Ear

‫الدكتور كان جايبها من غير‬

‫بيانات و شاور عليها على الصورة‬

‫‪Normal right ear drum‬‬

 Hand held speculum

used to straighten The external auditory canal is by pulling the pinna

upwards and backwards
Head mirror
 Pneumatic
Examination

used to
1)The mobility of the tympanic
membrane
2)Fistula test
‫عداها عشان شرحها فى األول‬
 Valsalva maneover

• Forced expiration with the mouth and nose closed.

• open eustachian tube
Rinne's Test :
Principle: It compares hearing by AC with hearing by BC in the same ear.
a) During hearing by air conduction ( AC )  sound passes through the external ear 
middle ear  inner ear. Therefore  it gains the advantage of middle ear
amplification.

b) During hearing by bone conduction ( BC )  sound passes directly to the inner ear
without passing through the middle ear. Therefore it does not gain the advantage
of middle ear amplification.

Method:
a) To test hearing by air conduction ( AC ) : the prongs of the vibrating tuning fork are
placed near the external canal.
b) To test hearing by bone conduction ( BC ) : the base of the vibrating tuning fork is
placed on the mastoid process.
Results:
Normally AC is better than BC. Called (Rinne positive).
Conductive HL BC is better than AC. Called (Rinne negative).
Sensori-neural HL AC is better than BC ,but both are reduced.Called (reduced Rinne
positive)
Weber's Test
Principle: It compares hearing by bone conduction in the two
ears.
So it is useful in case of unilateral hearing loss.

Method: The base of the vibrating tuning fork is placed on the

midline of the forehead or on the upper central incisor teeth.

Results:
• Normally :Sound is heard in the midline or equally in both
ears.
• Unilateral conductive HL :Sound is lateralized to the
diseased ear.
• Unilateral sensori-neural HL :Sound is lateralized to the
normal ear.
 Romberg's test:

•  The patient stands with eyes open and then closed

•  Normally the patient remains steady when the eyes are
open or closed
•  In vestibular dysfunction the patient is more unsteady
when the eyes are closed
pure tone audiogram
 causes of CD:
1)secretory otitis media
2)otosclerosis
3)wax accumulation
causes of mixed hearing
loss:
1)labyrinthitis
2) mixed otosclerosis
3)middle ear disease
causing invasion to inner
ear
causes of SNHL:
1)High tone occure in
Acoustic neuroma
 Hematoma Auris

COMPLICATIONS
1- Cartilage necrosis fibrosis  deformed auricle called
cauliflower ear.
2- Secondary infection : perichondritis
AETIOLOGY
1) Infected haematoma or laceration.
2) Infected surgical incision.
SYMPTOMS
1) General symptoms Fever, headache, anorexia and malaise.
2) Local symptoms The auricle  is swollen and painful.
SIGNS
1- General sign Fever.
2- Local signs
 The auricle  is swollen, reddish, hot and tender.
 The lobule  is free, because it has no cartilage.
COMPLICATION
Cartilage necrosis  fibrosis  deformed auricle called cauliflower ear.
TREATMENT
1) Antibiotic therapy.
2) Drainage ( by multiple small incisions )  debridement i.e. removal of
necrosed cartilage
in erysipelas the whole auricle ear lobe are included.
while in perichondritis the ear lobule is normal
Localised Otitis Externa (FURUNCULOSIS )
in bilateral and recurrent cases Blood sugar
test
NECROTIZING OTITIS EXTERNA
• severe pain occur mainly at night , discharging ear
Predisposing factors: 
1)Most commonly elderly uncontrolled diabetes
2)patients receiving immunosuppressive drugs
OTOMYCOSIS
DEFINITION: Fungal infection of the skin lining of the external canal.

AETIOLOGY Causative organisms Aspergillus niger ( black ) and Candida

albicans ( white ).

Predisposing factor Prolonged use of local antibiotics ear drops.

SYMPTOMS 1- Itching  the main symptom. 2- Hearing loss  when the

fungus mass occludes the external canal.

SIGN Speculum examination The lumen of the external canal contains a

whitish mass with black spots which resembles a wet newspaper.

TREATMENT 1- Removal of the fungus mass  by suction or ear wash. 2-

Anti–fungal ear drops and creams e.g. clotrimazole, nystatin or 2%
salicylic acid ( keratolytic ) in alcohol ( fungicidal )
HERPES ZOSTER OTICUS
‫الصورة اللى من المحاضرة ملقتهاش فى الكتاب فلو حدلقاهاهكون شاكرة‬
‫ليه‬
The triad of
a) herpes zoster oticus,
b) facial nerve palsy and
c) sensori-neural hearing loss and vertigo is called Ramsay-Hunt
syndrome.
 BULLOUS MYRINGITIS
Reddish bullae on the tympanic membrane .
Retracted drum
Signs of retraction ( due to negative middle ear
pressure ) 
a. the handle of malleus appears shortened ( i.e.
fore_x0002_shortened )
b. the lateral process of malleus is prominent,
c. the cone of light is distorted
d. its mobility is restricted ( by Siegle’s speculum or pneumatic
otoscope) .
• Occure in eustachian tube dysfunfction
acute catarrhal otitis media.
Stage of tubal catarrh ( salpingitis )
A. Pathology
The mucosal lining of the eustachian tube becomes oedematous and hyperaemic
eustachian tube obstruction  development of
negative middle ear pressure.

B. Symptoms
Hearing loss and tinnitus.( no earache)

C. Signs
Speculum examination: Retracted tympanic membrane
a) the handle of malleus appears shortened ( i.e. fore-shortened
b) the lateral process of malleus is prominent,
c) the cone of light is distorted &
d) its mobility is restricted ( by Siegle’s speculum or pneumatic otoscope ).
Tuning fork tests: Conductive hearing loss
If there is throbbing pain ......suppurative
acute suppurative otitis media
Stage of suppurative otitis media

A- Pathology: The middle ear exudate becomes

muco-purulent.

B- Symptoms
 General symptoms ( of inflammation )Fever, anorexia, headache and
malaise.
 Local symptoms
 Earache , severe and throbbing. Hearing loss and tinnitus.
C- Signs
 General sign Fever.
 Local signs
 Speculum examination: Bulging angry red tympanic membrane.
 Tuning fork tests: Conductive hearing loss
TREATMENT
I. Before perforation
A- Medical treatment
 Antibiotic therapy for 7-10 days.
 Analgesics / antipyretics.
 Decongestive nasal drops  to reduce oedema around Eustachian tube orifice
 improves ventilation and drainage of the middle ear.
B- Surgical treatment : Myringotomy
operation i.e. incision of the tympanic
membrane. When?
1) Failure of medical treatment ( i.e. persistent pain and fever ) for 48 hours.
2) Bulging tympanic membrane because myringotomy incision does
not cause loss of substance heals better than pathological perforation.
3) Development of cranial or intracranial complication.
II. Stage of perforation
A. Medical treatment
 Antibiotic therapy  better according to the results of sensitivity tests.
 Aural toilet, by repeated suction or dry mopping  to remove the ear discharge.
B. Surgical treatment
Myringotomy operation i.e. incision of the tympanic membrane. When? Small or high
perforation insufficient for adequate drainage.
Perforation of the drum by
pressure necrosis
4- Stage of tympanic membrane perforation
A- Pathology
The increased middle ear pressure  pressure necrosis of a part of pars tensa of
the
tympanic membrane  central perforation.

