegia,
paralytic squint and diplopia.
c. 9th, 10th. 11th, and 12th cranial nerves may be encroached
upon at the skull base, or in the parapharyngeal space by an
enlarged retropharyngeal node (node of Rouviere) There will
be palatopharyngolaryngeal paralysis (nasal regurge, nasal
tone of voice, hoarseness of voice, dysphagia, choking) due
to paralysis of 9th and 10th cranial nerves, dropping of the
 -324-

shoulder due to paralysis of the Uth cranial nerve, and

paralysis of one half of the tongue with dysarthria due to 12th
nerve paralysis.
d. 2nd, 7th and 8th nerves may be affected in advanced cases.
3. Sympathetic chain affection will lead to Homer*s syndrome
(ptosis, miosis, enophthalmos, anhydrosis, and hemifacial
flush).
4. Increased intracranial tension : headache, projectile vomiting,
blurring of vision and papilloedema. This is considered as a
terminal stage,
N.B. Trotter's triad of nasopharyngeal carcinoma (Diagnostic) include:
a. Immobile soft palate.
b. Unilateral conductive deafiiess.
c. Unilateral facial pain.
Investigations
1. Plain x-ray skull (lateral view and skull base view) shows a
nasopharyngeal soft tissue mass with bone erosion.
2. CT scan of the nasopharynx with contrast, shows the tumour as
an enhancing nasopharyngeal mass with bone erosion. It is
important to delineate extensions of the tumour, and nodal
metastasis particularly the impalpable node of Rouviere.
3. Biopsy and histopathological examination :
This is important to confirm the diagnosis, the biopsy is
obtained by one of the following methods :
a. Ednsocopic transnasal biopsy under local or general
anaesthesia.
b. Direct biopsy from the nasopharynx after retracting the soft
palate.
c. If the biopsies are repeatedly negative and clinically
nasopharyngeal carcinoma is highly suspected, blind
curettage of the nasopharynx and thorough histopathological
examiantion of the tissues obtained should be done.
4. Tympanogram may show secretory O.M.
5. Metastatic work up : chest x-ray, bone scan, and abdominal
ultrasound to detect distant metastasis.
Treatment
• Radiotherapy is the treatment of choice. It is given for both the
 »lrt

-325-

primary and to the neck, even if there are no clinically palpable

neck nodes.
The role of surgery in nasopharyngeal carcinoma is limited to the
performance of radical neck dissection if there are persistent
nodes after full dose of radiotherapy and the primary in the
nasopharynx is controlled (i.e. frequent negative biopsies,
denotes apparent cure by radiotherapy.
 -326-

Inflammatory conditions of the pharynx

A. Acute
1. Acute nonspecific pharyngitis (viral or bacterial).
2. Acute specific pharyngitis :
a. Diphtheria.
b. Vincent's angina.
c. Moniliasis.
3. Pharyngitis due to blood diseases :
a. Acute leukaemia.
b. Agranulocytosis.
4. pharyngitis as a part of systemic disease :
a. Infectious mononucleosis.
b. Viral exanthemata.
c. Aphthous ulceration.
B. Chronic
1. Chronic nonspecific pharyngitis.
2, Chronic specific pharyngitis :
a. Scleroma.
b. Syphilis.
c. T.B.
C. Inflammation of lymphoid tissye: Adenoiditis, and acute tonsillitis.
Acute tonsillitis
Acute nonspecific inflammation of the palatine (faucial) tonsils,
and it is usually associated with pharyngitis (pharyngotonsillitis). It is
most frequent in childhood, however, it does occur in adults.
Aetiology
Predisposing factors
1. Recurrent upper respiratoiy tract infections.
2. As an initial stage of some fevers e.g. measles, and scarlet fever.
3. Bad hygienic conditions and overcrowded places.
4. Lowered general resistance.
 ••H

-327-

Causative organisms:
1. Group A beta haemoiytic streptococci arc the commonest.
2. Haemophilus influenza, staphylococcus aureus, and
pneumococci.
3. It may start initially as viral tonsillitis followed by secondary
bacterial infection particularly in children. Common viruses
include; adenovirus, parainfluenza, and herpes simplex.
Pathology
1. Acute catarrhal tonsillitis: the inflammatory changes are marked on
the surface of the tonsils, with oedema and congestion of the
mucosa.
2. Acute follicular tonsillitis : the inflammatory changes are confined
to the crypts. First, there is infection of the lymphoid follicles with
formation of small abscesses, and thus the crypts become full with
pus that appears as yellowish spots on the surface of the tonsil.
Later, this purulent exudate coalesce to form a non adherent
yellowish membrane on the surface of the tonsils.
3. Acute parenchymatous tonsillitis : there is congestion and
enlargement of the whole tonsil without pus formation.
Clinical picture
Symptoms
1. High fever reaching 39-40*C with headache malaise and
anorexia.
2. Myalgia, arthralgia, backache and pain in the limbs.
3. Severe sorethroat and odynophagia with referred otalgia.
4. Change of voice (hot potato voice), if the size of the tonsils is
huge.
5. Foetor oris.
6. Dehydration may occur in children due to the high fever and
painful swallowing (odynophagia).
Sings
A. General
High temperature, with tachycardia that is proportionate to the
fever, and the patient looks severly ill.
B. Local
1. The tonsils appear swollen, congested and erythematous
(sometimes deeply red purple). There is hypertrophy of all
 -328-

lymphoid tissues. The oropharynx also appears red and

oedematous.
2. Yellowish white spots may be seen filling the crypts (acute
follicular tonsillitis). There may be a yellowish white
membrane on the surface of the tonsils that can be easily
wiped away.
S.There is oedema of the soft palate, and the tongue is coated.
There is foetor of breath.
4. Enlarged tender upper deep cervical (jugulodigastric) lymph
nodes.
Investigations
1. Swab from the tonsil for culture and sensitivity.
2. Blood picture shows leucocytosis.
3. High erythrocyte sedimentation rate.
Differential diagnosis
1. Scarlet fever, which is a streptococcal tonsillitis in which the
streptococci produce the erythrogenic toxin which results in an
erythematous rash. Usually there is hypertrophy of the posterior
pharyngeal wall which is characteristic.
2. Other causes of a membrane over the tonsils :
a. Vincent's angina.
b. Acute diphtheria.
c. Infectious mononucleosis.
d. Acute leukaemia and agranulocytosis.
Treatment
1. Bed rest, light diet, and adequate fluids.
2. Antibiotics : Benzyl penicillin, 600mg/6hours I.M. daily for Sdays.
After an intial response, continue on oral penicillins e.g.
amoxycillin and amoxycillin with calvulanic acid (anti P
lactamase). Cephalosporins and macrolides are a second option.
3. Analgesics and antipyretics.
4. Antiseptic mouth wash.
Complications of acute tonsillitis
A. Local
1. Pcritonsillal abscess (Quinsy).
2. Parapharyngeal abscess and retropharyngeal abscess.
3. Ludwig*s angina.
 -329-

4. Extension of infection leading to otitis media, laryngitis and

bronchitis.
5. Chronic tonsillitis and septic focus manifestations.
B. General
1. Delayed poststreptococcal infection :
a. Rheumatic fever.
b. Acute glomerulonephritis.
c. Fascial myositis (e.g. plantar fascitis).

Chronic tonsillitis
Aetiology
Repeated attacks of acute tonsillitis.
Clinical picture
Symptoms
1. History of recurrent attacks of acute tonsillitis. There may be a
history of a peritonsillar abscess.
2. Recurrent sore throJit and dysphagia, or the mere sensation of
irritation in the throat.
3. A nagging pain extending to the ear.
4. Foetor oris with bad taste in the mouth.
5. Recurrent enlargment of the cerivcal lymph nodes.
6. Snoring, sleep apnoea and hot potato voice if the tonsils are
markedly enlarged.
7. Septic focus manifestation; low grade fever, fatigue, anorexia,
headache, arthritis, backache, and joint pains.
Signs
1. Redness and persistent congestion of the anterior pillars in
abscence of acute infection.
2. The tonsils mr.y be enlarged with widening and irregularity of
their crypts.
3. Induration of the tonsils.
4. Unequal size of the tonsils.
5. Expressible pus on pressure, or an intratonsillar abscess.
6. Persistent enlargement of the jugulodigastric lymph nodes.
 -330-

Investigations
l.HighESR.
2. Elevated Antistreptolysin "O" titre (ASO) in case of infection by
group A beta haemolytic streptococcal infeciton.
Treatment
Tonsillectomy.

Acute faucial diphtheria

This is an acute specific infective disease and although it is rare
nowadays due to widespread immunization, it should be considered in
any pharyngeal infection particularly in those demonstrating a
membranous exudate.
Aetiology
It is caused by the Gram positive bacillus (corynebacterium
diphtheriae), which is transmitted by droplet infection from patients or
asymptomatic carriers. Diphtheria may occur either in:
1. The pharynx (faucial diphtheria) which is the commonest.
2. The larynx and nose are rarely affected primarily. Laryngeal and
nasal diphtheria are usually secondary to faucial diphtheria.
3. Conjunctiva (very rare).
Age; it usually affects young age groups up to 12 years.
Incubation period; is 2-6 days.
Pathology
- It is a membranous type of inflammation that affects the mucosal
surfaces. After intial infection the organism remains on the surface
of the mucous membrane and multiply, and doesnot invade the
deep tissues. The organism produces a powerful exotoxin that
diffuses and becomes absorbed in the circulation producing
toxaemia. The exotoxin has a high affinity to cardiac and neural
tissues.
- At an early stage, the affected side is severely congested. Very soon,
patches of necrosis occur in the superficial layer of the epithelium
that rapidly fuse together forming a necrotic dirty yellowish grey
membrane which becomes adherent to the tonsil. The membrane is
formed of large number of bacteria, fibrin, necrotic tissues, RBCs,
and inflammatory cells especially neutrophils.
- The subepithelial tissues, that escape neaosis respond by outpouring
 HI

-331-

of an exudate rich in fibrinogen and leucocytes. Fibrinogen, later

forms fibrin threads.
Clinical picture
Clinically diphtheria can vary form an asymptomatic carrier state to a
rapidly fatal toxic disease.
Symptoms
1, Insidious onset of low grade fever, headache, malaise, anorexia,
and there may be vomiting.
2. Severe sorethroat and dysphagia.
Signs
1. Low grade fever and severe toxaemia. In toxic cases, the
temperature is generally low or even subnormal. Fever may last
3-7 days, and sometimes longer.
2. There is severe tachycardia which is not proportionate to the
fever.
3. A false membrane is formed over the tonsil which is :
a. Unilateral and has a strong foetor.
b. At first a thin film, which becomes raised into a yellowish
white patch, and later turning to dirty greyish like
wash-Leather. It may become blackish with offensive odour.
c. Thick and fum, and if peeled off its stands at an edge.
d. Involves the faucial tonsil, and often exceeds the limits of the
tonsil to involve the fauces, soft palate and pharynx.
e. Adherent and leaves a bleeding surface when removed,
f Tends to reform rapidly after removal.
4. Albuminuria may occur, and it varies in degree from day to day.
It is generally found on the 4th to the 10th day.
5. Markedly enlarged tender cervical lymph nodes, on both sides of
the neck (Bull's neck).
Laryngeal diphtheria
- It is usually due to extension from faucial diphtheria, rarely it is
primarily lamgeal.
- At first, there is hoarseness of voice and a croupy cough. Later on,
there is stridor, dyspnoea, and cyanosis due to obstruction by the
diphtheritic membrane. The membrane here, lies over respiratory
epithelium, so it has a loose attachement and can be detached easily
without bleeding.
- The condition may be fatal and should be rapidly treated.
 ••••cr

-332-

Nasal diphtheria
- It may occur primarily in the nose or it may accompany faucial
diphtheria.
- There is unilateral sanguineous nasal discharge with the formation of
a dirty greyish memln'ane over the nasal mucosa. It is not easy to
see the membrane in the nasal cavity, although shreds and crusts
may be expelled. There are no manifestations of toxaemia in
primary nasal diphtheria.
Investigations
A. Throat swab is taken from the lesion and is examined by:
a. Direct smear stained with gram stain.
b. Culture on enriched medium (Loeffler's serum or blood
tellurite agar).
Complications
They may appear on the 2nd or 3rd week, and they are due to the
effect of the toxin on cardiac and neural tissues.
A. Cardiovascular; (appear in the 2nd week)
1. Toxic myocarditis.
2. Vagal neuritis, conduction defect and arrhythmias.
3. Acute circulatory failure.
4. Heart failure may be due to any of the above mentioned
complications. It may appear late at any time during
convalesccne if it is due to vagal neuritis.
5. Thromocytopenia.
B. Neurological; (occur in 10-20% of cases)
They may appear in 3-6 weeks after the onset of infection
1. Paralysis of the soft palate is the earliest and most common
neurological deficit. There is regurgitation of fluids through
the nose, nasal tone of voice and immobility of the soft
palate. It usually occurs during the 1st or 2nd weeks and
stays for 1-3 weeks.
2. Occular paralysis may appear in the 2nd or 3rd weeks. The
intrinsic muscles are affected more than the extrinsics.
Paralysis of the intrinsic muscles leads to loss of
accomodation and light reflexes, and paralysis of the
extrinsic muscles leads to diplopia and squint.
3. Hoarseness of voice and dysphagia due to laryngeal and
pharyngeal paralysis.
 '333-

4. Paralysis of the diaphragm and intercostal muscles, which

may lead to respiratory failure.
5. Peripheral neuritis, which may lead to hand and foot drop.
Occasionally, ascending polyneuritis (Guillan-Barre'
syndrome) may occur.
6. Paralysis of the lower part of the face and hemiplegia arc rare.
C. Respiratory
1. Laryngeal obstruction due to extension of the infection to the
larynx, laryngeal oedema, or detached necrotic pieces from
the pharynx.
2. Bronchopneumonia and lobar pneumonia.
3. Lung collapse and lung abscess.
4. Respiratory muscles paralysis and respiratory failure.
D. Kidney; toxic nephritis and albuminuria.
Differential diagnosis
Faucial diphtheria should be differentiated from causes of
membranous exudation and ulceration of the tonsils and pharynx.
1. Acute follicular tonsillitis

Acute Follicular tonsillitis Faucial diphtheria

Acute onset - Gradual insidious onset

High fever (39-40T)
Mild toxaemia
Flushed face
Full rapid pulse which is
proportionate to fever
Vomiting is uncommon
Exudation appears as yellowish
spots, confined to the tonsils,
and can be easily removed
without bleeding.
Bilateral
Throat swab is negative for
diphtheria
- Low grade fever (38*C)
- sever toxaemia
- Pallor
- Weak rapid pulse which is
disproportionate to fever.
- Vomiting is not uncommon.
- Exudation appear as a dirty
greyish membrane, often
exceeding limits of the tonsil,
and it is adherent and leaves a
bleeding surface when
removed.
- Unilateral
- Throat swab is positive for
diphtheria