B- Symptoms
 General symptoms ( of inflammation )  diminish.
 Local symptoms
1. Otorrhoea  starts.
2. Earache  diminishes.
3. Hearing loss and tinnitus.
Signs
 General sign Fever  diminishes.
 Local signs
 Speculum examination: - Perforated tympanic membrane. The perforation is
central in pars tensa.
- Otorrhoea  muco - purulent, pulsating & is blood-stained at the time of rupture.
- The middle ear mucosa (through the perforation ) hyperaemic &
oedematous.
 Tuning fork tests: Conductive hearing loss.
Postauricular mastoid abscess
Mastoiditis
DEFINITION
Inflammation of the bony walls of the mastoid air cells.
PATHOLOGY
1- Starts as osteitis of the bony walls of the mastoid air cells , necrosis of these bony walls ,
the air cells coalesce together , the mastoid process is converted to a single cavity full of pus ,
called coalescent mastoiditis
2- Pus then erodes the external surface ( i.e. cortex ) of the mastoid process forming a sub-
periosteal mastoid abscess.
3- Pus then bursts through the periosteum and skin  forming a mastoid fistula.
SYMPTOMS
General symptoms Fever, headache,anorexia and malaise.
Local symptoms
1- Earache severe and over the mastoid.
2- Otorrhoea  profuse.
3- Hearing loss and tinnitus  due to otitis media
.SIGNS
A- General examination Fever.
B- External examination
1) Coalescent mastoiditis Tenderness over the mastoid antrum ( largest air cell ), tip ( most
superficial cell ) and posterior border ( site of mastoid emissary vein ).
2) Mastoid abscess  external fluctuant swelling. It may be:
a) Post-auricular abscess: Behind the auricle pushing it outwards and forwards
b) Zygomatic abscess: Above and in front of the auricle
c) Bezold’s abscess: In the upper part of the neck deep to sterno-mastoid muscle.
C- Speculum examination
1. Otorrhoea  muco-purulent or purulent, profuse and recurs rapidly after
removal ( called reservoir sign ( diagnostic sign ).
2. Sagging i.e. bulging downwards of the postero-superior wall of the bony part of
the external auditory canal. It is due to periosteitis of the adjacent mastoid
antrum. It is an early and diagnostic sign
3. Tympanic membrane  usually perforated, but may be intact and hyperaemic.
INVESTIGATIONS
1. Imaging Plain x-ray or better CT scan  clouding ( opacity ) of the mastoid air
cells
2. Culture and sensitivity tests of the ear discharg
DIFFERENTIAL DIAGNOSIS : Furunculosis of the external auditory canal
TREATMENT
A- Medical treatment
Antibiotic therapy  better according to
the results of culture and sensitivity tests.
B- Surgical treatment
a. Myringotomy operation in case of intact tympanic membrane.
b. Cortical mastoidectomy operation in case of:
• Failure of conservative treatment (antibiotics & myringotomy ) for 48 hours.
•  Mastoid abscess.
•  Mastoiditis with other cranial or intra-cranial complication.
 Bezold's abscess
pus tunnels below the tip, deep to the
sternomastoid muscle in the neck.
 Zygomatic abscess :
above and in front of the auricle.
 Mastoid fistula
A fistula occurs when the abscess bursts through the
periosteum and soft tissues
Attic perforation
Tubo-tympanic disease

Tympanic membrane perforation :is central in pars tensa i.e.

surrounded by a complete rim of the tympanic membrane & does not
reach the annulus. . It has any size, any shape and smooth edges.
2) Tuning fork tests Conductive hearing loss.

INVESTIGATIONS:
1. Pure tone audiometry Mild or moderate conductive hearing loss
due to
a) tympanic membrane perforation &
b) impaired mobility of the ossicles by the middle ear discharge and
thickened mucosa.
The ossicles are usually intact.
2. CT scan Shows accurate extent of the disease.
3. Culture and sensitivity tests  of the ear discharge.
TREATMENT
Tympanoplasty operation after control of infection.
A. Control of infection
1. Regular aural toilet to remove the ear discharge by suction or dry mopping with a
cotton
tipped probe.
2. Antiseptic ( as 2% acetic acid ) & antibiotic / steroid ear drops; avoid ototoxic
drops.
3. Antibiotics therapy  better according to the results of sensitivity tests.
4. Avoid re-infection. How?
a) Treatment of predisposing factors as adenoiditis and sinusitis.
b) Avoid entry of water into the ear canal during head wash and swimming. How?
By putting an ear plug or a piece of cotton soaked with an ointment.
B. Tympanoplasty with or without mastoidectomy operation
1. Tympanoplasty operation It has two
aims
a) Healing : by eradication of irreversibly diseased tissues in the middle ear as
granulations and
polypi.
b) Hearing : by reconstruction of the middle ear hearing mechanism
2. Cortical mastoidectomy operation :is performed when conservative treatment fails
to control the otorrhoea. The operation is called tympanoplasty with mastoidectom.
RUPTURE OF THE TYMPANIC MEMBRANE
 GLOMUS TUMOUR
1- Pulsating tinnitus is the earliest manifestation of
glomus tympanicum then conductive deafness
INVESTIGATIONS
1. CT scan To assess condition of the middle ear and inner ear.
2. Audiological evaluation Conductive hearing loss.
TREATMENT
1. Hearing aid : for infants with bilateral atresia It is fitted as early as possible.
2. Surgical reconstruction of the external auditory canal  if the auditory system
has normal structure ( by CT scan ) and normal function by audiological
evaluation ).
Foreign Body (FB) Impaction
INCIDENCE : Most commonly children.
TYPES
1- Animate foreign bodies  as flies and larvae.
2- Inanimate foreign bodies
a) Non-vegetable foreign body  as bead and button.
b) Vegetable foreign body  as bean and pea. It swells with water impacted.
SYMPTOMS
1. History of foreign body insertion  may be present.
2. Hearing loss  when the foreign body occludes the external canal.
3. Animate foreign body  causes severe irritation and noise in the ear.
SIGN
The foreign body is easily detected on clinical examination. (see below, glass
bead &
insect FB)
TREATMENT
1- Animate foreign body  is killed by alcohol or oil before removal by
ear wash or instruments ( as
hooks and forceps ).
2- Inanimate foreign body
a) Non-vegetable foreign body  can be removed by ear wash or
instruments as hooks and forceps
b) Vegetable foreign body  is removed by instruments ( as hooks and
forceps ).
Ear wash is contraindicated because the
foreign body may swell  impacted.
N.B. General anaesthesia  is necessary in case of impacted foreign
body and uncooperative patients as children.
COMPLICATION
Injury of the external canal or the tympanic membrane. May be
produced by the
foreign body, or during unskilled attempts of removal.
WAX (CERUMEN) IMACTION
TREATMENT
Removal by ear wash or instruments. If the wax is hard it is softened before ear wash
By a wax solvent as hydrogen peroxide or
glycerine bicarbonate ear drops.