2. Acute membranous tonsillitis.

 -334-

3. Vincent's angina.
4. Infectious mononucleosis.
5. Acute leukaemia and agranulocytosis.
6. F.B. in the throat when coated over with mucus.
7. Ulcerative stomatitis.
Treatment
1. Hospitalization with good nursing. Isolation is mandatory untill
three consecutive daily swab cultures are negative.
2. Complete bed rest for at least three weeks to avoid cardiac
complications.
3. Specific diphtheria antitoxic serum, to neutralize the circulating
toxins. The dose is 40000-100.000 lU, I.M. or I.V., to be repeated
after 24-48 hours. In cases with severe toxaemia the dose is
100.000-200.000 LU. given I.V. The antitoxin should be given
immediately once diphtheria is suspected clinically without waiting
for the results of culture. It should be given within 48 hours in
order to neutralize the toxin before it becomes fixed to tissue.
- Appropriate skin senstivity test should be done before giving the
antitoxic serum to avoid sensitivity reactions and anaphylaxis to
the horse serum. It is done by injecting 0.05ml of diluted
antitoxin intradermally, if erythema larger than 1.5cm develops
in 20 minutes, this means sensitivity to the horse serum. In such
cases we have to start desensitization before giving the horse
serum, or shift to another serum e.g. sheep's serum.
- Steroids and antihistaminics should be given if sensitivity
reactions or anaphylaxis occur.
4. Antibiotics : penicillin 1/2-1 million I.U./day I.M. for 10 days. Oral
erythromycin may be given in pencillin allergic patients.
5. Glucose 50 cc of 25% solution given as I.V. drip to support the
cardiac muscles.
6. Vitamins and antipyretics.
7. Careful observation for the patients' airway, as tracheostomy may
be necessary if respiratory obstruction develops.
8. Treatment of complications if they arise:
a. Heart failure : Rest, O2, diuretics, digitalis and restrict salt in
diet
b. Respiratory failure : mechanical ventilation.
 -335-

c. Palatal and pharyngeal paralysis : nasogastric tube feeding.

d. Avoid foot drop by physiotherapy and keeping the foot in
dorsiflexion by applying a sand bag under the foot
Prophylaxis
1. Active immunization : Immunization against diphtheria is
compulsory in infants. The vaccine (formol toxoid) is given in
conjunction with tetanus and whooping cough vaccines (DPT) at
the ages of 2, 4, and 6 months. The dose is 0.5-1.5 ml given I.M.
Booster doses are given at the ages of 18 months and 5 years
(School age).
2. Passive immunization 50(X)-1(XX)0 lU : of antitoxic serum is given
LM. for contacts e.g doctors, nurses etc.. It my be combined with a
booster dose of the toxoid.

Infectious mononucleosis (glandular fever)

- This is an acute infective pharyngitis caused by Epstein Barr virus
(EBV). The virus can be isolated from blood, lymph nodes and
saliva of patients.
- It generally affects adolescents and young adults.
- It is probably transmitted by droplet infection.
Clinical picture
It varies from an asymptomatic state to a severe systemic illness. The
incubation period is 5-7 weeks.
1. Persistent fever, malaise, fatigue and headache.
2. Pharyngeal manifestations:
a. Severe sorethroat and dysphagia are the most common symptoms
(present in 80% of cases).
b. Marked hyperaemia, congestion and oedema of the pharyngeal
mucosa and tonsils.
c. Shallow yellow ulcers or a greyish white membrane may form on
the tonsils.
d. Palatal pctechiae arc present in 30% of cases.
3. Tender enlargement of the cervical lymph nodes.
4. A rubelliform skin rash that is almost invariable if ampicillin is
mistakenly prescribed for the condition.
5. Generalized lymphadenopathy may occur (discrete, and mobile
lymph nodes).
6. Splenomegaly occurs in 50% of cases and hepatomegaly in 10% of
cases.
 "W

-336-

Complications
1. Meningoencephalitis, myelitis, hepatitis, myocarditis, pericar-
ditis, and nephritis.
2. Ascending polyneuritis, and facial palsy.
3. Haemolytic anaemia, aplastic anaemia, and thrombocytopenia.
4. Splenic rupture may rarely occur.
5. Airway obstruction due to sloughing of a membrane over the
pharynx (rare).
Investigations
L Blood picture shows leucocytosis (particularly lymphocytosis
and monocytosis). Atypical forms of lymphocytes with
plcomorphism are present in 10-20% of cases.
2. Serological tests:
a. Positive Paul-Bunnel agglutination test
b. Positive monospot test
c. High or rising hetcrophilc antibody titre.
Treatment
It is mainly symptomatic in the form of:
1. Rest, light diet and fluids.
2. Analgesics, and antipyretics.
3. Antiseptic mouth wash.
4. Antibiotics to avoid secondary bacterial infection, but take care
not to prescribe ampicillin as it may cause a rubelliform rash.
5. Steriod; prednisone 40-80 mg/day to be tapered over 2 weeks,
and it is very effective in reducing the inflammation. It is given
only in severe cases.

Vincent's angina (gangrenous stomatitis)

This is an acute specific ulcerative inflammation of the pharynx
and mouth caused by a spirochaete called Borrelia vincenti and fusiform
bacillus, working in symbiosis. It affects the pharynx, tonsils, fauces and
gums.
Clinical picture
1. Low grade fever, headache and malaise.
2. Severe sorethroat and odynophagia with excessive salivation and
foetid breath.
 -337-

3. Ulcerations of the pharyngeal mucosa where the ulcers have deep

punched-out edges. A dirty greyish yellow inlaid membrane is seen
covering the tonsils, and occasionally, may extend to the pillars and
softpalate. It should be differentiated from the onlaid membrane in
diphtheria. The membrane can be wiped off easily leaving an ulcer
with punched out edges.
4. Enlarged tender submandibular lymph nodes.
5. Tender gingiva with ulceration and membrane formation.
Investigations
Swab obtained from the ulcers or from necrotic area, is cultured
and examined for the organisms.
Treatment
1. Antibiotics e.g. penicillin, tetracyclin, and erythromycin.
2. Hydrogen peroxide or sodium perborate mouth wash.
3. Adequate oral hygiene.
4. Adequate nutrition and vitamins.

Pharyngitis assocaited with blood diseases

I. Agranulocytosis
This is depression of the bone marrow with marked reduction in
formation of polymorph nuclear leucocytes (PNLs) leading to marked
leucopenia with relative lymphocytosis.
Aetiology
Bone marrow depression which may be :
A. Primary: Idiopathic.
B. Secondary : (to drug therapy)
1. Antibiotics e.g. chloramphenicol, sulpha.
2. Antimetabolites e.g. cyclophosphamide, methotrexate.
3. Antiemetics e.g. chloropromazine.
4. Antirheumatics e.g. phenylbutazone.
5. Radiation therapy.
6. Infective hepatitis.
7. Autoimmune.
Clinical picture
1. History of drug therapy.
2. Fever, and malaise, with prostration and marked rapid
deterioration of the general conditon.
 w

-338-

3. There is ulceration in the oral cavity, fauces, tonsils, and gums.

The ulcers have ragged edges, clean base, with little or no
surrounding inflammatory reaction. Later, it may become so
extensive and a form of gangrenous stomatitis may develop.
Investigations
1. Complete blood count (diagnostic), it shows decreased total
Icucocytic count (about 1000-2000 / cm3), decreased or absent
granulocytes, and relative lymphocytosis.
2. Bone marrow aspiration.
Treatment
1. Discontinuation of the offending drug.
2. Isolation of the patient in a sterile environment.
3. Antibiotics.
4. Fresh blood transfusion.
5. Bone marrow transplantation may be done.
n. Acute leukaemia
This is neoplastic proliferation of the precursors of the white blood
cells in the bone marrow leading to marked increase in the white blood
cells (leucocytosis) and appearance of immature cells (blasts). It may be
fatal in few days.
Clinical picture
1. Anaemia with fatigue, pallor, and prostration.
2. Thrombocytopenic purpura, with epistaxis and bleeding
tendency.
3. Intercurrent infections with fever, and sorethroat. The gingiva
are swollen purpulish and bleeding easily. The tonsils are
enlarged with exudative membrane or necrotic ulcers.
5. Generalized lymphadenopathy and splenomegaly.
6. Sternal tenderness.
Investigations
1. Complete blood count shows marked leucocytosis (the total
leucocytic count exceeds 100.000/cm3), increased blast cells,
decreased platelets (thrombocytopenia), and anaemia.
2. Bone marrow aspiration shows marked infiltration with blast
cells.
Treatment
Isolation of the patient, fresh blood transfusion, antibiotics, and
cytotoxic drugs.
 n

-339-

Acute nonspecific pharyngitis

Aetiology
It is usually a viral infection which is associated with viral upper
respiratory tract infection e.g. common cold, and influenza.
Seocndary bacterial infection then follows.
Predisposing factors
A. Gerneral
- Poor general resistance.
- High virulence of the organism.
- Overcrowdedness.
B. Local
- Postnasal discharge as in adenoids and sinusitis.
- Smoking.
Clinical picture
1. Fever, headache, malaise, and anorexia.
2. Sorethroat and dysphagia.
3. Diffuse congestion and hyperaemia of the whole pharyngeal
mucosa including the tonsils.
4. There may be tender enlargement of the cervical lymph nodes.
Treatment
1. Rest, light diet, and adequate fluids.
2. Systemic antibiotics.
3. Analgesics and antipyretics.
4. Antiseptic mouth wash and gargles.

Moniliasis (Candidiasis = oral thrush)

Aetiology
Predisposing factors
1. Prolonged antibiotic therapy.
2. Immunocompromized patients, and lowered general resistance as
in;
a. Patients receiving cytotoxic chemotherapy.
b. Malignancies.
c. Diabetes.
d. AIDS.
e. Malnutrition and hypovitaminosis.
Organism; Candida albicans.
 7
-340-

Clinical picture
1. Sorcthroat and dysphagia, but with no fever.
2. Milky white slightly raised patches are seen in the oropharynx,
and oral cavity (tongue and inner side of the cheeks).
Treatment
1. Discontinuation of antibiotics, adequate nutrition and vitamins.
2. Topical antifugal treatment:
a. Mycostatin (Nystatin) mouth paint
b. Gentain violet as mouth paint.
c. Daktarin oral gel.
3. Systemic antifungal drugs e.g. ketoconazol, may be needed in
severe systemic candidiasis.

Chronic nonspecific pharyngitis

Aetiology
1. Repeated attacks of acute pharyngitis.
2. Tobacco, alcohol, spicy food.
3. Prolonged exposure to dusty dry atmosphere.
4. Mouth breathing.
5. Septic teeth, and chronic tonsillitis.
6. Sinusitis, adenoiditis, enlarged turbinates, and nasal allergy.
7. Gout and rheumatoid arthritis.
8. Indigestion and reflux oesophagitis,
9. It may follow tonsillectomy.
Clinical picture
Symptoms
1. Persistent sorethroat and sensation of dryness in the throat.
2. A desire for frequent clearing the throat (hawking).
Signs
A. Simple catarrhal pharyngitis :
" Mild enlargment and congestion of the uvula, soft palate
and the posterior pharyngeal wall.
- Hypertrophy of the lymphoid tissue in the posterior and
lateral phaymgeal walls, with dilated vessels seen.
B. Hypertrophic (Granular) pharyngitits :
- Small nodules are seen in the posterior and lateral
pharyngeal walls.
- Enlarged lateral pharyngeal bands.
 -341-

C. Atrophic pharyngitis :
- It is frequently associated with atrophic rhinitis.
- Atrophic, pale, glazed pharyngeal mucosa, particularly that
of the posterior pharyngeal wall. There arc little or no
secretions.
Treatment
1. Avoidance of predisposing factors e.g. smoking, spicy food, and
treatment of sinusitis and nasal allergy.
2. Local treatment:
a. Mandl's paint (KI + menthol + glycerin) or 1% zinc chloride.
b. Magnesium citrate gargles, to gargle with one half and
swallow the other half. Mg. is a heavy ion and so opens the
bowel, and citrates dissolves the sticky mucus.
c. Electrical or chemical cautery of the nodules in the
hypertrophic type or ablation by CO2 laser.
d. Spraying the throat with warm alkaline wash followed by
applicadon of an oily spray in the atrophic type.
3. Antibiotics.
4. HI antagonists e.g. cimetidine and Ranitine, and omeperazolc
for treatment of gastric reflux.

Chronic speific pharyngitis

A. Syphilis :
1. Primary syphilis : Chancer of the pharynx is rare, but it may affect
the tonsils (which is the second most common extragenital site of
chancer. It appears as a unilateral, cartilageous hard, reddish,
painless nodule which persists for several weeks. The cervical
lymph nodes are enlarged.
2. Secondary syphilis : First, it takes the form of diffuse erythema of
the palate and fauces with mild enlargement of the tonsils. Later,
mucous patches are seen on the tonsils, fauces, tongue, and inner
aspect of the cheek. They appear as bluish grey, rounded, slightly
raised patches which are surrounded by a zone of erythema, later
on, they coalesce and ulcerate to form a snail track ulcer. There are
other signs of secondary syphilis including diffuse maculopapular
skin rash, fever, and generalized lymphadenopathy.
3. Tertiary syphilis : Gumma is the typical lesion, which appear as a
hard, purple swelling on the palate, posterior pharyngeal wall, and
 - 342 -

less frequently on the valleculae and tonsils. Later on, they

ulcerate, and die ulcers have deep punched-out edges, indurated
margins, and necrotic yellowish floor (wash - leather apperance).
Postsyphilitic complications
1. Perforation of the hard palate.
2. Adhesion between the soft palate and the posterior pharyngeal
wall.
B. Tuberculosis
It is usually secondary to pulmonary tuberculosis or as a part of
miliary T.B., rarely it is primarily pharyngeal. There are minute grey
or yellow tubercles seen on the fauces, and palate, that soonly
ulcerate. The ulcers are superficial, shallow, with undermined edges,
bluish margins, and a yellow caseous floor. There is severe
odynophagia and sorethroat.
C. Pharyngoscleroma
It is usually secondary to and in association with rhinoscleroma.
Clinical picture
1. Painless hard induration without ulceration.
2. Glazed atr(q)hic pharyngeal mucosa with no or littie secretions.
3. Granulations and greenish crustations in the pharynx.
4. Fibrosis and adhesions between the soft palate and the posterior
pharyngeal wall leading to pharyngeal stenosis.

Septic focus
A septic focus is a state of chronic bacteraemia or toxaemia
secondary to chronic infection in a part of the body. The bacterial toxins
can produce many systemic manifestations on different organs of the
body, including the following:
1. Anaemia, fatigue and anorexia.
2. Low grade fever and headache.
3. Heart : Rheumatic fever, rheumatic activity and infective
endocarditis.
4. Kidney: acute and subacute nephritis, and albuminuria.
5. Lungs: bronchiectasis.
6. Eyes: iridocyclitis.
7. Skin: dermatitis.
8. Myalgias, arthralgia, anthritis, and plantar fasciitis.
 -343-

- A septic focus may be ;

1. Chronic tonsillitis.
2. Chronic sinusitis.
3. Cholecystitis.
4. Prostatitis.
5. Salpingitis and cervicitis.
6. Colitis.