Ear Wash
INDICATIONS: 1- Wax accumulation.
2- Otomycosis.
3- Foreign body in the external auditory canal.
CONTRAINDICATIONS:
1) Impacted and large vegetable foreign body in the external auditory canal.
2) Tympanic membrane perforation ( traumatic or inflammatory ).
3) Bacterial otitis externa.
TECHNIQUE:
1- The patient is seated with a basin under his ear ( to avoid soiling his clothes ).
2- The auricle is pulled upwards and backwards ( to straighten the external auditory
canal )
3- The used water should be sterile ( to avoid infection ) and at body temperature
( to avoid caloric stimulation of the inner ear ).
4.The jet of water should be gentle and is directed towards the postero-superior wall
of the external auditory canal ( to avoid injury of the tympanic membrane ).
5- The external auditory canal is dried and examined.
EAR WASH
OTITIS MEDIA WITH EFFUSION (Secretory Otitis Media)
DEFINITION
Accumulation of a non-purulent sero-mucoid effusion
in the middle ear.
INCIDENCE
The commonest cause of conductive hearing loss in children.
PATHOGENESIS
a) Eustachian tube obstruction or dysfunction ,improper middle ear
ventilation development of negative middle ear pressure. The middle
ear mucosa tries to equalize this negative pressure by production of an
effusion which consists of
 transudate  from the blood vessels
 mucus  due to increased activity of themucus glands and goblet
cells.
AETIOLOGY
1- Eustachian tube obstruction
a. Nasopharyngeal oedema  due to infection, allergy or radiotherapy.
b. Nasopharyngeal tonsil hypertrophy i.e. adenoids.
c. Nasopharyngeal tumours.
2- Eustachian tube muscles dysfunction: Cleft palate and paralysed palate.
3- Inadequate treatment of acute otitis media
 Inadequate antibiotic therapy ( improper antibiotic,
 inadequate dose or short course )  the infection is inactivated, but not resolved.
SYMPTOMS
1. Hearing loss and tinnitus.
2. A bubbling sound may be heard in the ear.
SIGNS
a- Speculum examination The tympanic membrane shows
i. Signs of retraction ( due to negative middle ear pressure ) 
a. the handle of malleus appears shortened ( i.e. fore_x0002_shortened )
b. the lateral process of malleus is prominent,
c. the cone of light is distorted
d. its mobility is restricted ( by Siegle’s speculum or pneumatic otoscope) .
ii. Signs of middle ear effusion :
a) its colour is yellow to dull grey,
b) fluid level ( called hair line ) may appear as biconcave line &air bubbles may be
present.
c)Tuning fork tests Conductive hearing loss.
INVESTIGATIONS
i. Pure tone audiometry Conductive hearing loss.
ii. Tympanometry Type B i.e. flat curve  diagnostic.
TREATMENT
Conservative treatment
a) Treatment of predisposing factors.
b) Antibiotics therapy  to prevent recurrent infection.
c) Auto-inflation of the eustachian tube by chewing gum and Valsalva’s
manoeuvre i.e. forced expiration with both mouth and nose closed.
d) Corticosteroids and mucolytics controversial.
Surgical treatment : How? Myringotomy and insertion of a ventilation
tube. The tube is either:
a) temporary ( i.e. is extruded spontaneously after 3 – 6 months ) as
grommet tube, or
b) permanent as T - tube. When? After failure of conservative treatment
for several weeks … Why? To ventilate and drain the middle ear i.e. it is a
substitute for the eustachian tube.
 Adult patient with unilateral O.M should suspect nasopharyngeal
carcinoma untill proved otherwise
Used for surgical ttt of secretory O.M
T- tube in cleft palate or pararlysed palate
GLOMUS TYMPANICUM
INCIDENCE
Frequency Rare.
Age Commonly 40 - 50 years.
Sex More common in females.
ORIGIN
Arises from the non-chromaffn paraganglionic tissues ( chemo-receptor
which lie
a) on the promontory  called glomus tympanicum, or
b) on the jugular bulb ( near the floor of the middle ear ) called glomus jugulare.
PATHOLOGY
A highly vascular benign tumour.
BEHAVIOUR
Although microscopically benign  it is an aggressive locally destructive tumour
CLINICAL PICTURE
A- Otological manifestations
1- Pulsating tinnitus  the earliest manifestation of glomus tympanicum.
2- Bloody otorrhoea  when it perforates the tympanic membrane
3- Speculum examination 
a) Initially a red mass behind an intact tympanic membrane. producing a
characteristic sun-rising appearance.The mass blanches on compression by a
pneumatic otoscope or Siegle’s speculum  called Brown’s sign
b) When the tumour perforates the tympanic membrane a red vascular
mass appears in the external auditory canal. It bleeds profusely on
touch.
4- Gradual progressive hearing loss initially conductive,then becomes
mixed after invasion of the inner ear.
B- Neurological manifestations
1) Jugular foramen syndrome ( i.e. IX, X and XI cranial nerves paralysis )
theearliest manifestation of glomus jugulare.
2) Facial and hypoglossal nerves paralysis later on.
INVESTIGATIONS
1) CT scan & MRI To assess tumour extension.
2) Angiography & MR angiography To cofirm the
diagnosis and show the feeding vessel.
3) Biopsy Better avoided , because it may cause profuse
bleeding.
TREATMENT:
Surgical excision. Better after embolization of the feeding vessel in order
to decrease
Pneumatic otoscope
Left facial nerve paralysis
CLINICAL PICTURE OF MOTOR
FACIAL NERVE PARALYSISSYMPTOMS
1. Inability to close the eye firmly.
2. Deviation of the angle of the mouth.
3. Food collects between the cheek and teeth.
4. Hyper-acusis ( phonophobia ) i.e. increased sensitivity to loud sounds.
EXAMINATION
A. Motor tone ( i.e. at rest )
1) Loss of forehead corrugations ( occipito_x0002_frontalis ).
2) Loss of the naso-labial fold ( levator anguli oris ).
3) Drooping of the angle of the mouth ( levator anguli oris ).
4) Drippling of saliva ( orbicularis oris ).
B. Motor power ( i.e. during active movements )
1) Inability to elevate the eyebrow ( occipito-frontalis ).
2) Inability to close the eye firmly ( orbicularis occuli ).
3) Inability to whistle ( orbicularis oris ).
4) Inability to blow ( buccinator ).
5) Deviation of the mouth to the healthy side on smiling ( levator anguli
oris ).
CT- scan of temporal abscess
CLINICAL PICTURE
1) Invasion stage :Localized area of encephalitis. Fever, headache,
anorexia and malaise.
2) Latent stage
Formation of an abscess surrounded by a capsule of glial tissue.
a) The above manifestations improve and the patient feels and looks well.
b) Its duration is variable.
3) Manifest stage The abscess cavity enlarges.
A. Manifestations of increased intra-cranial pressure :
Severe persistent headache. ,Projectile vomiting i.e. not related to meals
and not preceded by nausea. ,Papilloedema  blurred vision , Marked
increase of the intra-cranial pressure pressure on the medullary centers :
slow pulse, slow respiration, subnormal temperature and slow
cerebration.
B. Localising manifestations
I. Temporal lobe abscess:
• Contralateral hemiplegia : due to pressure on the cortical motor area.
• Contralateral hemi anaesthesia due to pressure on the cortical sensory
area.
• Homonymous hemianopia i.e. loss of vision in the temporal
visual fields due to pressure on the optic radiation.