Suppurations related to the pharynx

I. Peritonsillar abscess (Quinsy)
A peritonsillar abscess is a collection of pus between the fibrous
capsule of the tonsil, usually at its upper pole, and the superior
constrictor muscle of the pharynx.
Aetiology
- It usually occurs as a complication of acute tonsillitis, or it may
apparently arise denovo with no preceding tonsillitis.
- It starts by infection in the depth of one of the tonsillar crypts
(usually the crypta magna), which becomes sealed off as a result
of adhesions from recurrent infections, then infection escapes
through the capsule of the tonsil, and thus a peritonsillar abscess
forms,
- The abscess usually forms above the tonsil in 98% of cases (i.e.
anterosuperior), but it may be lateral to or behind the tonsil.
- Organisms : It is usually a mixed aerobic and anaerobic infection.
Clinical picture
The patient is usually a fit young adult with a previous history of
repealed attacks of acute tonsillitis.
Symptoms
1. Sorethroat usually precedes the abscess by 2-3 days which
becomes more severe and unilateral.
2. High fever, rigors, headache, and malaise. Fever becomes
hectic with pus formation.
3. Severe dysphagia and odynophagia with drippling of saliva
(the patient is unable to swallow his saliva due to severe
pain).
4. Intense unilateral neck pain which is maximum behind the
 -344-

angle of the mandible and often radiates to the ipsilateral ear.

Pain becomes throbbing with pus formation.
5. Foetor oris.
6. Trismus and torticollis.
Signs
1. Fever, tachycardia, pallor and toxic facies.
2. Torticollis towards the affected side.
3. Trismus, which may be severe and makes the examination
difficult.
4. Oropharyngeal examination reveals asymmetrical marked
oedema and hypremia of the soft palate, and a swelling above
and lateral to die tonsil which is displaced downwards and
medially. The uvula is oedematous and displaced to the other
side. The swelling is at first indurated (cellulitis), later on
pitting oedema can be elicited on probing, indicating pus
formation.
5. Enlarged firm, tender jugulodigastric lymph nodes on the
same side.
Differential diagnosis
1. Parapharyngeal swelling e.g. pleomorphic adenoma of deep lobe of
parotid, minor salivary gland tumours, neurogenic tumours,
lymphoma, and aneurysm of the carotid artery.
2. Anaplastic carcinoma Oymphoepithelioma) of the tonsil.
3. Acute leukaemia.
4. Abscess related to the upper molar tooth.
Complications
1. Laryngeal oedema and stridor, particularly in children.
2. Pyaemia and septicaemia.
3. Rupture of the abscess and inhalation of pus.
4. Cervical cellulitis.
5. Haemorrhage.
6. Parapharyngeal abscess (every quinsy should be considered as a
potential parapharyngeal space suppuration).
Treatment
A. During the stage of peritonsillar cellulitis (before pus
foramtion)
1. Parenteral antibiotics.
 -345-

2. Antiseptic mouth gargles,

3. Antipyretics, analgesics, bed rest, light diet and adequate
fluids.
Never incise at this stage as it may lead to spreading cervical
cellulitis and septicaemia.
B. During the stage of peritonsillar abscess (Pus formation)
- This is indicated by hectic fever, throbbing pain, pitting
oedema on probing, and aspiration by a needle brings pus.
1. Parenteral antibiotics to be continued after incision and
drainage.
2. Incision and drainage under local anaesthesia, however,
general anaesthia can be resorted to in uncooperative
patients. (Fig.78)
- Sites of incision :
1. Most bulging point.
2. At the midpoint of a line drawn from the base of the uvula
to the last upper molar tooth.
2. 1/2 cm lateral to the point of crossing of tow lines; a
vertical line along the anterior pillar, and a horizontal line
along the base of the uvula.
4. Through the crypta magna.
- The knife must be guarded in order not to go deep and injure
big vessels.
- After incision, dissection is done by a forceps using the
Hilton's method to open pus loculations.
C. Tonsillectomy should be done 4-6 weeks after drainage in order
to avoid recurrence. Occasionally, quinsy tonsillectomy (i.e.
drainage of the quinsy and doing tonsillectomy in the same
sitting), is done in cases of posterior location of the abscess
(behind the tonsil).

f"''g 78 quinsy
 -m—'*^

-346-

11. parapharyngeal abscess

This is a collection of pus in the parapharyngeal space.
Aetiology
It is due to spread of infection to the parapharyngeal space as in the
following conditions:
1. Peritonsillar abscess.
2. Acute tonsillitis, and after tonsillectomy operation.
3. Suppuration in the retropharyngeal space, the submandibular
space and parotid spaces.
4. Petrositis and mastoiditis.
5. Infected last molar tooth.
6. Penetrating foreign body.
Clinical picture
Symptoms
1. Fever, headache, malaise and anorexia. There may be rigors and
sweating. Fever becomes hectic with pus formation.
2. Severe odynophagia with drippling of saliva.
3. Intense unilateral neck pain, maximum behind the angle of the
mandible and often radiates to the ipsilateral ear. Pain becomes
throbbing with pus formation.
4. Change of voice.
5. Unilateral neck swelling in the upper lateral part of the neck.
6. Trismus and torticollis,
*
Signs
1. Fever, tachycardia and toxic facies.
2. Torticollis towards the affected side.
3. Beck's triad:
a. Trismus due to irritation of medial pterygoid muscle.
b. Tender firm external swelling on the lateral side of the upper
part of the neck, mainly below and behind the angle of the
mandible. The swelling lies deep to the stemomastoid muscle
and may point along its anterior border.
c. Swelling in the lateral wall of the pharynx, pushing the tonsil
(which is normal) medially. Pitting oedema or fluctuation can
be elicited on probing (indicates pus formation).

1
 -347-

Investigations
1. CT scan of the pharynx and neck.
2. Blood picture shows leucocytosis.
3. Elevated ESR.
Differential diagnosis
All parapharyngeal swellings (e.g. salivary gland tumours
especially pleomorphic adenoma and adenoidcystic carcinoma,
neurogenic tumours especially vagal shwannnoma, chemodectoma, and
lymphoma. Aortic aneurysm may cause a swelling in the parapharyngeal
space).
Complications
1. Laryngeal oedema and airway obstruction.
2. Thrombosis of the internal jugular vein which may lead to septic
emboli, so ligation of the vein or the facial veins may be needed
during surgery.
3. Erosion and rupture of the carotid artery (fatal).
4. Mediastinitis.
Treatment
1. Hospitalization, rest, light diet and excessive fluids.
2. Parenteral broad spectrum antibiotics.
3. Analgesics and antipyretics.
4. Incision and drainage : It is done by an external incision along
the anterior border of the stemomastoid muscle.
- Indications of incision and drainage :
1, Pus formation (Hectic fever, throbbing pain, and pitting
oedema).
2, Severe sepsis.
3, Hemorrhage.
4, Subcutaneous emphysema.
5, Neurological deficit.
- If these indications are not present, start medical treatment
with aggressive antibiotic therapy, with regular strict
observation. If there is persistent fever or worsening of
symptoms in 24-48 hours do surgical drainage.
Anatomy of the parapharyngeal space
The parapharyngeal space lies on either side of the superior part of
the pharynx (the oropharynx and the nasopharynx).
 •t-i

-348-

• Boundaries
a. Laterally, it is bounded by the parotid gland, parotid fascia, and
the medial pteiygoid muscle.
b. Medially, it is related to the pharynx, separated from it by the
superior constrictor muscle. Posterior to the pharynx, this space
communicates with the retropharyngeal space.
c. Superiorly, it is limited by the base of the skull.
d. Inferiorly, it is limited by the fascia surrounding the
submandibular gland.
Contents
1. The cartoid sheath with the internal carotid artery, internal
jugular vein, and the vagus nerve.
2. Styloid group of muscles.
3. The last four cranial nerves.
4. Cervical sympathetic chain.
5. Mandibular division of the trigeminal nerve.
6. Ascending palatine and ascending pharyngeal artery.
7. Lymph nodes, and minor salivary glands.
III. Retropharyngeal abscess
This is a collection of pus in the rctopharyngeal space between the
buccopharyngeal fascia of the posterior pharynged wall, and the
prevertebral fascia. It occurs in two forms, either, acute retropharyngeal
abscess in children or chronic form in adults.
A. Acute retropharyngeal abscess
Aetiology
- Acute suppuration in a retropharyngeal lymph node (gland of
Henlc) following an upper respiratory tract infection (e.g.
infection in the nose, pharynx, tonsils, and adenoids).. It occurs
primarily in children up to 4 years, and it is rare after that age as
this node atrophies by the age of 5 years.
- It is predisposed by :
a. Lowered general resistance, and defective nourishment.
b. Tuberculosis.
c. Rickets.
- Occasionally, a foreign body which has perforated the posterior
pharyngeal mucosa will give rise to an abscess.
 -349-

Clinical picture
Symptoms
1. Fever, headache, malaise, anorexia. Fever becomes hectic
with pus formation.
2. Severe dysphagia with drooling of saliva.
3. Foetor oris.
4. Nasal obstruction if the abscess spreads high up obstructing
the posterior nares.
5. Stridor and airway obstruction may occur due to laryngeal
oedema.
Signs
L Fever, tachycardia, and toxic facies.
2. Torticollis with the neck flexed forwards. Backward extension
of the neck causes stretch of the prevertebral muscles and
severe pain.
3. A swelling is seen in the posterior pharyngeal wall to one side
of the midline, which is fluctuant on probing. There is also
marked hypremia .and congestion of the posterior pharyngeal
wall.
4. Enlarged tender cervical lymph nodes.
N.B. : Aspiration with a fine needle may be done to exclude
various vascular malformations.
Investigations
1. Plain x-ray neck lateral view, shows widening of the prevertebral
space, with normal vertebral bodies.
2. CT scan of the skull base is diagnostic.
3. Blood picture shows leucocytosis.
4. Elevated ESR.
Treatment
1. Tracheostomy may be necessary to relieve upper airway
obstruction if it occurs.
2. Incision and drainage : It is done through the transoral route,
under general anaesthesia with the patient lying in the
trendlenberg position (the head is lower than the body). First
aspirate pus with a needle to exclude an aneurysm. A vertical
incision is done in the posterior pharyngeal wall over the abscess
to drain the pus. Care should be taken during intubation to avoid
 -350-

rupturing the abscess with the tube and inhalation of pus, so,
blind nasal intubation is contraindicated in this situation.
3. Parentral antibiotics, after evacuation of pus.
B. Chronic retropharyngeal abscess (cold abscess = pott's disease of
the spine).
Aetiology
It occurs in adults and is relatively uncommon. It is always due to
tuberculous infection, which has spread through the anterior
longitudinal ligament of the cervical spine to reach the
retropharyngeal space. This tuberculous infection is due to
reactivation of a domiant tuberculous focus as a result of decreased
immunity.
Clinical picture
1. In early stages there are few symptoms and signs.
2. Odynophagia, slight sorethroat and pain in the neck which
inceascs on neck movement.
3. Tenderness and rigidity of the cervical spine.
4. There may be marked bulge of the posterior pharyngeal wall in
the midline.
5. Associated pulmonary T.B. may be present
6. Mainfestations of T.B. toxaemia (night fever, night sweating.
loss of weight, and anorexia) may be present
7. There may be neurological signs, and occasionally, the patient
may present with symptoms and signs of spinal cord
con:5)ression. It must be remembered that the spine may be quite
unstable and thus manipulation may precipitate a neurological
event
Investigations
1. Plain x-ray cervical spine lateral view shows widened
prevertebral space with destroyed bodies of cervical vertebrae,
decreased disc spaces, and loss of normal curvature of the
cervical spine.
, 2. Investigations for T.B. : increased ESR, sputum analysis for
T.B., needle biopsy, and tuberculine test
3. Blood picture shows lymphoc)^osis.
4. Chest x-ray to exclude assocaited pulmonary T.B.

Mi^U
 =5

-351-

Treatment
1. Antituberculous chemotherapy.
2. Incision and drainage of the abscess, via an incision along the
posterior border of the stemomastoid muscle, Transoral drainage
should be avoided as this paves the way for secondary bacterial
infection.
3. Orthopaedic management,
IV. Ludwig's angina
This is a submandibular space suppuration involving the floor of
the mouth and the neck.
Aetiology
1. Dental causes represent 80-90% of cases,
a. Infection of the lower teeth, and peridontal abscess.
b. After extraction of a sepdc tooth.
2. Occasionally, it is observed with acute parotitis, submandibular
sialadenitis, specific fevers, and cutaneous infection.
- It occurs more commonly in patients with decreased resistance
particularly diabetics.
- Organisms : It is commonly a mixed aerobic and anerobic
infection.
Clinical picture
- There is usually a history of tooth extraction or dental infection.
1. Fever, headache, and malaise.
2. Severe pain especially over the floor of the mouth with
dysphagia and drooling of saliva,
3. Muffled voice.
4. Massive brawny hard tender neck swelling involving the
submental and the submandibular regions. First, the swelling is
indurated (cellulitis), later on, fluctuation is elicited (pus
formation). The overlying skin is red, hot, and oedematous.
5. Swollen oedematous floor of mouth with the tongue pushed
upwards and backwards.
6. Respiratory obstruction with dyspnoea and stridor due to
laryngeal oedema, or upward displacement of the tongue.
Treatment
1. Bed rest in the semisitting position to avoid respiratory
obstruction.
 -352-

2. Massive parenteral antibiotics.

3. Analgesics and andpyretics.
4. Secure airway: a tracheostomy set should be always available as
respiratory obstruction may occur suddenly, and in such case an
urgent tracheostomy should be done.
5. Surgical treatment:
A free incision should be made for decompression. It is either a
transverse submadibular incision, or midline vertical incision
from the chin to the hyoid bone. The incision is deepened
through the deep fascia and the mylohyoid muscle. On incision,
the tissues appear frozen with a serous foul discharge, later on,
after few days the discharge becomes purulent. The incison
should be left open with drains.

Tonsillectomy
The tonsils have a certain protective role in the body, but when they
are diseased, they become a source of trouble to the patient, and
necessitates their removal
Indications of tonsillectomy
1. Repeated attacks of acute tonsillitis (three or more episodes per
year). This is the most common indication.
2. Peritonsillar abscess even if it occured once, because it is liable to
recur.
3. Diphtheria carriers (as a protective measure).
4. Tonsillar hypertrophy which causes :
a. Obstructive sleep apnoea or corepulmonale. It is usually
associated with adenoid hypertrophy, and often
adenotonsillectomy is required.
b. Difficulty in swallowing.
c. Recurrent imtative cough.
N.B. : adenotonsillar hypertrophy may be due to recurrent acute
inflammation, or longstanding chronic inflammation.
5. Tonsillitis causing febrile convulsions.
6. Chronic tonsillitis acting as a septic focus with :
a. Recurrent sorethroat
b. Recurrent upper respiratory tract infection.
c. Recurrent otitis media, pharyngitis and bronchitis.
 -353-

d. Foetor oris.
e. Septic focus manifestations.
7. Rheumatic fever, rheumatic heart disease and glomerulonephritis
due to beta haemolytic streptococcal infection.
8. Tumours or cysts of the tonsils which require unilateral
tonsillectomy :
a. Bengin tumours e.g. papilloma, fibroma, mixed salivary tumours
and cysts (rare).
b. Malignant tumours or when malignancy is suspected. Here,
tonsillectomy is done as an excisional biopsy.
c. As an end stage when searching for an occult primary when there
is enlarged malignant metastatic cervical lymph node and the
primary is not detected. Here, remove the ipsilateral tonsil.
9. Cervical adenitis e.g. T.B., if they are a localized group and not
resolving with medical treatment.
10. Impacted F.B. e.g. tonsillolithiasis and fish bone if it is deeply
inserted in the tonsil.
11. Persistent or recurrent, tonsillar haemorrhage, due to superficial
telangectasia or a spurter.
12. Trauma to the tonsils.
i Contraindications of tonsillectomy
1. Blood dyscrasia e.g. haemophilia, Von-Willebrand disease,
leukaemia, and purpura.
2. Patients on aspirin (e.g. for the treatment of rheumatic fever or
cardiac patients), and non steroidal antiinflammatory drugs,
because to they lead to coagulopathy and thrombocytopathy with
bleeding tendency. In such case, the operation should be postponed
for two weeks, and the patient should receive vitamin K.
preoperadvely and intraoperatively.
3. Uncontrolled systemic disease e.g. diabetes, heart failure, and
hypertension.
4. Active rheumatic fever.
5. Exanthemata e.g. measles, mumps, and chicken pox.
6. Presence of acute infection e.g.
a. During acute tonsillitis.
b. Acute upper respiratory tract infection e.g. rhinitis, sinusitis, and
bronchitis.
 -354-

- The operation should be postponed for two weeks after recovery.