• Hallucinations of smell and taste ( uncinate fits ) due to

pressure on uncinate gyrus.
• Nominal aphasia i.e. inability to name common objects due to
pressure on the speech centres, if the abscess is in the
dominant hemisphere
patient with discharging ear then fever , rigors and
sweating ....lateral sinus thrombophelebitis
PATHOLOGY
1- Peri-phlebitis Localized inflammation
around the sinus i.e. peri-sinus abscess.
2- Endo-phlebitis The inflammation spreads to the sinus intima  formation of
athrombus.
3- Complications
a) Occlusion of the sinus lumen forming  an occluding thrombus.
b) Spread of the thrombus proximally and distally forming  a propagating
thrombus.
c) Infection of the thrombus forming  an infected thrombus which breaks down
forming
 showers of septic emboli which enter the circulation.
CLINICAL PICTURE
A- Manifestations of blood infection
1) Fever either:
a) pyaemic i.e. intermittent ( malaria-like ). Occurs in irregular attacks, between
which the patient is relatively well. The rise of temperature is accompanied
by rigors and is due to escape of septic emboli to the blood stream,
b) septicaemic i.e. continuous and high ( typhoid-like ).
2) Headache, anorexia and malaise..
3) Pallor due to anaemia as a result of septicaemia and toxaemia
B- Manifestations of thrombus extension
1) Downwards : to the internal jugular vein ,the vein becomes tender and cord
like.
2) Upwards : to the superior sagittal sinus ,impedance of CSF drainage ,increased
intra-cranial pressure i.e. otitic hydrocephalus ,severe headache, projectile
vomiting, blurred vision and papilloedema.
3) Forwards :to the superior petrosal sinus, to the cavernous sinus , lid oedema,
conjunctival chemosis , proptosis, papilloedema, ptosis, dilated pupil and
ophthalmoplegia.
4) Laterally : to the mastoid emissaryvein , tender oedematous swelling over the
mastoid process called Griesinger’s sign.

INVESTIGATIONS
1) Magnetic resonance angiography :Diagnostic.
2) Blood culture during an attack of fever.
TREATMENT
1) Medical treatment
a) Antibiotic therapy  better according to the results of culture and sensitivity
tests.
b) Anti-coagulant therapy  in the presence of manifestations of thrombus
extension.
- Cavernous Sinus Thrombo-phlebitis
DEFINITION
Inflammation of the cavernous venous sinus.
CLINICAL PICTURE
1- Manifestations of blood infection :High fever, rigors and poor general condition.
2- Orbital manifestations
a) Manifestations of venous obstruction Lid oedema,conjunctival chemosis, proptosis
and papilloedema. Why? Because cavernous sinus thrombo-phlebitis Þ impairment of drainage
of the ophthalmic veins Þ orbital oedema.
b) Manifestations of cranial nerves paralysis Ptosis, dilated pupil and ophthalmoplegia. Why?
Due to paralysis of the 3rd, 4th & 6th cranial nerves which pass through the cavernous sinus.
3- The other side is commonly involved. Why? Due to
spread of infection along the inter-cavernous communicating sinuses.
INVESTIGATIONS
MRI and MRA ( angiography ) Diagnostic.
TREATMENT
1- Massive antibiotic therapy. The antibiotic should cross the blood brain barrier as
cephalosporins ( 3rd generation ), chloramphenicol and metronidazole.
2- Anti-coagulants Þ heparin.
2- Surgical drainage of the paranasal sinuses infection Þ when the patient’s general condition
allows.
PROGNOSIS
Poor and high morbidity ( permanent loss of vision & ophthalmoplegia ) and mortality rates.
MRI-T1
Cerebellar abscess
a) Equilibrium disorders:
 Vertigo and nystagmus.
 Ataxia ( i.e. staggered gait ) and positive Romberg’s test.
b) Motor disorders:  Ipsilateral intention tremors.
 Ipsilateral muscle incoordination  dysmetria on finger - to -
nose test.
 Ipsilateral dys-diadokokinesia i.e. inability to perform rapid
alternating
movements as pronation and supination of the forearm.
c) Staccato ( syllabic ) speech i.e. each syllable is pronounced
as if it is a
separate word.
Meningitis
secondary to
O.M
Meningitis secondary to O.M
Nose
• By nasal speculum: -
Examine for discharge, crusts, deviations and swellings.
• Visible structures:
Anterior part of:
 Nasal septum
 Floor of the nose
 Middle and inferior turbinate
 Middle and inferior meatus.
• It is a recent method for inspecting the nose with a
• rigid endoscope.
• It gives brilliant illumination & excellent
• visualization.
• INCIDENCE
The nasal bones are one of the most commonly fractured bones in the body.
• TYPE
Usually compound i.e. accompanied by laceration of the skin and / or the nasal mucosa.
• AETIOLOGY
Direct trauma to the nose Ÿ as a blow or car accident.
• SYMPTOMS
1) History of trauma.
2) Pain Ÿ transient at the time of injury.
3) Epistaxis Ÿ due to injury of the nasal mucosa.
4) Deformity Ÿ due to oedema and displacement of the nasal bones.
5) Nasal obstruction Ÿ due to septum deviation and haematoma
• SIGNS
1- Inspection
a) External swelling Ÿ due to oedema.
b) Deformity Ÿ due to external swelling and displacement of the nasal bones.
x When the blow comes from the front Ÿ the nasal bones are depressed.
x When the blow comes from the side Ÿ the nasal bones are deviated.
c) Black eye Ÿ due to peri-orbital ecchymosis.
2- Palpation: -Tenderness and crepitus Ÿ on palpation of the nasal bones.
3- Anterior rhinoscopy
a) Mucosal lacerations Ÿ may be present.
b) Septum deviation and haematoma Ÿ may be present.
• X - RAY : Of medico-legal importance.
 TREATMENT
a. Recent cases i.e. first hours, before development of oedema. Ÿ
Immediate reduction either manually or with instrument as Walsham’ s forceps followed by
fixation of bones with splints.
2) Intermediate cases i.e. when oedema masks the landmarks. Ÿ
Wait for one week ( till oedema subsides ) Ÿ treat as recent cases.
a. Late cases i.e. mal-united fracture Ÿ Rhinoplasty operation to re-fracture Ÿ reduce Ÿ fixate
the nasal bones.
MRI - T1( CSF ‫)اسود‬
CONGENITAL CHOANAL
ATRESIA
CONGENITAL CHOANAL ATRESIA
• Congenital closure of the posterior nasal opening (choana) which may be:
- Unilateral (75%) or bilateral (25%).
- Bony (90%) or membranous (10%).
- Complete or incomplete.
• Symptoms:
- Unilateral: usually asymptomatic at birth and presents later in life by:
x Unilateral persistent nasal obstruction
x Unilateral persistent nasal discharge.
- Bilateral: presents as an emergency birth because the neonate is obligatory nasal breather
during the first few weeks Why? Because the larynx is high and the epiglottis lies behind the
soft palate.
- Cyclic asphyxia: The neonate strives to breath while the lips are tightly closedÆcyanosis Æ
increased CO2 Æ muscle relaxationÆ Mouth opens with a few gulping respirationÆ the mouth
closes again and so on. (‫)مهمه‬
- If the neonate is not properly managedÆ Death from respiratory obstruction
- If the neonate passes asphyxia, there may be
x Bilateral persistent nasal obstruction
x Bilateral persistent mucoid nasal discharge
• Signs:
- Air flow test: no fogging
- Failure of rubber catheter or colored drops to pass through the nose to the pharynx.
- Endoscopic examination shows closure of the posterior choana.
• Investigations:
- CT scan.
- Plain X ray after instillation of lipidol
• Treatment:
- Bilateral cases ( emergency case)
- Insert and maintain an oral airway or McGovern nipple which is a baby bottle nipple with an
open tip or use an oropharyngeal airway.
Surgical:
Early:
- Perforation of the atretic plate by sinuscope.
- Endotracheal intubation or tracheostomy may be needed
Late:
- Transpalatal repair.
- Transnasal excision by sinuscope.
If unilateral in old child and present with offensive discharge : foreign body
 McGovern nipple