7. During epidemics of poliomyelitis.
8. Menestruation pregnancy.
9. Peritonsillar abscess; the operation is done after 6 weeks, however,
quinsy tonsillectomy is done cases of posteriorly located
peritonsillar abscess.
Preoperative preparation
A. Good history taking and physical examination to exclude any
contraindication for the operation and assure fittness for general
anaesthesia. The following points are important:
1. Exclude acute tonsillitis and fever.
2.. History of bleeding tendency (e.g. bleeding during circumcision,
haemoarthrosis, subcutaneous ecchymosis). This is more
important than laboratory investigations.
3. Adequate chest and heart examination.
4. Exclude Rheumatic fever and Rheumatic activity.
5. History of intake of salicylates or nonsteroidal anti-inflammatory
drugs.
B. Investigations
1. Complete blood picture including HB%, to detect anaemia or
thrombocytopenia.
2. Coagulation profile.
a. Bleeding time (normal 3-5 minutes).
b. Clotting time (normal: 4-10 minutes).
c. Prothrombin time (normal: 12 seconds).
d. Prothrombin concentration (normal: 100%.).
e. Partial thromboplastin time (normal: 25-45 seconds).
3. Blood grouping and Rh compatibility.
4. Erythrocyte sedimentation rate (normal: First hour is 5-10
minutes).
5. Fasting blood sugar.
6. Urine analysis for albumin and sugar.
7. Liver and kidney function tests, if there is a history suggestive of
hepatic or renal trouble.
C. Antibiotics are given five days prior to surgery.
D. Iron supplements, vitamin C and vitamin K are given. Vitamin K is
 -355-

very important as most children are already receiving antibiotics

which kill the flora forming vitamin K in the large intestine.
E. The patient should be fasting six hours before surgery.
F. On the morning of surgery, check the vital signs, temperature, and
examine the tonsils for inflammation.
G. Sedation several hours before surgery.
H. Atropine 1/2 hours before surgery to dry the pharyngeal secretions
(now, many anaesthetists prefere not to give as it causes severe
tachycardia; they use scopolamine).
Technique of the operation
- Anaesthesia
General intubation anaesthesia either nasally or orally using a
cuffed endotracheal tube. It must be deep to abolish the cough and
swallowing reflexes, but the protective laryngeal reflexes should be
restored rapidly after anaesthesia to avoid aspiration of blood clots
or vomitus.
- Local anaesthesia can be used in adults and the operation is
performed in the sitting position.
- Position of th patient
The patient lies supine with the neck extended by a sandbag
placed under the shoulders.
- Procedure : (Dissection method) (Fig.79)
- The mouth is opened using a Boyle-Davis mouth gag.
- If adenoidectomy is going to be done, the adenoids are removed first
with the neck in the flexed position, and the nasopharynx is packed
with a piece of gauze to control bleeding, and the pack is removed
at the end of the operation.
- The tonsil is grasped by a tonsil holding forceps, and pulled
medially. The anterior pillar is then incised, and by sharp dissection
the plane of cleavage is obtained (this is the plane between the
capsule of the tonsil and its muscular bed. The upper pole of the
tonsil is held by an artery forces and is cut by a sissor. Then the
tonsil is removed by blunt dissection in the same plane of cleavage
(i.e. extracapsular), till its lower pole. Then the lower pole is held
by a clamp forceps and ligated (the lower pole contains the major
blood supply of the tonsil, secure haemostasis by ligature, or
sometimes by underruning sutures of any bleeding point. Minute
mucosal bleeding can be secured by bipolar coagulation.
 -356-

Thc nasopharyngeal pack is removed (if adenoidectomy was

performed).
Relax the mouth gag, and observe the pharynx and the tonsillar bed
untill swallowing returns in order to detect any primary
haemorrhage.
The patient should not be extubated untill the cough reflex returns, to
avoid aspiration.

Fig.79, tonsillectomy by
dissection

Otiier methods for tonsillectomy

1. Laser tonsillectomy (mentioned later). It is done now in some
centers as it causes less pain postoperatively.
2. Cryosurgery : freezing the tonsils, which is recommended in
cases with blood disease as haemophilia.
N.B. : Removal of the tonsil by the guilotine (Guillotine method)
was used in the past. It has many disadvantages and more
frequent complications, particularly incomplete removal and
postoperative haemorrhage.
Postoperative care
1. The patient is placed in the tonsillectomy position, on his side, with
the lower leg flexed and the other one extended. The upper arm of
the patient is placed under his cheek, and the other arm behind him.
A pillow is placed behind the patient to prevent him from rolling on
his back. This position prevents backfalling of the tongue and
aspiration and helps to detect bleeding or vomiting.
 I •'1,1

-357-

2. In the recovery room :

a. Observe for respiratory obstruction, and cyanosis (face of the
patient) this is very important. Also observe for primary
haemorrhage or vomiting.
b. The following should be available; suction apparatus, pulse
oxymeter, electronic ECG, laryngoscope, tongue foreceps, and
nasopharyngeal airway.
c. Pethidin is given I.M., after regaining all reflexes to avoid
depression of the respiratory center.
3. Observation in the ward for :
a. Vital signs : A weak rapid pulse and hypotension denote
bleeding.
b. Frequent swallowing, spitting of fresh blood, or vomiting of dark
blood denotes bleeding.
c. Respiration : irregular respiration and cyanosis indicates
respiratory obstruction, and the patient should be returned
rapidly to the operating theatre.
4. Medications :
a. Systemic antibiotics for 10 days.
b. Analgesics and antipyretics (use only paracetamol, or
novalgine).
c. Decongestant nasal drops.
d. Vitamins and iron supplements.
5. Feeding :
- It starts 4 hours after surgery to avoid vomiting and ileus.
- In the first day semisolids (better tolerated), and cold drinks are
given.
- From the 2nd to the 8th day, avoid hard, spicy and hot food.
Swallowing is painful, but it is highly important to use the
deglutition muscles early. The more the patient eats and drinks,
the quicker tlie pain dissapears.
Complications of tonsillectomy
A. Complications from anaesthesia
1. Injury of the teeth, oral cavity, oropharynx or the larynx during
intubation.
2. Cardiac arrest.
3. Aspiration of vomitus or blood.
 • %

-358-

4. Succinyl choline apnoea.

5. Extubation glottic spasm and laryngeal oedema.
6. Anaphylaxis from the anaesthesia (rare).
B* Haemorrhage (posttonsillectomy bleeding)
1. Primary haemorrhage : This occurs immediately after
tonsillectomy and it may be due to :
a. Bad aggressive technique with the dissection going off the
plane of cleavage.
b. Bleeding tendency e.g. Von-Willebrand's disease, intake of
salicylates or NSAE)s prior to surgery (i.e. bad preoperative
preparation).
c. Operating on an acutely infected tonsils.
Treatment
1. Ligation of the bleeding point or underruning by sutures.
2. Suturing the pillars together, if it is a generalized ooze.
3. External carotid artery ligation may be needed in severe
cases, if bleeding doesnot stop.
4. Correction of shock and fresh blood transfusion in severe
cases.
2. Reactionary haemorrhage : This occurs during the first 24
hours after the operation. It may be due to :
a. Rise of B.P. after recovery from anaesthesia, where the
collapsed vessels open again.
b. Slipped ligature.
c. Bleeding tendency.
The condition is suspected when there is frequent swallowing,
spitting of fresh blood and vomiting of large amounts of dark
blood. In severe cases there is a weak rapid pulse, hypotension,
pallor, sweating and cold extremities and these indicate shock.
Treatment ;
1, If it is only mild oozing conservative treatment may be
sufficient, but take care as the patient may be swallowing
the blood instead of spitting it. Conservative management
includes:
a. Sedation, coagulants, and H2O2 mouth gargles.
b. Removal of all blood clots from the tonsillar bed.
c. Temporary firm pressure of the tonsillar bed using a
 -359-

sponge moistened with H2O2 may be applied for some

minutes, by the use of a special clamps (post
tonsillectomy bleeding clamp).
2. If bleeding is severe, or persistent despite the conservative
measures, do not hesitate to take the patient back to the
operating theatre, where he is reanaesthetized again, and
all blood clots are removed then do :
a. Ligature or underruning sutures of the bleeding points.
b. If bleeding still persists the anterior and posterior pillars
are sutured together over a rolled pad of iodoform
gauze or gelfoam, and if left for 24-48 hours.
c. External carotid ligation may be needed in failed all
measures to control bleeding.
3. Correction of shock and blood transfusion may be needed
while simultaneously managing bleeding.
3. Secondary haemorrhage: This is delayed bleeding that may
occur on the 5th to the 12th day. It is due to infection which may
result from inadequate feeding or inadequate antibiotics.
Sometimes taking salycilates, NSAIDs, or cephalosporins can
cause bleeding due to their antiplatelet effect. There is usually
mild pyrexia.
Treatment
1. Secondary haemorrhage is usually mild and stops with
conservative treatment in the form of:
a. Systemic parenteral antibiotics for 4 days.
b. Removal of all blood clots from the tonsillar bed.
c. H2O2 mouth gargle, sedation, and rest.
d. Proper feeding.
e. Haemostatic pressure may be required.
2. Sometimes, bleeding is severe or persistent, and in such case,
the patient is reanaesthetized and bleeding is dealt with by :
a. Ligature or underruing sutures, but Uiis is usually difficult
due to friability of tissues, and may even cause more
bleeding.
b. Suturing die anterior and posterior pillars together over a
pack.
c. Blood transfusion and antishock measures may be
required.
 -360-

C. Respiratory complications
1. Respiratory obstruction: This is the most serious complication
and it may be life threatening, so it must be recognized early and
rapidly managed. It may be due to :
a. Laryngeal spasm which may be due to extubation spasm or
irritation of the vocal cord by secretion or blood.
b. Falling back of the tongue which occurs when the patient is
still deep under anaesthesia (incomplete recovery) and is sent
to bed, lying on his back.
c. Inhaled RB. (e.g. blood clot, secretions, neglected loose pack,
a piece of gauze or a tooth), that may slip down to the larynx
or even to the bifurcation of the trachea.
d. Inhaled vomitus due to bad preoperative preparation.
c. Laryngeal oedema from intubation; due to over sized tube, or
forcible intubation, particularly if the child has an undetected
subglottic naiTOwing.
- Respiratory obstruction is detected by:
a. Inspiratory stridor, croupy cough and rising pulse.
b. Over working aea nasi, with suprasternal, supraclavicular
and intercostal retractions.
c. Diminished air entery, with low O2 saturation and
increased CO2 tension (detected by oxymeter).
d. Bradycardia and cyanosis are late signs.
Treatment
L Pull the tongue out of the mouth by a tongue foreceps and
push the mandible forwards.
2. Suction of secretions, blood or vomitus, or removal of F.B.,
by the aid of a laryngoscope.
3. Reintubation and administration of 02 under pressure in cases
of laryngeal spasm.
4. Steroids and O2 in laryngeal oedema.
5. Tracheostomy may be needed.
2. Atelectasis:
It is due to inhaled F.B., and it may be unilateral or bilateral. In
mild cases, there is slight peripheral cyanosis, mild pyrexia and
dysoonea. In severe cases it may be fatal.
3. Respiratory infection; bronchopneumonia, lobar pneumonia, or
 -361-

lung abscess. It is due to aspiration of blood clots, vomitus or

secretions.
D. Infections
1. Otitis media.
2. Parapharyngeal abscess.
3. Cervical adenitis.
4. Bacteraemia and septicaemia,
E. Trauma
1. Dental injury from intubation, or the mouth gag.
2. Mandibular joint dislocation from vigorous opening of the
mouth.
3. Injury of the uvula, tongue, lips, posterior pharyngeal wall, or the
soft palate.
4. Atrophy of the uvula due to injury of the uvular artery.
F. Incomplete removal
If there are residual remnants of the tonsils, they regrow again and
become frequentiy infected. In this condition a revision surgery is
indicated.

Stomatitis and oropharyngeal ulcerations

Classincation
/. Local causes
1. Trauma
2. Infections:
a. Bacterial:
- acute : - Phar>'ngitis, tonsillitis.
- Vincent's angina
- Faucial diphtheria
- Chronic - Tuberculosis.
- Syphilis.
b. Viral - Herp angina
- Herpes simplex.
- Herpes zoster
-AIDS
c. Fungal: moniliasis (candidiasis)
3. Allergic stomatitis.
 ir -C

- 362 -

4. Malignant ulcer.
5. Dyspeptic ulcer.
6. Precancerous'lesions.
//. Miscellaneous causes
1. Blood diseases: - Agranulocytosis.
- Acute leukaemia.
2. Vitamin deficiencies - Vitaminc A deficiency
- Vitamin C deficiency (scurvy)
3. Metabolic disorders; diabetes; and uraemia.
4. Skin disease: - Pemphigus.
- Erythema multiforme.
- Lichen planus.
- Lupus erythematosus.
5. Recurrent aphthous stomatitis.
6. Behcet's disease.
7. Cancrum oris.
8. Stomatitis due to metals and drugs.
N.B. : Most of the abovelisted causes have been already discussed. The
most common features of causes not mentioned before; include :
A. Traumatic ulcers
1. Mechanical trauma due to a stiff bristles on a tooth brush, fish bone,
accidental cheek biting, illfitting denture and jagged teeth.
Traumatic ulcers have punched out serrated edges, soft base with
reddish granulations in the floor. They heal in few days.
2. Thermal bums due to intake of hot food, usually affects the anterior
part of the palate and the tongue.
3. Chemical injuries include intake of corrosives (eg. caustic potash),
where it forms multiple ulcerations with yellowish sloughs. Aspirin
bum is anothr form of chemical injury.
4. Tobacco smoking produces inflammatory patches with excessive
keratinization.
5. Radiotherapy for the treatment of head and neck malignancies lead
to dryness of the oral mucosa (xerostomia), with atrophy of
papillae of the tongue and sometimes ulceration.
Treatment of traumatic cases:
a. Topical antibiotics with hydrocortisone (orobase).
 •^jmKw

- 363 -

b. Coating the lips and the oral mucosa with a lubricant e.g. liquid
paraffin.
B. Viral stomatitis
Viral ulcers are shallow, rounded, and symmetrical. They are
surrounded by inflammation and tissue tags due to ruptured
vesicles.
1. Herpes simplex
- The type I herpes simplex virus affects the oral cavity, the
oropharynx, and is transmitted by close personal contact,
while type II generally gives rise to genital infection.
- Clinical picture : infection with type I herpes simplex virus is
preceded by a prodroma of fever, headache malaise, and
usually there is foetor oris. It usually affects children and
causes severe vesicular and ulcerative stomatitis. The
vesicles are multiple and small, affecting the lips, gums,
tongue, buccal mucosa, soft palate, and occasionally
spreading to the oropharynx. Vesicles, soon rupture to form
multiple, shallow, painful ulcers surrounded by a hypraemic
zone.
- Investigations
a. Scrappings from the base of a fresh lesion, and
examination by a direct smear stained with Giemsa stain
reveals multinucleated giant cells, ballooning of the
nuclei, with intranuclear inclusoin bodies.
b. Viral culture and immunofluoresence.
- Treatment
a. Topical anaesthetic spray, mouth wash, antipyretics,,
analgesics, soft diet and fluids.
b. Antiviral drugs e.g. Acyclovir.
2. Herpes zoster
It is caused by varicella zoster virus (which causes chicken-pox). It
is due to reactivation of virus particles which have remained in the
cranial nerve nuclei, or ganglia. The vesicular eruption can occur along
the distribution of the 5th, 9th and 10th cranial nerves (i.e. palate, tonsils,
and posterior pharyngeal wall). There is severe pain on swallowing,
vesicless and shallow ulcers that heal rapidly. It is usually accompanied
by herpes zoster oticus.
 -364-

3. Herpangina
It is a self-limiting vescicular eruption caused by coxsakie virus,
that may occur in epidemics. To distinguish the case from herpes
simplex; the erythema and vesicles lie posterior, affecting the tonsils,
pillars, and the soft palate. Vesicles rupture to form shallow ulcers with
punched out edges, gray craters, and are surrounded by a deeply red
areola.
4. AIDS
It is caused by human immunodeficiency virus (HIV). It is
transmitted by sexual contact, parenteral blood and blood products, and
prcnatally from the mother to her baby. Otolaryngologic manifestations
include, persistent oral thrush, gingivitis, oropharyngeal candidiasis,
herpetic ulcers and cervical lymphadenopathy. Kaposi's sarcoma may
affect the E.A.C, nose, nasopharynx, and larynx.
Allergic stomatitis
It is due to chemical or contact allergy (e.g. lip stick, mouth wash,
tooth paste, asprin, and acriflavin). It is characterized by the formation of
vesicles that rupture to form shallow ulcers. •
Precancerous lesions
Leukoplakia; which appear as a raised white area usually on the
inner side of the check, dorsum of the tongue and the lower lip. It has an
illdefined border, and no surrounding inflammation.
Dyspeptic ulcers
They are related to constipation, diarrhea, and hyperacidity. The
ulcers are small, superficial, painful, with punched out edges. They
usually occur in the oral cavity and tongue.
Vitamin deficiencies
1. Vitamin B deficiency produces glossitis with red glazed swollen
tongue and Assuring of the angle of the mouth.
2. Riboflavin deficiency produces cracked red lips and fissured
tongue.
3. Vitamin C deficiency (scurvy) produces swollen gums, that are
spongy and bleed easily. There are patches of discoloration on the
palate.
Metabolic diseases
1. Diabetes : Xerostomia, red painful tongue, purple spongy bleeding
gingiva and loosening of teeth.
2. Uraemia; brown coated tongue with characteristic odour.
 ^

-365-

Stomatitis with skin diseases

1. Pemphigus
It is a disease of skin and mucosa of unknown aetiology; possibly it
is autoimmune. There are irregularly scattered bullae that rupture to form
irregular painful ulcers. There are two forms; pemphigus vulgaris (the
severe form), and pemphigus vegetans (the milder form). Biopsy and
microscopic examination shows the intraepithelial lesion, with
acanthoslysis. It is treated mainly by steroids, and immunosuppressive
drugs.
2. Bullous pemphigoid
A less severe disease affecting mainly children below 5 years, and
old persons above 60 years. Biopsy and microscopic examination shows
that the lesion is subepithelial with no acanthoslysis.
3. Erythema multiforme
This is a self limiting disease of the skin and mucosa. The aetiology
is unknown, but it may be a delayed hypersensitivity reaction to drugs
(e.g. penicillin) or infections (e.g. mycoplasma). There are vesicles and
bullae in the oral cavity that rupture quickly to form ulcers that are
friable, bleed easily and are covered with a white pseudomembrane.
Treatment is topical steroids in severe cases.
Recurrent aphthous stomatitis
The aetiology is unknown but it may an abnormal immunological
response to oral bacterial infection. Other theories that were postulated
include, viral infection, psychogenic, endocrinal disturbances, anaemia
and an autoimmune reaction. The buccal and labial mucosa shows
multiple, superficial, painful ulcers in an otherwise healthy person.
Treatment consists of mouth wash with 250mg tetracycline capsule
dissolved in 50ml water 4 times daily, topical steroids and recently
levamezole.
Cancrum oris
This is a rapidly spreading ulceration of the gums, tongue and
buccal mucosa, with sloughing, bone exposure and rapidly developing
gangrene. It may affect the face, eyes and ears. It particularly occurs in
children with low resistance, leukaemias, diabetics, and immunocompro-
mized.
Stomatitis due to metals & drugs
This occurs with metals (e.g. mercury, lead, and gold), and drugs
(e.g. epanutine, antidepressants, and cytotoxic drugs). The ulcers are
large, deep, necrotic, with irregular edges, and lack a surrounding zone of
inflammation.
 • ^

-366-

Plummer Vinson syndrome

(Paterson - Brown Kelly Syndrome)
This is a chronic inflammatory pharyngo-oesophagitis.
Aetiology
Iron deficiency, which causes atrophy of the mucosa and
submucosal fibrosis, with stricture and web formation.
Clinical picture
1. Dysphagia due to stricture or web formation that usually occur at
the pharyngo-oesophageal junction.
2. Iron deficiency anaemia (hypochromic microcytic).
3. Koilonychia (spooning of the nail), and brittle nails.
4. Fissured angles of the mouth, and glossitis.
5. Achlorhydria due to atrophic gastritis.
6. Splenomegaly in 15% of cases.
The condition is precancerous, and may lead to postcricoid carcinoma.
Treatment
1. Proper nutrition and iron supplements (oral or parenteral) for
correction of anaemia.
2. Repeated dilatation of a strictue or a web.
3. Regular follow up by barium swallow and endoscopy is essential as
the condition is precancerous.

Hypopharyngeal carcinoma
Malignant hypopharyngeal tumours are almost exclusively
squamous cell carcinomas.
Age : Old age avove 50 years, however, postcricoid carcinoma may
occur in younger age groups if it develops on top of
pulmmer-vinson syndrome (20-40 years). In Egypt
postcricoid carcinoma occur even at an earlier age.
Sex : Males are more commonly affected than females, but in Europe
postcricoid carcinoma is more common in females. In Egypt,
males and females are equally affected, and it is mostiy
postcricoid rather than pyriform fossa carcinoma.
Predisposing factors
1. Plummer-vision syndrome (hyposiderosis) predisposes to
postcricoid carcinoma.
 -367-

2. Niacin deficiency especially in pellagra, which is due to maize

eating that was common in the past and not nowadays.
3. Excessive tobaco smoking and alcohol consumption.
4. It may be irradiation induced.
Pathology
Sites
1. Pyriform fossa tumours (50%). The pyriform fossa (sinus)
extends from the pharyngoepiglottic fold to the upper end of the
oesophagus. It is bounded laterally by the thyroid cartilage and
medially by the aryepiglottic fold, arytenoid cartilage and
cricoid cartilage.
2. Postcricoid tumours (40%). The post cricoid area
(pharyngo-oesophageal junction) extends from the level of the
arytenoid cartilages to the inferior border of the cricoid
cartilage.
3. Posterior pharyngeal wall tumours (10%).
Microscopically
- It is almost always squamous cell carcinoma with variable
degrees of differentiation, but they are usually poorly
differentiated. It may be keratinizing or non keratinizing.
- Non squamous hypopharyngeal malignancies are generally minor
salivary gland in origin (usually adenoid cystic carcinoma) or
mesenchymal (e.g. plasmacytoma).
Spread
A. Direct spread of the primary tumour
It has a high tendency towards submucosal extensions of 10mm or
more. Furthermore, it may be multicenteric with involvement of the
oesophagus. This is important when considering the resection margins.
1. Pyriform fossa tumours
a. Tumours which involve the lateral wall may invade through the
thyrohyoid membrane and become palpable in the neck and this
may be mistaken for nodal metastasis. Extrapharyngeal spread
to the soft tissues of the neck (carotid sheath and thyroid gland)
may occur.
b. Tumours on the medial wall invades the supraglottic larynx
(aryepiglottic fold, paraglottic space, and postcricoid region.
Invasion of the paraglottic space causes fixation of the vocal
cord.
 T

-368-

2. Postcricoid tumours; it may extend anteriorly to the larynx,

laterally to the pyriform fossa, downwards to the oesophagus and
posteriorly to the prevertebral muscles and fascia (inoperable).
Extrapharyngeal spread to the thyroid gland, and soft tissues of the
neck occurs in advanced cases. A submucosal spread of 10mm or
more must be bom in mind when considering the resection
margins.
3. Posterior pharyngeal wall tumours; may spread upwards to the
oropharynx, downwards to the cervical oesophagus and posteriorly
to the prevertebral muscles and fascia.
B, Lymphatic spread
Nodal metastasis in hypopharyngeal tumours is common and early.
It metasatizes to the deep cervical lymph nodes (upper, lower and middle
groups). Paratracheal and mediastinal nodal metastasis occur in
postcricoid tumours. Bilateral lymph node metastasis may occur from
tumours that crossed the midline (postcricoid).
C. Blood spread; Late, to lung, liver and bones.
Clinical picture
Symptoms
1. Gradual progressive dysphagia, firt to solids, later to solids and
fluids. It occurs early in postcricoid and posterior pharyngeal
wall tumour than pyriform tumours. Indefinite vague symptoms
as mere discomfort in the throat, sense of a lump in the throat or
sticking of food on swallowing should be interpreted with
suspicion as this may indicate an early malignancy.
2. Pain in the throat; usually lateralized and often radiating to the
ipsilateral ear in pyriform tumours.
3. Regurgitation and chocking.
4. Hoarseness of voice due to :
a. Vocal cord fixation as a result of infiltration of the paraglottic
space or the cricoarytenoid joint (i.e. extension to the larynx).
b. Infiltration of the recurrent laryngeal nerve in the
tracheo-oesophageal groove due to extralaryngeal spread,
which leads to vocal cord paralysis, (more common with
postcricoid tumours).
5. Stridor and airway obstruction due to tumour extension to the
larynx or bilateral vocal cord paralysis.
6. A painless neck mass of gradual onset and progressive course,
 •tp«l

- -S:

may be due to nodal metastasis, or exrralaryngeal spread to the

soft tissues of the neck.
7. Progressive weight loss.
8. Spitting of blood due to haemorrhage and necrosis or injury by
solid food.
9. Symptoms suggestive of distant metastasis (late);
a. Chest; chest pain, dysponea, and haemoptysis.
b. Liver; Jaundice, and pain in the right hypochondrium.
c. Bones; bony pains and pathologicl fractures.
Signs
A. General
1. Cachexia and underweight.
2. Manifestation of hyposiderosis (plummer vinson syndrome).
3. Patient usually sits in the barking dog position to allow easy
respiration.
4. Signs of distant metastasis (late) e.g. pleural effusion, ascites,
hard tender liver and fractures.
B. Local
1. Examination of the hypopharynx and larynx (by a mirror,
flexible endoscope, or rigid endoscope); may reveal; (Fig.80)
a. The upper edge of postcricoid tumours.
b. Pyriform or posterior wall tumour.
c. Froth (saliva) in the pyriform fossa or the postcricoid region.
d. Invasion of the larynx and state of the airway.
e. Fixation or paralysis of the cords.
f. Oedema of the arytenoids in postcricoid and pyriform
tumours.

Fig 80 postcricoid
carcinoma
 -370-

2. Examination of the neck; may reveal:

a. Enlarged painless cervical lymph nodes; a report on the- site,
number, size, and bilaterality. Early, they are firm and
mobile, and later become hard and fixed. Cervical nodal
metastasis may be the only presentation of pyriform fossa
tumours as it is one of the silent areas.
b. The larynx is pushed forwards.
c. Absent laryngeal click :on side way movement of the larynx
on the vertebral column (Positive Moure's sign).
d. Fixation of the larynx to the vertebral column indicates
invasion of the prevertebral muscles and fascia (inoperable).
Investigations
1. Plain x-ray soft tissue lateral view shows widening of the
prevertebral space in postcicoid tumours.
2. Barium swallow shows an irregular filling defect, and helps to
assess the lower extent of the tumour.
3. CT scan of the neck shows the tumour (enhancing soft tissue
mass), its extensions, extrapharyngeal spread and cervical nodal
metastasis. This is important for accurate staging.
4. Endoscopy and Biopsy
Endoscopic examination (hypopharyngoscopy,
oesophagoscopy and direct laryngoscopy) to detect extent of
the tumour for staging, and to decide tfie treatment modality
and type of pharyngeal repair. It is important to detect the
lower extent of the tumour and invasion of the larynx.
- Biopsy is taken for histopathological examination to confirm
the diagnosis.
- Bronchoscopy is essential to evaluate extension to the posterior
wall of the trachea.
5. Metastatic work up; abdominal ultrasound, bone scan, and chest
x-ray.
6. Routine preoperative investigations; ECG, liver and kidney
function tests. Blood picture, and a full coagulation profile.
7. Evaluation of the nutritional status of the patient and daily body
weight is important.
Treatment
Hypopharyngeal carcinoma carries an unfavourable prognosis with
an overall 5-years survival rate of 30%.
 -371-

A, Surgery

pyriform fossa tumors tese tumors usuallypresent late and a

total phangolarngectomy is required.
2. Postcricoid tumours; Total laryngopharyngectomy, with or
without oesophagectomy to eradicate multicenteric lesions, or if
there is skin lesions due to submucosal spread. Radical neck
dissection is usually needed due to high incidence of nodal
metastasis.
3. Posterior pharyngeal wall tumours; total laryngopharyngectomy
with or without oesophagectomy.
- Partial pharyngectomy in early cases may be resorted to through a
lateral pharyngotomy approach, or peroral CO2 laser ablation,
although such situations are not common in pracdce.
- Patients with hypopharyngeal carcinoma are usually debilitated, so
hyperalimentadon is needed through a nasogastric tube if possible,
or by intravenous hyperalimentation (aminoacids and intralipids),
in order to have a weight gain to tolerate the surgical procedure.
Management of the neck nodes
Because of the high incidence of nodal metastasis in
hypopharyngeal carcinoma, neck dissection is mandatory, taking in
consideration dissection of the paratracheal and mediastinal lymph
nodes.
Reconstruction of the removed pharynx after total
laryngopharyngectomy :
1, Total laryngopharyngectomy with oesophagectomy
a. Gastric pull up; where the stomach is mobilized through the
chest up to the neck, and anastomsis is done between the fundus
of the stomach and the remaining part of the oropharynx. This is
the best method.
b. Colon interposition.
2. Total laryngopharyngectomy without oesophagectomy
a. Free vascularized flaps e.g. jejunal loop or fasciocutaneous radial
forearm flap. This needs a highly skilled microvascular
technique.
b. Pctoralis major myocutaneous flap or deltopectoral flap.
B. Radiotherapy
This is not the primary treatment modality as hypopharyngeal
carcinomas are not radioresponsive. Furthermore, they are usually
 p a
m

-372-

advanced at the time of diagnosis. Radiotherapy is generally resorted to

as a palliative treatment for inoperable cases.
Adjuvant postoperative radiotherapy is indicated in :
a. Narrow or invaded resection margins.
b. Invasion of adipose tissue.
c. Positive nodal metastasis histopathologically.
d. Alltemativc to neck disseciton.
N.B, : Combined therapy in the form of surgery and postoperative
radiotherapy improves the locoregional control.
C. Palliative treatment
Indications
1. Recurrence after surgery.
2. Inoperable cases :
a. Poor gereral condition or surgical unfittness.
b. Fixation to the vertebral column.
c. Paralysed vocal cord.
d. Massive fixed nodes or bilaterd nodes.
e. Extrapharyngeal or extraoesophageal spread.
f Distant metastasis.
Methods
1. Adequate alimenation by ryle feeding or gastrostomy.
2. Tracheostomy if there is respiratory obstruction.
3. Laser debulking.
4. Pain killers.
5. Radiotherapy and/or chemotherapy.