baby bottle nipple with an open tip used in treatment of Bilateral choanal atresia
Modified Oropharyngeal
airway
‫نفس استخدام الي فوق‬
FOREIGN BODY IMPACTION
• INCIDENCE
Most commonly children.
• TYPES
1) Vegetable foreign bodies Such as pea and bean. Their fatty acids are irritating Ÿ inflammatory
reaction.
2) Non-vegetable foreign bodies Such as button and bead and disc battery
• SYMPTOMS
1) Unilateral offensive nasal discharge; may be blood-stained Ÿ pathognomonic.
2) Unilateral persistent nasal obstruction.
• SIGNS
1) Unilateral offensive purulent nasal discharge; may be blood-stained.
2) The foreign body is seen by clinical or endoscopic examination.
• COMPLICATIONS
1. Rhinitis and sinusitis.
2. Formation of rhinolith i.e. a nasal stone. How? Due to precipitation of calcium salts from the
nasal secretions on a foreign body, blood clot or inspissated mucus.
• TREATMENT
x Removal Ÿ by a hook or forceps.
x General anaesthesia Ÿ is necessary if the patient is uncooperative .
Fracture nasal bone
‫لما تيجي الصورة دي اخد بالي المريض في انهي مرحله يعني معاه‬
Edema ‫وال ال‬
‫هنا مافيش يبقي هنختار اول حاجه‬
Recent cases i.e. first hours, before development of oedema. Ÿ
Immediate reduction either manually or with instrument as Walsham’ s forceps followed by
fixation of bones with splints.
‫قولته فوق‬
nasal examination and also examination of other ENT organs.
X- ray Fracture nasal bone CT Fracture nasal bone
X - RAY : Of medico-legal importance
Deviated septum is corrected by Ashe’s forceps
Reduction of fracture by Walsham forceps
ACUTE SINUSITIS
• DEFINITION
Acute inflammation of the muco-periosteal lining of one or more of the paranasal sinuses.
• CAUSATIVE ORGANISMS
1- Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis.
2- Anaerobic organisms Ÿ in maxillary sinusitis of dental origin.
• ROUTES & SOURCES OF INFECTION
1- Nasal route
a) Infection reaches the sinus via its ostium.
b) Acute rhinitis Ÿ commonest.
c) Swimming and diving in polluted water.
d) Nasal packing.
e) Nasal foreign body.
2- Dental route Causes maxillary sinusitis.
a) Infection of the 2nd premolar or 1st molar teeth.
b) Oro-antral fistula.
3- External route
a) Compound fracture of the sinus.
b) Penetrating foreign bodies as gunshots.
• SYMPTOMS
A- General symptoms Fever, headache, anorexia and malaise.
B- Local symptoms
Nasal obstruction Vaso-active i.e. alternates from side to side.
Nasal discharge
a) muco-purulent or purulent Ÿ according to the severity of infection,
b) scanty or profuse Ÿ according to the degree of obstruction of the sinus ostia,
c) post-nasal or nasal in sinusitis of the anterior group of sinuses & post-nasal in sinusitis of
the posterior group of sinuses,
d) offensive Ÿ in maxillary sinusitis of dental origin ( anaerobic organisms ).
3- Hyposmia or anosmia Due to nasal obstruction.
Dental maxillary sinusitis causes cacosmia.
4- Facial pain : Severe and increases by straining & leaning forwards. It is due to accumulation
of discharge in the sinus under tension ( tension pain)
a) Ethmoidal sinusitis Ÿ between the eyes.
b) Maxillary sinusitis Ÿ over the cheek.
c) Frontal sinusitis Ÿ over the forehead. It is characteristically
periodic i.e. starts in the morning, decreases at noon and subsides in
the afternoon.
d) Sphenoidal sinusitis Ÿ behind the eye
SIGNS
1. General signs Fever; higher in children.
2. External examination: Tenderness over the affected sinus
a) Ethmoidal sinusitis Ÿ over the medial canthus.
b) Maxillary sinusitis Ÿ over the cheek.
c) Frontal sinusitis Ÿ over the floor of the sinus ( at the roof of the orbit )
3. Anterior rhinoscopy
- Swelling and hyperaemia of the nasal mucosa Ÿ in the middle meatus and / or superior
meatus. - - Muco-purulent or purulent discharge Ÿ
a. in the middle meatus Ÿ in anterior ethmoidal, maxillary and frontal sinusitis.
b. in the superior meatus Ÿ in posterior ethmoidal sinusitis.
c. in the spheno-ethmoidal recess Ÿ in sphenoidal sinusitis.
INVESTIGATIONS
A- Radiological examination
Usually not necessary because the diagnosis
evident by clinical examination.
1) Plain x-ray Opacity or air-fluid level.
2) CT scan Used only in case of failure of
medical treatment Æ for proper assessment
of the disease & in case of suspected
complications.
B- Culture and sensitivity tests of the discharge
TREATMENT
1- Medical treatment
A- General measures
x Antibiotics for 10 – 14 days.
x Decongestants.
x Supportive & symptomatic measures Ÿ rest,
ample fluid intake, analgesics and antipyretic
B- Local measures
1) Nasal decongestants.
2) Steam inhalation.
2- Surgical treatment When? Only:
a) when medical treatment fails &
b) when complications threaten or occur. Better avoided because it may lead to osteitis or
osteomyelitis of the sinus wall.

How? Endoscopic widening of the natural ostium of the affected sinus.