Pharyngeal pouch (Zenker's diverticulum)

This is herniation of the pharyngeal mucosa as a pulsion sac
through a potentially weakened area in the posterior part of the
pharyngeal wall known as Killian's dehisence, which lies between the
upper oblique fibres of the inferior constrictor muscle (thyropharyngeus),
and the lower transverse fibres of the same muscle (cricopharyngeus).
Aetiology
1. Spasm or failure of relaxation of the cricopharyngeal sphincter
(lower transverse fibres of inferior constrictor muscle).
2. Premature closure of the cricopharyngeal sphincter;
 - 373 -

The cricopharyngeal sphincter is normally closed except during

swallowing, where the upper thyropharyngeus contracts to push food
down, if at this stage the cncopharyngeus is still contracting this will
lead to progressive rise of the intralaryngeal pressure and herniation of
the pharyngeal mucosa.
Clinical picture
- Age, 40 years and above.
- Sex; males are more commonly affected.
Symptoms
1. It may be asymptomatic in case of small pouch.
2. Dysphagia of prolonged duration.
3. Regurgitation of undigested food of foul odour.
4. Neck swelling usually on the left side.
5. Progressive loss of weight due to oesophageal obstruction or
malignant change.
Signs
1. Unilateral neck swelling usually on the left side (as the
oesophagus is a left sided structure in the neck and not in the
midline. The swelling is cystic, compressible, empties on
pressure with a gurgling sensation, and lies under the
steromastoid muscle.
2. Indirect laryngoscopy may show froth in the pyriform fossa or
regurgitation of undigested food.
Complications
1. Oesophageal obstruction.
2. Malignant change.
3. Repeated chest infection.
Investigations
1. Barium swallow, shows a retort shaped swelling with a smooth
contour.
2. Oesophagoscopy shows the orifice of the pouch with retained
food and secretions. Sometimes the puch is so huge that the
endoscope can pass through it with perforation of the pouch.
Treatment
1. No treatment is required in asymptomatic cases.
2. Symptomatic cases :
a. Small pouch; cither do :
- Repeated dilatation.
 -374-

- Cricopharyngeal myotomy.
- Endoscopic crush and stapling.
b. Large pouch isexcised (diverticulectomy) with cricopharyn-
geal myotomy.

The occult (hidden) primary

Most carcinomas of the head and neck metastasize to the lymph
nodes of the deep cervical chain but an enlarged lymph node may be the
only presenting feature of such a carcinoma (i.e. hidden primary).
An occult primary may be in one of the silent areas of the head and
neck, or from a tumour below the level of the clavicle.
A. Silent areas in the head and neck include
1. Nasopharynx, particularly the fossa of RosenmuUer.
2. The base of the tongue and the valecula.
3. The tonsillar crypts.
4. Thyroid gland (papillary or follicular carcinoma).
5. Supraglottic larynx (The ventricles and the epiglottis).
6. Pyriform fossa.
7. Floor of mouth.
8. Maxillary sinus (very rare).
B. A tumour below the level of the clavicle may be
1. Bronchongenic carcinoma.
2. Carcinoma of the breast
3. Stomach and intestine (metastasize to the left lower deep
cervical lymph nodes known as virchow*s glands).
N.B. : Rarely, a diagnosis of branchiogenic carcinoma (carcinoma
of branchial cell origin) may be considered. This usully
occurs at a young age, and may feel clinicaUy exactly like a
malignant lymph node.
Management of a case of occult primary
/. Adequate history
1. There is a history of a painless neck mass of insidious onset and
rapidly increasing in size. ;
2. Ask about the following :
a. Symptoms suggestive of a disease in the head and neck, (e.g.
dysphagia, hoarseness, sorethroat, nasal obstruction, and
otalgia).
 b. Pulmonary symptoms (e.g. cough, haemoptysis and dyspnoea).
c. Gastric symptoms; indigesuon, and dyspepsia.
d. Progressive loss of weight.
//. Examination
1. Examin the lump for site, size, number, consistency, bilaterality,
and for fixation to deep structures.
2. Examiantion of other lymph nodes.
3. Full head and neck examination.
4. Examination of the abdomen,
///. Investigations
A. Radiological
1. Plain radiographs of the head and neck.
2. CT scan from the skull base down to the chest.
3. Thyroid scan.
4. Barium swallow, meals, and enema.
B. Complete blood picture and erythrocyte sedimentation rate.
C. Fine needle aspkadon from the lump.
D. Endoscopy under general anaesthesia
- Endoscopy, including nasopharyngoscopy, oesophagoscopy,
laryngoscopy, bronchoscopy, and hypopharyngoscopy. Biopsy
should be taken from any suspicious lesion, however, blind
biopsies should be taken from the fossa of Rosenmuller, base of
tongue and pyriform sinus on the same side of the lump even if
there is no suspicious lesion.
- After endoscoy palpate the base of the tongue and tonsils as
tumours in these areas are better felt than seen. Finally, remove
the tonsil on the same side of the lesion for muldple sections and
histological examiantion
N.B. : Never rush to excise a neck node before exhausting the search
for a primary, because of the following :
a. Spillage of the tumour cells in the neck may occur during
surgery.
b. Tlie pathological examination if proved to be squamous cell
carcinoma; the biopsy did not give a clue to the site of the
primary tumour.
c. The biopsy incision can interfere later on with the plan of
neck dissecuon incision.
d. If the node removed was the only single node, the patient may
have a false sense of security, as if cured, and doesnot
show-up again.
 MMuaa

-376-

Snoring and sleep apnoea

- Sleep apnoea, is a disorder of intermittent cessation of respiration
during sleep that lasts for seconds or longer. The cessation of air flow
is usually measured at the nose and lips.
- Sleep aponca consists of three types :
1. Central sleep apnoea; the cessation of air flow is due to transient
lack of the respiratory effort.
2. Obstructive sleep apnoea (OSA); there is temporary upper airway
obstruction with normal respiratory effort
3. Mixed sleep apnoea; exhibits components of both central and
obstructive apnoea, but is condisered a variant of OSA.
Obstructive sleep apnoea is the most common type and often
involves the otolaryngologist's care.
Snoring is the sound produced as a result of passage of air via the
oropharynx producing vibrations of the soft palate. The relaxed tone of
the muscles in this area is believed to contribute to the excessive
vibrations assocaited with snoring.
Causes of obstructive sleep apnoea
Any condition causing narrowing of the upper airway; the
oropharynx, hypopharynx and supraglottic larynx may lead to OSA.
A. Nasopbryngeal causes
1. Large nasopharyngeal tumours e.g. angiofibroma.
2. Huge adenoids,
3. Anterior and large posterior nasal packs in children.
B. Oropharyngeal causes
1. Marked adenotonsillar hypertrophy.
2. Large lax uvula and soft palate with excessive mucosal folds.
3. Excessive redundant lax faucial pillars.
4. Large oropharyngeal tumours.
C. Hypopharyngeal causes
1. Macroglossia (Huge tongue).
2. Microganthia (receding mandible).
3. Hypopharyngeal tumours.
4. Oedema due to radiotherapy.
There are certain causes that exacerbates OSA, and these include :
1. Nasal problems e.g., devaited septum, nasal polypi, hypertro-
phied turbinates, and other causes of nasal obstruction.
 - 377 -

2. Alcohol and sedatives.

3. Obesity.
Clinical picture
1. There is loud snoring during sleep, which is followed by a period of
apnoea, leading to ai'ousal from sleep. Arousal is due to hypoxia
and hypercapnia, then the patient returns to sleep again (i.e.
interrupted restless sleep lythm). The spouse may witness periods
of apnoea, and frequent arousals at night.
2. There may be night mares, and nocturnal enuresis and abnormal
positions during sleep.
3. There are symptoms of sleep deprivation including day time
hypersomnolence, headache, lack of concentration, and impaired
day performance.
4. Impotence, hypertension, and obesity are usually associated with
OSA.
5. Examination may reveal:
a. About 70% of patients are overweight.
b. Short thick neck.
c. Systemic hypertension.
d. Oropharyngeal examinaion may show :
- Low hanging redundant palate and large uvula.
- Large (kissing) tonsils.
- Excessive pharyngeal mucosal folds.
- Narrow oropharyngeal isthmus.
- Large tongue.
e. Examin the larynx, nasopharyx and nose for any obstructive
lesion.
N.B. : Although snoring indicates some degree of obstructed
breathing, and although patients who have OSA are loud
snorers, yet not all people who snore have OSA (i.e. most
snoring is not pathologic).
Investigations
1. Polysomnography, is the most sensitive and specific test in the
evaluation of OSA. It measures eye movements
(electro-occulography), brain activity (EEC), cardiac rythm (ECG),
pulse oximetery (to measure 02 and C02 saturations), nasal and
oral airflow, and respiratory movements (chest & abdominal
 -378-

movements). It allows correct diagnosis, estimation of the

magnitude of the problem, and differentiates between obstructive
and central sleep apnoea.
2. Multiple sleep latency test; provides objective assessment for the
tendency to sleep.
3. Respiratory function tests.
4. Flexible endoscopy of the naso, ore, and hypopharynx. Muller's
manouver is performed by asking the patient to snore with the
mouth closed, which may show collapse in the area.
5. CT scan at the level of the oro-hypopharynx.
6. X-ray head and neck.
7. Rhinomanometeric studies for nasal resistance.
N.B. : The diagnosis of obstructive sleep apnoea syndrome is made
when there is more than 5 epispdes of arousal per night hour
sleep, or 30 per night sleep.
- The apnoea index is the periods of apnoea occuring / 1 hour night
sleep.
Complications
If left untreated, chronic OS A may lead to:
L Cor puhnonale and heart failure.
2. Cardiac arrhythmias.
3. Idiopathic hypertension.
4. It may be fatal and cause nocturnal death.
5. Personality changes.
Treatment
A. Medical
1. Weight reduction.
2. Avoid drugs that depress the CNS e.g. alcohol.
3. Progestion, which is respiratory stimulus (doubtful).
4. Theophylline; increases the hypoxic drive.
5. Protriptyline (non sedating tricyclic anti-depressant).
6. Oxygen therapy.
7. Nasopharyngeal intubation.
8. Tongue retaining devices.
9. Nasal continuous positive air pressure, applied through a mask
which is kept over night.
 -379-

B. Surgical
- To bypass the obstruction, and to prevent collapse of soft tissues
at the site of obstruction.
- It must be remembered that general intubation anaesthesia is
difficult, and one should be always ready for tracheostomy.
Intraoperative steroids should be given (to decrease oedema),
and extubation is done only when the padent is fully awake.
- Operations performed
1. Uvulopalatopharyngoplasy (UVPP); this is the most common
procedur performed. This procedure entails removal of the
tonsils, part of the posterior pharyngeal wall medial to the
posterior pillar, variable part of the soft palate, the uvula, with
trimjning of the faucial pillars. The amount of soft tissues
removed varies according to the mucosal redundancy. It can be
done by surgery or laser (laser assisted
uvulopalatopharyngoplasy). The latter can be done under local
anaesthesia if the padent is cooperative.
2. Midline glossectomy by laser, where we remove the portion
between the foramen ceacum and the valecula in the midline.
This is done in case of huge base of the tongue.
3. Mandibular advancement in case of receding mandible.
4. Hyoid expansion.
5. Tracheostomy, cures 100% of patients with OSA, and it is
indicated in OSA, with failed all measures, or if there are
complications.
6. Adenoidectomy should be done if it is the cause of OSA in
children without hesitation as OSA is a major cause of sudden
infant death syndrome.
N.B. : Treatment of any assocaited nasal problem should be carried
out e.g. turbinectomy, SMR, and polypectomy, and this should
be performed prior to the treatment of OSA.
 -380-

THE OESOPHAGUS
Anatomy of the oesophagus
- The oesophagus is a fibromuscular tube which extends from the lower
end of the laryngopharynx (opposite the lower border of the 6th
cervical vertebra) to the stomach (opposite the lower border of the
11 th thoracic vertebra).
- It consists of three parts
1. Cervical part.
2. Thoracic part.
3. Abdominal part
- It has three anatomical narrowings
1. At its upper end just below the cricopharyngeal sphincter (about 15
cm from the central incisors).
2. At the crossing of the aortic arch and the left main bronchus (about
25 cm from the central incisors).
3. At its lower part, at the oesophageal hiatus of the diaphragm (about
40 cm firom the central incisors).
Relations of the cervical part
Anteriorly : Trachea, thyroid gland.
Posteriorly : Prevertebral muscles and fascia, and the bodies of the
cervical vertebrae.
Laterally : Carotid sheath, lobes of the thyroid gland, and the
recurrent laryngeal nerve in the tracheo-oesophageal
grove.

Dysphagia
Dysphagia is defined as difficulty or pain on swallowing and/or the
sensation of the act of swallowing.
Classiflcation of the causes
I. Oesophageal causes
A. Causes in the lumen
- Foreign body is the commonest cause of temporary oesophageal
obstruction.
B. Causes in the wall
L Congenital diseases:
a. Congenital atresia or stenosis of the oesophagus.
 *V

b. Tracheo-oesophageal fistula (the commonest anomaly).

2. Traumatic :
a. Foreign body.
b. Oesophagoscopy and instrumentation.
c. Chemical : ingestion of corrosives which lead to stricture
formation later on.
d. External injury (rare).
e. Rupture of a normal oesophagus (rare).
3. Inflammatory :
a. Acute ulcerations of the oesophagus from :
- Corrosives.
- Drugs, and specific fevers, e.g. typhoid and scarlet feua.
- Persistent vomiting.
- Moniliasis.
b. Chronic inflammatory changes in :
- Reflux oesophagitis especially in sliding hiatus hernia.
- Peptic ulceration of the lower end oesophagus.
- T.B., syphilis, crhon's disease.
- Pulmmer vinson syndrome.
- Scleroderma.
4. Neoplastic :
a. Benign tumours (rare): e.g. leiomyoma, fibroma.
b. Malignant tumours : carcinoma.
5. Neurological : (functional disorders of the swallowing
mechanism)
a. Paralytic : paralysis of the pharyngeal and oesophageal
muscles dut to :
- Central lesion e.g. bulbar palsy, cerebrovascular stroke,
poliomyelitis.
- Peripheral (nerve) lesion e.g. postdiphtheritic neuritis,
andlead poisoning.
- Neuromuscular disorder e.g. myasthenia gravis.
b. Incoordinated motility :
- Pharyngeal pouch (mentioned before).
- Cricopharyngeal achalasia.
- Achalasia of the cardia,
- Diffuse oesophageal spasm.
 -382-

C. Pressure on the oesophagus from outside

1. In the cervical region (upper 1/3)
a. Malignant thyroid tumour.
b. Huge multinodular goiter.
c. Enlarged cervical lymph nodes e.g. metastasis, and
lymphoma.
d. Pharyngeal pouch.
e. Aneurysm of the carotid artery.
f. Pott's disease of the cervical spine with cold abscess.
g. Osteophytes of the cervical vertebrae.
2. In the thorax (middle 1/3)
a. Mediastinal tumours.
b. Pericardial effusion.
c. Enlarged left atrium.
d. Bronchogenic carcinoma,
e. Aneurysm of the aorta.
f. Dysphagia lusoria : compression by an abnormal right
subclavian artery or a double aorta (very rare).
3. In the abdomen Qover 1/3)
a. Enlarged left lobe of liver.
b. Paraoesophageal hiatus hernia.
IL Extraoesophageal causes
1 Nasal
Nasal obstruction in infants (e.g. adenoids), and nasopharyngeal
fibroma. They cause difficulty in feeding.
2. Oral
a. Congenital: cleft palate.
b. Traumatic : injuries, corrosives, palatal tear.
c. Inflammatory:
- Stomatitis & ulcerations of mouth, gums and tongue.
- Glossitis, dental sepsis.
- Sialadenitis.
- Ludwig's angina.
d. Tumours of the oral cavity eg. carcinoma of tongue, palate,
tonsils, and floor of mouth.
 -383-

3. Pharyngeal
a. Congenital: web, stricture.
b. Traumatic : lacerations, corrosives.
c. Inflammatonr' :
- acute and chroaic pharsngitis.
- acute and chronic tonsillitis.
- Quinsy.
- retropharyngeal abscess.
- Parapharyngeal abscess.
- pulmmer vinson syndrome.
d. Tumours:
- Oropharyngeal carcinoma.
- Hypopharyngeal carcinoma.
4. Laryngeal
a. Perichondritis,
b. T.B.
c. Any lesion involving the inlet of the larynx (epiglottis,
arytenoids, aryepiglottic folds) e.g.
- supraglottic carcinoma.
- epiglottis.
- oedema of arytenoids,
d. Laryngopharyngeal malignancies.

Foreign body in the oesophagus

Types of foreign bodies
The type of foreign body differs according to age :
1. Children playing with coins or buttons may put them into their
mouth where they may slip backwards and get swallowed.
2. In adults, it may be a fish or meat bone, a lump of meat, and
dentures in old people.
3. Safety pins, and nails. Razor blades in suicidal attempts and with
prisoners.
The commonest are coins, bones, and safety pins.
Site of lodgment
- Many foreign bodies especially when rounded, smooth, and
relatively small pass down to the stomach.
 -384-

- Foreign bodies usually lodge at sites of anatomical constrictions of

the oesophagus, (the cricopharyngeal sphincter, crossing of the arch
of aorta and left bronchus, and oesophageal opening of the
diaphragm).
a. Large foreign body and coins usually lodge in the upper part of
the oesophagus below the region of the cricopharyngeal
narrowing.
b. Meat, soft and small foreign body may lodge above a previous
stricture (e.g. firbosis or carcinoma).
c. Sharp foreign body may lodge anywhere but most commonly in
the upper end of the oesophagus.
In oesophageal malignancy and strictures, absolute dysphagia may
occur due to lodgment of a small foreign body.
Clinical picture
1. History of swallowing of a F.B. is given by the parents of the child
or by the patient himself if older. Adults are often able to point to
the exact site of obstruction.
2. Initial symptoms at the time of swallowing include coughing,
gagging, chocking and vomiting actions which may return the
object to the mouth.
3. Dysphagia and regurgitation of food and fluids, later, blood if sharp
F.B, with retrosternal dull aching pain.
4. In sharp F.B., there is severe dyphagia, with severe pain referred to
the back, or to the ear.
5. In smooth and small F.B., the patient later becomes accomodated to
its presence, and a symptomless period follows, and the F.B. may
remain there for weeks.
6. If perforation of the oesophagus occurs, there will be fever and
severe toxaemia due to mediastinitis.
7- Examination:
- Observe the patient during swallowing.
- Examine the mouth, pharynx, tonsils, and base of tongue.
- Examine the neck, for tenderness, swelling or surgical
emphysema (injury to the oesophagus).
Investigations
1. Plain x-ray neck and chest: may reveal an opaque F.B. e.g. coin,
pins.
 -385-

2. Barium swallow : F.B. may appear as a filling defect.

3. Oesophagoscopy under general anaesthesia.
Treatment
- Knowledge of the nature, size and the shape of the F.B. is ver\'
importani.
A, The F.B. is removed by oesophagoscopy under general
anaesthesia, and the size of the oesophagoscope varies with age :
a. Coins can be removed easily with a hypopharyngoscope and a
crocodile forceps. During its removal the coin is turned to lie
in a coronal plane to avoid slipping.
b. Sharp F.B. : do not remove it before noting the position of the
sharp edge, and the sharp edge is grapled and taken out.
c. A denture or a large bone can be divided insitiu by a scissor
before removal.
B. External approach (cervical or transthoracic oesophagotomy) in
impacted F.B, perioesophagids after unsuccessful attempts, and
perforation of the oesophagus.
Complications of a F.B. in the oesophagus
1. Oesophagitis and ulceration which may cause perforation of the
oesophagus.
2. Stricture formation.
3. Mediastinal emphysema, mediastinitis, pneumothorax, empyema.
4. Tracheo-oesophageal fistula.

Corrosive oesophagitis and post corrosive stricture

Swallowing corrosives is a common incident in the country, and it
is the commonest cause of non malignant strictures of the oesophagus. It
is usually swallowed accidentally in children or as a suicidal attempt in
adults :
1. Caustic potash (concentrated solution of potassium hydroxide), is
used by some people for washing and whitening clothes. A child
may drink the solution by mistake assuming it is milk, and most
cases therefore occur between the age of 2-5 years.
2. Rarely lysol, phenol or sulphuric acid are taken by adults in suicidal
attempts or by mistake.
 -386-

A. stage of corrosive oesophagitis

Clinical picture
1. Immediately after ingestion of the caustic material there is severe
burning pain in the mouth, tongue and pharynx with intense pain on
swallowing.
2. Severe dysphagia, salivation, and regurgitation.
3. Laryngeal oedema may occur causing respiratory obstruction and
stridor especially in children.
4. Shock and dehydration which varies according to the severity.
5. Local examination reeals : pedema, and white sloughs in the mouth,
pharynx and tongue.
6. There may be skin bums around the mouth, in the neck or upper
chest.
N.B. : Early oesophagoscopy is contraindicated as it may cause
perforation of the oesophagus due to friability of tissues.
Complications
1. Shock and dehydration.
2. Acute disturbances in the electrolyte balance and renal functions.
3. Perforation of the Oesophagus with bleeding and mediastinitis.
4. Laryngeal oedema and stridor.
5. Bronchopneumonia and chest infection due to inhaled
regurgitaion.
6. Trachco-ocsophageal fistulae.
7. Post corrosive stricture formation : There is a subsequent stage
after the intial reaction has subsided, during which, dysphagia
lessens and the patient can swallow with mild difficulty, later
on, dysphagia reappears due to stricture formation.
Traetment
1. Immediate neutralization of the caustic by diluted lemon juice or
vinegar (Potash is a strong alkali).
2. A mixture of milk and egg white is given.
3. Management of shock and correction of electrolyte imbalance if
present.
4. Parenteral antibiotics.
5. Tracheostomy if there is severe respiratory obstruction.
6. Olive oil is given frequently.
7. Steroids to decrease oedema and subsequent fibrosis and
stricture formation.
 - ?87 -

8. Nourishment is maintained by I.V. regiemens untill the patient

can swallow.
N.B. : Nowadays, a small nasogastic tube is introduced to ensure
adequate nourishment, and to maintain the lumen of the
oesophagus.
B. Stage of past corrosive stricture
- Strictures due to corrosives ingestion usually occur at sites of normal
narrowing as mentioned before. The stricture may be a short
segment or at multiple levels, and the area above may be dilated.
- It usually develops in the range of 2-3 weeks due to fibrous tissue
formation.
Clinical pictue
1. Dysphagia reappears (after tlie initial reaction and latent stage)
with the formation of the stricture. It is progressive, first may be
mild and intermittent to solids, but later on, to both solids and
fiuid (absolute). Sudden complete oesophageal obstruction with
absolute dysphagia may occur due to corking of the lumen by a
foreign body impacted over the stricture.
2. Malnutrition, dehydration, and starvation may occur especially
in children if inadequately nourished.
3. Recurrent chest infection due to regurgitation and aspiration of
the regurge (spill over).
Investigations
1. Plain x-ray chest and neck.
2. Barium swallow : shows the stricture as an irregular segment
with narrowing of the lumen of the oesophagus. It may be
multiple with small prestenotic dilatation above the stricture.
Strictures due to congnital defect or instrumental trauma, appear
regular and involve a short segment.
3. Oesophagoscopy shows:
a. The lumen of the oesophagus either central or eccentric.
b. The oesophagus is slightly dilated above a narrow stricture
with debris and food particles.
2. Near the stricture, the mucosa is dull and thickened.
d. The stricture appears pale with loss of elasticity of the
oesophagus.
 -388-

Treatment
A. Permeable stricture : regular dilatation through rigid
oesophagoscopy using gum-elastic bougies or rubber mounted
metallic dilators. They are introduced in increasing sizes till an
adequate lumen is reached. Care should be taken not to perforate
the oesophagus by forcible dilatation of a severly stenotic
segment as the oesophagus has no serosal covering, or the
dilator goes through a blind pouch due to the irregular nature of
the stricture. After dilatation, the patient must be hospitalized for
at least 24 hours in order to check for any oesophageal injury,
and nothing per mouth is allowed in the first 12 hours.
B. Impermeable (non dilatable) stricture :
1. Temporary feeding gastrostomy.
2. Surgery.
a. Resection of the stricture and reanastomosis by a free
jejunal loop or gastric pull up.
b. Colon bypass to overcome the stricture using the
transverse colon.
c. OesophagOgastrostomy or oesophagojejunostomy.
3. oesophageal stents.
Surgery is indicated in :
a. Failed repeated dilatation.
b. Long, narrow, tortuous stricture.
c. Complications e.g. perforation or necrosis of the oesophagus.

Achalasia of the cardia (cardiospasm)

This is marked dilatation of the lower two thirds of the oesophagus
stopping short of the diaphragmatic orifice.
Aetiology
Neuromuscular incordination of the lower oesophageal sphincter
which is due to degeneration of Auerbach's plexus in the wall of
the oesophagus. This leads to cither:
1. Failure of relaxation of the cardiac sphincter.
2. Spasm of the cardiac sphincter.
Pathology
There is marked dilatation of the lower two thirds of the
oesophagus. It is first fusiform or spindle shaped, then becomes sigmoid
 - 3S9 -

in shape. Tne wall of the oesophagus is thickened due to hypertrophy of

the muscle coat. There will be stagnation of food and fluid leading to
oesophagitis and ulceration, and later on fibrosis and stricture formation
adding more to the problem.
Clinical picture
1. The patient is usually a neurotic subject, about 30-40 years in
age.
2. Long standing intermittent dysphagia, which is more to fluids
than to solids as fluids need a highly coordinated act of
swallowing while solids descend by gravity. Periods of
remission always occur (to distinguish from stricture). It may
increase by emotional stress.
3. Regurgitation of undigested food free from HCL and gastric
secretions.
4. Dull aching retrosternal pain or fullness may be present, after
meals.
•5. The patient, despite long standing dysphagia is of nonnal built
(no loss of weight), as the dilated oesophagus empties its
contents after a while into the stomach.
Complications
1. Ulceration then fibrosis and stricture formation.
2. Pulmonary complications lead to recurrent chest infections and
aspiration pneumonia.
3. Columnar lined lower end of the oesophagus (Barret's
oesophagus) which may predispose to malignancy (rare).
Investigations
1. Barium swallow; shows huge dilatation of the lower end of the
oesophagus, fusiform in shape with narrow smooth tapered
lower end, with marked narrowing at the cardia. Absent air
bubble in the fundus of the stomach.
2. Oesophagoscopy; marked dilatation of the oesophagus with
narrow central or eccentric orifice below the dilatation, stagnant
secretions, fluids and food particles, of foul odour. There may be
oesophagitis and ulceration of the walls of Uie oesophagus.
Treatment
A. Medical
1. Reassurance, sedatives and psychotherapy.
2. Amyl-nitrite before meals for relaxation of the cardia.
3. Vitamin B,
 -390-

B. Repeated dilatation may be useful in early cases.

C. Surgical
1, Heller's cardiomyotomy ; This consists of vetical incision of
circular muscle fibres of the gastro-oesophageal (cardiac)
sphincter, down to the mucosa which is left intact to bulge.
This is done as an alternative to dilatation, or if dilatation
fails.
2. Cardibplasty : a vertical incision in the muscle coat of the
cardiac sphincter is done, and then it is sutured transversely
to widen the lumen.

Tumours of the oesophagus

L Benign tumours
They arc very rare and include:
1, Leiomyomata : These are the most common benign oesophageal
tumours. They are seen in the middle or lower third of the
oesophagus. They are asymptomatic when small, but later as
they become large, the patient starts to complain of dysphagia,
retrosternal fullness or pressure. Treatment is by endoscopic
excision.
2. Fibromas, myxomas, lipomas and papillomas : They are usually
located in the upper part of the oesophagus, they may be sessile
or pedunculated. Treatment is surgical excision either
endoscopically or by lateral neck or thoracic incision.
IL Malignant tumours
Carcinoriia of the oesophagus is more common in males above 60
years. Althoug hit may occur in young ages.
Predisposing factors
1. Smoking.
2. Alcohols, spicy food.
3. Achalasia of the cardia.
4. Oesophagitis and long standing ulceration.
5. Plummer Vinson syndrome (predisposes also to postcricoid
carinoma).
Pathology
Sites
a. Cervical oesophagus is the least common, may be due to
extension from hypopharyngeal carcinoma.