Why? To restore normal ventilation and drainage of the affected sinus through its natural ostium
How?
a) Maxillary sinusitis Ÿ endoscopic middle meatal antrotomy.
b) Frontal sinusitis Ÿ endoscopic frontal sinusotomy.
c) Sphenoidal sinusitis Ÿ endoscopic sphenoidotomy.
d) Ethmoidal sinusitis Ÿ endoscopic ethmoidectomy
ATROPHIC RHINITIS
AETIOLOGY
A- Primary atrophic rhinitis No cause can be detected. It may be due to
1) Endocrinal disturbance Oestrogen deficiency is suggested because Ÿ it is common in females,
usually starts at puberty and symptoms increase during menses.
2) Auto-immune disturbance.
3) Autonomic disturbance Nasal sympathetic over-activity Ÿ vaso-constriction & ischaemia
4) Infection Suppurative sinusitis in childhood.
B- Secondary atrophic rhinitis A cause can be detected.
1- Infective Nasal granulomata as scleroma
2- Iatrogenic
a) Radiotherapy.
b) Total surgical excision of the inferior turbinate
PATHOLOGY
1) End-arteritis or peri-arteritis of the nasal terminal arterioles Ÿ ischaemia.
2) Atrophy of the nasal epithelium with destruction of the cilia Ÿ stasis of nasal secretions.
3) Atrophy of the nasal glands Ÿ diminished nasal secretions Ÿ formation of crusts.
4) Atrophy of the nerves Ÿ anosmia and dullness of the sensation of air.
5) Atrophy of the bony turbinates Ÿ wide roomy ) nasal cavity.
6) Secondary infection by proteolytic saprophytic organisms as Klebsiella ozaena Ÿ putrefaction
of the crusts Ÿproduction of a foul odour ( called ozaena )
SYMPTOMS
1) Nasal discharge Ÿ greenish, crusty & has foul odour.
2) Nasal obstruction ( inspite of the roomy nose ) Ÿ due to a) accumulation of crusts or dullness
of the sensation of air as a result of atrophy of the sensory nerves.
3) Anosmia Ÿ due to atrophy of the olfactory mucosa Ÿ the patient does not smell his own bad
odour.
4) Epistaxis Ÿ due to separation of the crusts.
SIGNS
1) The nasal cavity Ÿ is roomy and lined with greenish offensive crusts.
2) The nasal mucosa Ÿ is pale, dry and atrophic.
3) The turbinates Ÿ are atrophic.
TREATMENT
A- Medical treatment
Treatment of the cause Ÿ in case of secondary atrophic rhinitis.
1) Nasal douching with alkaline nasal lotion Ÿ to separate the crusts.
2) Oily nasal drops as paraffin ( lubricant ) Ÿ to prevent adherence of the new crusts.
3) Menthol nasal drops Ÿ to mask the foul odour.
4) Glucose 25% in glycerine nasal pack Ÿ to diminish foetor. How? It inhibits
growth of the proteolytic saprophytic organisms which are responsible for the foul
odour..
5) Local oestrogen and oral potassium
iodide Ÿ to stimulate the nasal glands.
B- Surgical treatment
Narrowing the roomy nasal cavities till the nasal mucosa regenerates.
When? Failure of medical treatment to control the patient’s symptoms. How?
Submucosal insertion of a graft as fat, bone, cartilage or teflon.
Closure of the nostril(s) for 6 – 24 months Ÿ by skin flaps from the vestibule.
Histopathology of RHINOSCLEROMA
Frequency The commonest specific infective chronic rhinitis ( granuloma ) in Egypt.
it is endemic in some areas as El-Sharkeyah and El-Kalyobeyah.
Sex & Age Commonly females 15 – 25 years.
Site It starts in the nose ( called rhino-scleroma ) and may spread to Ÿ the pharynx )called
pharyngo-scleroma ), the larynx ( called laryngo-scleroma )
and the lacrimal passages ( called dacryoscleroma ).
AETIOLOGY
Causative organism Klebsiella Rhinoscleromatis ( Frisch bacillus )
Mode of transmission Unknown. It is only slightly contagious.
PATHOLOGY
1. Stage of invasion Similar to acute non-specific rhinitis.
2. Active stage Either atrophic or nodular form. Both may occur simultaneously.
a. Atrophic form Similar to atrophic rhinitis.
b. Nodular form The submucosa is infiltrated by granulomatous tissue characterized by:
i. Mikulicz cells Ÿ large foamy cell with a central nucleus and vacuolated cytoplasm.
The vacuoles contain the Frisch bacilli Ÿ gram negative intra-cellular diplo-bacilli.
These cells are pathognomoic of scleroma.
ii. Russel bodies Ÿ bright red oval or rounded bodies devoid of nuclei. They
represent plasma cells undergoing hyaline degeneration.
iii. Plasma cells and lymphocytes.
3. Fibrotic stage
Healing occurs by extensive fibrosis.
CLINICAL PICTURE
1- Stage of invasion Similar to a prolonged attack of acute non-specific rhinitis that does not
respond to the usual lines of treatment.
2- Either atrophic or nodular form. Both may occur simultaneously.
Atrophic form Æ Similar to atrophic rhinitis.
Nodular form
ƒ Bilateral discrete reddish non ulcerating firm nodules appear at the muco-
ƒ cutaneous junction between the nasal cavity and the vestibule.
They spread and coalesce Ÿ fill the nasal cavities, broaden the nose.
3- Fibrotic stage Concentric narrowing of the nasal cavities
INVESTIGATIONS
x Biopsy Shows the typical histological picture of scleroma.
x Culture and sensitivity tests.
TREATMENT
A- Medical treatment
x Antibiotics Ÿ rifampicin ( 300 mg bd. ), quinolones, 3rd generation of cephalosporins or better
according to the results of sensitivity tests.
x In the atrophic stage Ÿ similar to atrophic rhinitis.
B- Surgical treatment
x Removal of the granulomatous masses or fibrous tissue Ÿ better by laser surgery.
x Rhinoplasty operation Ÿ to correct nasal deformities
AETIOLOGY
Prolonged obstruction of the natural ostium of the paranasal sinuses in :
1- Anatomical conditions as deviated nasal septum or enlarged middle turbinate.
2- Pathological conditions as nasal allergy or nasal polypi.
3- Incomplete resolution of acute sinusitis due to :
a) inadequate treatment ( inadequate dose or short course of antibiotics therapy ),
b) resistant organisms or recurrent infections or
c) low patient’s resistance.
CAUSATIVE ORGANISMS
Mixed aerobic and anaerobic organisms.
SYMPTOMS
Similar to symptoms of acute sinusitis; but
1- General symptoms Ÿ absent.
2- Local symptoms Ÿ pain is dull. It is due to
absorption of air from the sinus as a result of obstruction of its ostium vacuum pain ).
SIGNS
Anterior rhinoscopy Muco-purulent or purulent discharge Ÿ similar to acute sinusitis.
INVESTIGATIONS
A. Radiological examination
1- Plain x-ray Of limited value. It shows Ÿ opacity or thickening of the mucosal lining.
2- CT scan Should be done because it shows. opacity or thickening of the mucosal lining of the
affected sinus
B. Culture and sensitivity tests of the discharge
TREATMENT
1- Medical treatment
A- - General measures
x Antibiotics, better according to culture and sensitivity tests.
x Mucolytics.
B- Local measures
x Nasal decongestants.
x Alkaline nasal lotion.
2- Surgical treatment When?
x When medical treatment fails
x When complications threaten or occur.
How? Functional endoscopic sinus surgery ( FESS ). Why? To restore normal ventilation and
drainage of the affected sinuses through their natural ostia Ÿ allows
the sinus mucosa to return to its normal functioning state. How?
1. Endoscopic removal of the cause of ostium obstruction as polypi and enlarged middle
turbinate.
2. Endoscopic widening of the natural ostium of the affected sinus. How?
a) Maxillary sinusitis Ÿ endoscopic middle meatal antrotomy.
b) Frontal sinusitisŸ endoscopic frontal sinusotomy.
c) Sphenoidal sinusitis Ÿ endoscopic sphenoidotomy.
d) Ethmoidal sinusitis Ÿ endoscopic ethmoidectomy.
SEPTAL HEMATOMA
DEFINITION