••••MP
 -391 -

b. Middle 1/3 (thoracic part) is the commonest.

c. Lower 1/3 if the next common.
Gross picture
a. Malignant ulcer : ulcer with raised everted edges, rough
haemorrhagic necrodc floor and indurated base.
b. Cauliflower mass.
c. Deeply infiltrative stricture (Schirrous type).
Microscopically
- Squamous cell carcinoma is the commonest (95%).
- Ade/3ocarcfonoma may occur in the lower 1/3 (5%) it may be
due to ectopic gastric mucosa.
Spread
A. Direct spread to surrounding structures
- Recurrent laryngeal nerves.
- Lungs, pleura, trachea, bronchi.
- Prevertebral fascia and muscles, and vertebrae.
- Stomach and aorta. .
B. Lymphatic spread
1. Upper 1/3 : to the lower deep cervical lymph nodes.
2. Middle 1/3 : to the mediastinal lymph nodes.
3. Lower 1/3 : Coeliac lymph nodes.
C. Blood spread : Liver and lungs.
Clinical picture
1. Gradual progressive dysphagia of short duration which is first to
solids, later to both solids and fluids. Absolute dysphagia may
rarely occur due to impaction of solid food on the growth.
2. Regurgitation of undigested food, may be mixed with blood.
3. Severe retrosternal pain indicates extraoesophageal spread.
4. Hoarseness of voice due to paralysis of the recurrent laryngeal
nerve.
5. Progressive loss of weight and cachexia.
6. Manifestations of distant metastasis later on.
Complications
1. Perforation of the oesophagus and mediastinitis.
2. Pulmonary complications : Aspiration pneumonia, and infiltra-
tion of the trachea and bronchi.
 -392-

3. Paralysis of the recuirent laryngeal nerve.

4. Diaphragmatic paralysis due to infiltration of the phrenic nerve.
5. Severe haemoirhage due to erosion of big vessels.
Investigations
1. Barium swallow; shows an irregular filling defect with
shouldering and rat tail appearance.
2. CT scan; to detect site and extension of the tumour,
extraocsophageal spread, and lymph node metastasis.
3. Oesophagoscopy and biopsy.
4. Bronchosopy to detect infiltration of the trachea.
5. Chest x-ray, abdominal sonar, and bone scan to detect distant
metastasis.
Treatment
Most cases are inoperable at the time of diagnosis.
A. Operable cases (Radical resection)
1. Carcinoma of upper third : total laryngopharyngectomy and
oesophagectomy with immediate reconstruction by gastric
pullup after mobilization of the stomach.
2. Carcinoma of middle 1/3 : The oesophagus is resected till one
inch above the tumour (safety margin), and then the stomach
is mobilized and connected to the oesophagus
(oesophago-gastrostomy). It carries a high incidence of
leakage and mediastinitis.
3. Carinoma of the lower 1/3 : surgery is the best, as many
growths arc adenocarcinoma and are radioresistant. The
lower part of the oesophagus till one inch above the tumour,
the upper 3/5 of stomach, spleen, omentum, and tail of
pancreas are resected, then reanastomosis is done by
ocsophago-jejunostomy or oesophagogastrostomy.
B. Inoperable cases
1. Distant metastasis.
2. Extaoesophageal spread : lungs, mediastinum.
- Palliative treatment:
1. Gastrostomy or oesophageal stent eg. souttar's tube for
feeding.
2. Pain killers.
5. Palliative oesophago jejunostomy.
 -393-

Stricture of the oesophagus

I. Malignant stricture (see cancer oesophagus)
II. Non malignant stricture
1. Congenital stricture : rare, usually single and occurs at the lower
third, and they have all the three layers of the oesophagus present,
so they are less liable to perforation.
2. Traumatic : during dilatation :
a. Accidental:
- Corrosive stricture : commonest (60%)<
- Very hot fluid ingestion in children.
- Foreign body : either during removal, or neglected foreign
body due to perioesophagitis, and subsequent fibrosis.
- External injury.
b. Surgical : after oesophageal resection (stricture at Uie suture
line).
3. Inflammatory :
a. Reflux oesophagitis : in hiatus hernia repeated vomiting, causes
ulceration of the lower oesophagus.
b. Peptic ulceration of the lower end of the oesophagus due to
ectopic gastric mucosa.
c. Chronic oesophagitis:
- Plummer vison syndrome.
- Tuberculosis, syphilis.
- Scleroederma, Crohn's disease.
- Occasionally typhoid fever and scarlet fever.

Perforation of the oesophagus

This is a fatal condition occuring mainly during clumpsy
unexperienced attempts at oesophagoscopy, extraction of a foreign body,
or dilatation of a stricture. It may be due to malignant growth, or direct
external injury.
Clinical picture
1. Severe retrosternal pain and severe dysphagia.
2. Dyspnoea sdue to development of mediastinitis or empyema.
3. Swelling and tenderness in the neck.
 -394-

4. Crepitus over the neck due to surgical emphysema.

5. Soon, the patient experiences severe illness, fever and increasing
toxaemia due to mediastinitis or empyema.
6. There may be severe haemorrhage if it happens during
instrumentation.
7. Shock and electrolytes imbalance may occur.
Treatment
1. Control shock.
2. Nothing is given by mouth and nutrition is maintained by
intravenous alimentation or temporary feeding gastrostomy.
3. Heavy courses of parenteral broad spectrum antibiotics.
4. Insertion of an intercostal tube to be connected to an underwater
seal, which may be inserted bilaterally.

Oesophagoscopy
This is performance of direct examination of the oesophagus using
a rigid oesophagoscope under general anaesthesia, or flexible fiberoptic
oesophagoscope under local anaesthesia and sedation. The length and
diameter of the oesophagoscopy varies according to the age of the
patient.
Indications
A, Diagnostic
1. Examination of the oesophagus e.g. stricture and achalasia.
2. To take a biopsy from any suspicious lesion.
B. Therapeutic
1. Extraction of a foreign body.
2. Dilatation of a non malignant stricture eg. postcorrosive
stricture.
3. Excision of benign tumour or a web.
4. Application of stent in oesophageal carcinoma.
Contraindications
1. Acute necrotic ulceration from caustics (no oesophagoscopy
before 3 weeks).
3. Advanced organic disease in a dehydrated patient.
3. Aneurysm of the aorta.
4. Marked kyphosis.
 -395-

5, Extreme varicosities in the oesophageal mucosa.

6. Vascular tumours.
Complications
1. Perforation of the oesophagus.
2. Haemorrhage.
3. Injury of the teeth, tongue, lips and pharynx.
 -396-

Laser in ENT
What is Laser ?
Laser is the abbreviation of Light Amplification by Stimulated
Emission of Radiation. The differences between Laser beam and ordinary
light beam is that ordinary light contains many wave lengths, out of
phase and in many directions (divergent), while on the contrary, laser
light contains only on wave length (monochromatic) all parallel and all in
one phase (coherent).
How is Laser used in Medicine ?
As laser beam has a very high energy, when it is directed to any
tissue it causes evaporation of the water content and the organic material
is burnt to carbon then oxidized to CO2, thus all tissues in front of the
laser beam are cut The laser beam acts exactly like a scalpel but the cut
made is clean, very precise, and doesn't bleed as the beam seals the blood
vessels.
What are the types of laser used in medicine ?
Many types are available according to the material from which the
light is emitted. They differ in their physical characteristics as wave
length, visibility and biophysical effects on tissues.
1. Carbon Dioxide laser
It has a wave length of 10.6 microns, it is absorbed by water in soft
tissues. The output beam is invisible and so, it should be aligned with a
visible beam and for this a red emitting Helium-Neon laser is used.
The delivery of the carbon dioxide laser can be manipulated to
meet various laser-tissue interactions by changing the power, the duration
and the spot size. To achieve vaporization we can use the large defocused
spot, low power and timed exposure, while to achieve a cutting effect,
surgeons select the smallest focused spot size, high power output and
continuous or superpulsed exposure time.
Advantages of CO2 laser
- It provides the surgeon with a non touch technique to vaporize
tissues in a precise manner, preserving the histological margins.
- Minimal post operative pain due to sealing of the cut ends of the
nerve fibres.
- Less operative bleeding.
- Less postoperative oedema and minimal scarring.
 -397-

Disadvantages of CO2 laser

- It can't be transmitted through fiberoptic filaments.
- It cannot seal blood vessels more than 0.5 mm in diameter.
2. Argon laser
Preoduces visible blue green light with a wave length of 488-415
nm. The energy can be transmitted through clear aqueous tissues as it has
a low water absorption, certain tissue pigments as melanin and
haemoglobin effectively absorb the argon laser light. It can be used with
flexible fiber delivery system.
3. Neodymium : Yttrium Aluminium Garnet (Nd : YAG)
It produces invisible light that has a wave length of 1.06 |im. It can
be transmitted through clear liquids and its absorption depends on
pigments. Precise control of damage is not possible and thermal
coagulation and necrosis may extend 4 mm from the impact site making
it excellent tool for tissue coagulaUons. It can also be transmitted through
flexible fiberoptic system.
4. Holmium laser
Produce invisible light wave with wave length of 2.1 |im. Its
thermal effect is less than YAG laser but more than CO2 laser also it
provides haemostasis better than C02 laser, but not as good as YAG
laser. It is the best bone removing laser and can be delivered through a
fiberoptic system.
5. KTP/532 laser
The potassium tetanyl phophate laser produces a visible 532 ]xm
beam witli a green light. It can be selected for procedures requiring
precise surgical excision due to its very small spot size and minimal
damage to surrounding tissues. It could be transmitted through fiberoptic
systems.
6. Semiconductor diode laser.
7. Pulsed yellow dye laser.
- What are the uses of laser in E,N.T ?
A laser should only be used when it offers significant advantages
over established, conventional techniques.
A. Uses of laser in laryngology
• Vocal cord nodules : Laser is very helpful because the beam can
be focused to a small spot, very precisely directed and the
nodules are gradually shaved off the edge of normal cord.
• Polyps and Cysts.
 -398-

• Reinke's oedema : stripping of the vocal cord can be carried out

with precision and without damage to the underiying cord.
• Subglottic stenosis; either congenital or acquired. Acquired
subglottic stenosis in our country is mainly due to scleroma but
another important cause is post-intubation due to prolonged
intubation in the ICU.
The stenotic area is removed preferably using the micro-trapdoor
technique and then a stent may be introduced and left in place for a
period of 2-14 months.
• Bilateral abductor paralysis : Usually following injury of the
recurrent laryngeal nerve in thyroid operations. Laser posterior
cordectomy and/or arytenoidectomy create a space for respiration
but voice result are poor.
• Vocal cord webs : The webs are divided using the laser.
• Malignant neoplasms. Laser is used for resection of early (Tl) glottic
tumour and for palliation and debulking of inoperable advanced
tumours (as mentioned before);
B-Uses of laser in the oral cavity and oro-pharynx
- Snoring : LAUP operation (laser assisted uvulopalatoplasty) has
added significant benefits over the conventional uvulopalatoplasty
in terms of bloodless surgery, postoperative morbidity and the
length of stay of the patient in hospital. Also LAUP operation could
be done under local anaesthesia.
- The ti^hnique of LAUP involves vaporization of a 2cm wide portion
of the palatal mucosa extending from hard palate to the free border
of the soft palate and also varporization of variable length of the
uvula. The deep penetraton of this laser bum causes sufficient
fibrosis of the underlying tissues to stiffen the palate and reduce the
palate flutter which is one of the causes of snoring.
- Tonsillectomy : laser tonsillectomy can be done by two techniques.
a. Laser cryptolysis : superficial vaporization of tonsillar crypts. It
is done underlocal anaesthesia on multiple sessions.
b. Laser tonsillectomy by dissection of the tonsil from its bed by
laser.
- Lingual tonsillectomy to treat hypertrophy of lingual tonsillitis.
- Haemangioma of the check or tongue.
- Excision of pre malignant lesions as leukoplakia.
- Partial resection of tongue base in case of obstructive sleep apnoea
caused by hypertrophy of tongue base.
 -399-

3. Uses of laser in nasal surgery

A. External rhinologic laser surgery. Laser can be used for excision of
rhinophyma which is an advanced form of acne rosacea, excision
of hypertrophic scars or keloids, photocoagulation of vascular or
pigmented cutaneous lesions e.g. telangectasia, port wine stains,
pyogenic granuloma, tatoos.
B. Intranasal laser surgery :
1. Laser turbenictomy for the treatment of hypertrophy of inferior
turbinates.
Advantages of laser tubrinectomy over conventional turbinectomy are

- Can be done under local anaesthesia.

- Minimizes the intraoperative bleeding.
- Avoidance of tight postoperative packing.
2. Photocoagulation of hereditary hemorrhagic telangectasia
(Rendu-Weber-Osler's disease) by YAG or ktp/532 laser.
3. Laser in Endoscopic sinus srugery: YAG laser is used to do
uncinectomy and to widen the maxillary sinus ostium.
4. Laser nasal polypectomy.
5. Endonasal laser-assisted dacryocytorhinostomy (ELDCR): YAG
laser with blunt hemispherical tip is inserted via the lacrimal
punctum to creat an intranasal ostium and then silicon tube is
left in place for 6 months.
F. Laser vidian neurectomy as a surgical management for idiopathic
vasomotor rhinitis.
G. Laser septoplasty to ablate anteriorly seated septal spurs.
H. Laser management of choanal atresia,
4. Uses of Laser in otology
1. Laser stapedotomy : Argon laser is used to divide the stapedius
tendon and crure of the stapes and then to perforate the footplate.
2. Laser myringotomy : C02 laser is used to create a small opening in
the drum. This hole has been suggested to remain open for a period
of weeks. During this time the middle ear mucosa may return to
normal and consequently a grommet tube may not be needed.
3. Removal of grannulation tissue from middle ear in tympanoplasty.
4. Excision of auricular lesions.
5. Removal of acoustic neuromas and other CPA lesions after this
tumours has been exposed conventionally.
 Neck swellings

Midline neck swellings

1. Thyroglossal cyst: it arises from the tongue at the
foramen caecum and it's due to persistent
thyroglossal duct. It may be lingual, submental,
suprahyoid, transhyoid, or infrahyoid.
The cyst moves up and down with deglutition. It's
treated by excision of the cyst with its tract (Sistrunk's
operation).

2. Thyroid cartilage: pericodritis, malignant

infiltration.
3. Thyroid isthmus: thyroid nodule.
4. Lymph nodes: prelaryngeal (Delphine node) or
pretracheal lymph node enlargement.
5. Dermoid cyst.
6. Thymus tumors.

Lateral neck swellings

1. Lymph gland enlargement (lymphoadenopathy)

2. Thyroid gland.
3. Branchial cysts.
4. Carotid body tumor.
5. Laryngocele.
6. Pharyngeal pouch.
7. Neurofibroma.
8. Sternomastoid muscle tumor.
9. Cystic hygroma.