Collection of blood Ÿ between the septal cartilage and its perichondrium.
AETIOLOGY
a. Direct trauma to the nose Ÿ as a blow or car accident.
b. Septum operation Ÿ as submucous resection and septoplasty operations.
SYMPTOMS
1- History of trauma.
2- Bilateral persistent nasal obstruction.
SIGN
Bilateral smooth red soft swelling of the septum.
COMPLICATION
1- Cartilage necrosis Ÿ supra-
tip depression of the nasal dorsum.
2- Secondary infection Ÿseptal abscess.
TREATMENT
1) Antibiotics.
2) Incision and drainage of the Haematoma.
3) Tight nasal packing Ÿ to avoid re-collection of blood.
ABSCESS OF THE SEPTUM
DEFINITION
Collection of pus Ÿ between the septal cartilage and its perichondrium.
AETIOLOGY
Secondary infection of septal haematoma.
SYMPTOMS
A- General symptoms
Fever, headache, anorexia and malaise.
B- Local symptoms
1- Severe throbbing nasal pain.
2- Bilateral persistent nasal obstruction.
SIGNS
1. fever .
2. Tender nasal dorsum.
3. Bilateral smooth red tender soft swelling of the septum.
COMPLICATIONS
1- Cartilage necrosis Ÿ supra-tip depression of the nasal dorsum.
2- Cartilage and mucosal necrosis septal perforation.
3- cavernous sinus thrombophlebites ‫مهم‬
TREATMENT
Similar to septal haematoma.
BILATERAL NASAL POLYPI
DEFINITION
Bilateral multiple polypi which arise from the ethmoidal sinuses.
INCIDENCE
Frequency Much more common than the antro-choanal polyp.
Age Adults.
Side Bilateral.
Number Multiple.
AETIOLOGY
1- Allergic rhinitis Ÿ commonest.
2- Chronic ethmoidal sinusitis.
3- Allergic fungal sinusitis.
SYMPTOMS
1- Bilateral persistent nasal obstruction.
2- Bilateral mucoid nasal discharge.
SIGN
Bilateral multiple pale grayish glistening smooth soft pedunculated ( grape-like ) masses Ÿ
which arise from the middle and superior meati. In severe cases Ÿ the polypi .
may protrude through the anterior nares.
CT SCAN
Shows the extent of the polypi.
BEHAVIOUR
Recurrence Common.
TREATMENT
A- Surgical treatment The main line of treatment.
1- Ethmoidectomy operation ( better endoscopic ) Ÿ treatment of choice.
2- Polypectomy i.e. excision of the polypi Ÿ high recurrence rate.
B- Medical treatment
1- Systemic steroids Ÿ for small polypi ( called medical polypectomy ).
2- Anti-histaminics and local steroid sprays Ÿ post-operatively to avoid
recurrence
ANTROCHOANAL POLYP
DEFINITION
Unilateral single polyp which arises within the maxillary sinus ( antrum ) Ÿ
then passes through its ostium to enter the nasal cavity Ÿ then passes backwards through the
choana to enter the
nasopharynx.
INCIDENCE
Frequency Much less
common than the
ethmoidal polypi.
Age Teenagers.
Side Unilateral.
Number Single.
AETIOLOGY
Unknown. May be inflammatory or a retention cyst.
SYMPTOMS
1- Unilateral persistent nasal obstruction.
2- Unilateral mucoid nasal discharge.
SIGN
Unilateral single pale grayish glistening smooth soft pedunculated mass Ÿ which arises from the
middle meatus Ÿ passes backwards to the choana
CT SCAN
Diagnostic.
BEHAVIOUR
Recurrence Uncommon.
TREATMENT Always surgical.
1) Endoscopic polypectomy with widening of the natural ostium of the maxillary sinus Ÿ
treatment of choice.
2) Polypectomy i.e. excision of the polypi Ÿ high recurrence rate.
3) Radical antrum ( Caldwell-Luc ) operation Ÿ may be done in recurrent cases.
 NASOPHARYNGEAL ANGIOFIBROMA
Teenager with sever epistaxis
. Cancer maxillary sinus
1- Nasal manifestations
Nasal obstruction.
Offensive nasal discharge.
Epistaxis.
Ulcerating friable nasal mass.
2- Oral manifestations
Persistent dental pain in the upper premolar and molar teeth.
Loose teeth.
Palatal swelling and ulceration.
Oro-antral fistula.
Trismus ( invasion of the pterygoid muscles in the pterygo-palatine fossa ).
3- Orbital manifestations
Proptosis Ÿ upward.
Epiphora ( invasion of the naso-lacrimal duct ).
Fixation of the eye ball Ÿ diplopia.
4- Facial manifestations
Cheek swellings
Facial paraesthesia ( invasion of the maxillary nerve in the pterygo-palatine fossa ).
5- Cervical manifestations
Enlarged submandibular & upper deep cervical lymph nodes ( late &
uncommon ).
INVESTIGATIONS
1- CT scan & MRI To assess tumour extension and lymph
nodes involvement.
2- Biopsy To confirm the diagnosis. It is obtained from the
nasal mass or endoscopically from the sinus.
3- Metastatic work-up Chest x-ray, brain CT scan, bone scan
& abdomen ultrasound.
TREATMENT Combined surgical excision and radiotherapy.
A- SURGICAL TREATMENT
1. Cancer maxillary sinus
a) Partial maxillectomy: When? When the tumour is limited to a part of the maxillary sinus. How?
Through lateral rhinotomy or mid-facial degloving.
b) Total maxillectomy: When? When the tumour involves the whole maxillary
sinus how? Throoough Furgeson incision to remove the Maxilla including the palate.
The palate is reconstructed by Dental prosthesis .
Adenoids
DEFINITION
Hypertrophy of the pharyngeal ( nasopharyngeal ) tonsil, sufficient to produce symptoms.
N.B. Adenoids is the commonest nasopharyngeal swelling.
INCIDENCE
Age Children.
AETIOLOGY
1) Physiological hypertrophy Occurs at the age of 3 - 8
years. Then, the pharyngeal tonsil gradually regresses in
size  to become atrophic at puberty.
2) Pathological hypertrophy Due to recurrent upper
respiratory infections.
SYMPTOMS
1- Bilateral nasal obstruction 
 Mouth breathing.
 Speech hypo-nasality.
 Difficult suckling in infants.
 Snoring and obstructive sleep apnea.
2- Bilateral nasal discharge
 Mucoid or muco-purulent  due to mechanical obstruction of the choanae.
 Nasal  excoriation of the nasal vestibule and upper lip.
 Post-nasal ( gummy egg white )  nocturnal cough,
 laryngismus stridulus and gastro-intestinal disturbances as loss of appetite and morning
vomiting.
SIGNS
 Posterior rhinoscopy Shows the adenoids, but is difficult. Digital
 palpation: condemned , as it is painfull
 Endoscopic examination The best.
INVESTIGATION
Lateral plain x-ray of the nasopharynx A soft tissue shadow (short arrow) narrowing the airway
(long arrow)  diagnostic.
COMPLICATIONS
1- Obstructive sleep apnea
2- Descending infections
3- Adenoids facies
TREATMENT
Adenoidectomy operation when adenoids is symptomatic or complicated.
Adenoids facies Due to under-development of the middle 1/3 of the face.
a) Nose Pinched nostrils.
b) Mouth Open mouth, short upper lip, protruding upper incisors, high arched palate
and receding mandible.
c) Face Idiot expressionless look
Inflatable balloon with anterior and posterior pack
Treatment :
A. Emergency treatment (1st Aid treatment) :
1. Position :
- Sitting with the head flexed and chin to chest (unless
shocked).
- Compress Little's area from outside by thumb and forefinger for 15 minutes, and apply
cold compresses on the bridge of the nose to induce reflex vasoconstriction.
- Cotton wool soaked in adrenaline, ephedrine or any nasal drops introduced in the nose with
the patient in the previous position.
2. Anterior nasal pack : if the first aids fail to control bleeding.
Can be done by :
a) A Vaseline gauze; A Vaseline gauze, 50-75 cm. long and 2cms. wide, introduced into the nose
in layers, from before backwards and from below upwards and is left for 24 hours.
b) Inflatable balloon.
c) Merocel sponge tampon
3. Posterior nasal pack :
a) A Foley’s catheter can be used as shown below or Inflatable balloon for posterior pack.
b) Posterior nasal pack using gauze sponge.
x A rubber catheter is introduced into the nose and taken out from the mouth.
x Tie its oral end to the thread of an already prepared post. nasal pack formed of a gauze
sponge folded into a tight roll ( about 5cmx3cm)
Pull the silk of the pack from the nose and push the pack itself behind the palate into the
nasopharynx.
x Tie the 2 threads ( coming from the nose over the collumella over a small piece of gauze( to
avoid necrosis of the collumella by the threads). Do anterior nasal pack and leave for 24-48
hours. Sedatives and antibiotics (to prevent 2ry infection).
B. CURATIVE :
Bleeding point cautery after local anesthesia by :
1- Electrical cautery
2- Caustics: silver nitrate 50-75% solution or chromic acid crystals.
3- Depending on the bleeding source, various vessels can be ligated through transnasal
a) endoscopic route, or by
b) a transmaxillary route in the pterygopalatine fossa.
4- Ligation of the external carotid artery (rare).
Stage of sub-periosteal abscess
Frontal osteomyelitis: Forehead fluctuant swelling
called Pott’s puffy tumour
CLINICAL PICTURE
1- Painless slowly growing bony swelling. When the bone is thinned out Ÿ
the swelling gives an egg-shell crackling sensation.
a) Ethmoidal mucocele Ÿ at the medial canthus.
2- Large mucocele produces proptosis.
a) Ethmoidal mucocele Ÿ proptosis is directed laterally.
INVESTIGATIONS
1- CT scan Diagnostic.
2- Plain x–ray Opacification and expansion of the
sinus.
TREATMENT
1- Surgical drainage of the sinus and the mucocele.
2- Treatment of the cause of obstruction in secondary mucocele
CLINICAL PICTURE
1- Painless slowly growing bony swelling. When the bone is thinned out Ÿ
the swelling gives an egg-shell crackling sensation.
a) Frontal mucocele Ÿ in the medial part of the roof of the orbit.
2- Large mucocele produces proptosis.
a) Frontal mucocele Ÿ proptosis is directed downwards and laterally
INVESTIGATIONS
1- CT scan Diagnostic.
2- Plain x–ray Opacification and expansion of the
sinus. The frontal sinus loses its characteristic scalloped appearance.
TREATMENT
1- Surgical drainage of the sinus and the mucocele.
2- Treatment of the cause of obstruction in secondary mucocele
Stage of orbital cellulitis
Pathology Inflammation of the orbital contents
without pus formation
Symptoms Fever, headache, anorexia, maliase and
pain in the eye.
Signs Conjunctival chemosis, limitation of eye movements, ophthalmoplegia and
diminution of vision. These manifestations are revrsible with treatment
1- Stage of sub-periosteal abscess
Pathology Collection of pus between the orbital periosteum and lamina papyracea.
Symptom Throbbing pain in the eye.
Signs Proptosis and lateral displacement of the globe. These manifestations are
revrsible with treatment
2- Stage of orbital abscess
Pathology Collection of pus within the orbit.
Symptoms Poor general condition, impaired vision & severe throbbing pain in the eye.
Signs Irreversible
ophthalmoplegia and irreversible /impairment of vision.
INVESTIGATIONS
1- CT scan Diagnostic.
2- Fundus examination.
COMPLICATIONS
Cavernous sinus thrombo-phlebitis. ‫مهمه‬
TREATMENT
1- Massive antibiotic therapy.
2- Surgical drainage of the paranasal sinuses and orbital infections.
Cavernous Sinus Thrombo-phlebitis
DEFINITION
Inflammation of the cavernous venous sinus.
CLINICAL PICTURE
1- Manifestations of blood infection
High fever, rigors and poor general condition.
2- Orbital manifestations
a) Manifestations of venous obstruction Lid oedema,
conjunctival chemosis, proptosis
and papilloedema. Why? Because cavernous sinus
thrombo-phlebitis Ÿ impairment of drainage of the
ophthalmic veins Ÿ orbital oedema.
b) Manifestations of cranial nerves paralysis Ptosis,
dilated pupil and ophthalmoplegia.
Why? Due to paralysis of the 3rd, 4th & 6th cranial
nerves which pass through the cavernous sinus.
3- The other side is commonly involved. Why? Due to
spread of infection along the inter-cavernous communicating sinuses
INVESTIGATIONS
MRI and MRA ( angiography ) Diagnostic.
TREATMENT
1- Massive antibiotic therapy. The antibiotic should cross the blood brain barrier
as cephalosporins ( 3rd generation ), chloramphenicol and metronidazole.
2- Anti-coagulants Ÿ heparin.
2- Surgical drainage of the paranasal sinuses infection Ÿ when the patient’s
general condition allows.
PROGNOSIS
Poor Ÿ high morbidity ( permanent loss of vision & ophthalmoplegia ) and mortality rates
CEREBROSPINAL FLUID RHINORRHEA
DEFINITION
Leakage of cerebro-spinal fluid from the nose.
SITE
1) A defect in the roof of the nasal cavity i.e. the cribriform plate.
2) A defect in the roof of the frontal, ethmoidal or sphenoidal sinuses.
AETIOLOGY
1) Congenital Bone dehiscence.
2) Traumatic
a) Surgical Ÿ intra-nasal, cranial ( skull base ) and intra cranial operations.
b) Accidental Ÿ skull base fracture.
3) Inflammatory Nasal syphilis.
4) Neoplastic Intra-nasal, cranial ( skull base ) and intracranial tumours.
5) Idiopathic No cause can be detected.
CLINICAL PICTURE
The rhinorrhoea is Ÿ
• unilateral,
• watery,
• clear colorless,
• salty Ÿ due to high chloride content,
• does not stiffen in a handkerchief Ÿ because it does not contain mucus &
• increases on straining & leaning forwards Ÿ due to increase of the intra-cranial pressure.
COMPLICATIONS
1- Meningitis Ÿ due to secondary infection.
2- Pneumo-cephalus ( i.e. air in the intra-cranial cavity ) due to forcible nose
blowing.
TREATMENT
A- Conservative treatment
1) Rest in the semi-sitting position Ÿ to
decrease the intra-cranial pressure.
2) Avoid straining & leaning forwards Ÿ to avoid increase of the intra-cranial
pressure.
3) Avoid nose blowing Ÿ to avoid pneumocephalus.
4) Avoid nasal drops and nasal packing Ÿ to avoid meningitis.
5) Antibiotics, which cross the blood brain barrier Ÿ to avoid meningitis.
B- Surgical treatment
z When? Failure of conservative treatment for 2 – 3 weeks.
z How? Closure of the defect by
A graft ( mucosa, fascia or muscle ) & /or
™ A mucosal flap ( from the septum ) through Ÿ an endoscopic, external or trans-
cranial approach
Oro-antral Fistula
DEFINITION
A fistula between the oral cavity and the maxillary sinus ( antrum ).
AETIOLOGY
1) Traumatic
a) Extraction of the 2nd premolar or 1st molar tooth ( commonest ).
b) Radical antrum operation Ÿ when the sub-labial incision does not heal.
2) Inflammatory
c) Osteomyelitis of the maxilla.
d) Nasal syphilis.
3) Neoplastic
e) Cancer maxilla.
f) Cancer palate.
SYMPTOMS
a) The patient can blow air from his nose into his mouth.
b) Unilateral nasal regurgitation of fluids.
c) Unilateral offensive nasal discharge Ÿ due to maxillary
d) sinusitis of dental origin.
SIGNS
a) The fistula can be seen through the oral cavity.
b) A probe can be introduced through the fistula from the oral cavity to the maxillary sinus
However, this may disturb healing of the fistula.
INVESTIGATIONS
Plain x-ray & CT scan Maxillary sinusitis.
TREATMENT
Early small fistula Direct suturing of the mucosal edges of the fistula.
Late or large fistula Surgical closure of the fistula by a buccal or palatal flap.
Treatment of maxillary sinusitis ( if present )
Radical antrum operation
Pharynx
Tongue depressor
 Tongue depressor
Wooden is preferred
TECHNIQUE:+
The patient  opens his mouth and breathe quietly through the mouth.
The examiner 
 uses a tongue depressor depress the tongue gently and firmly.The
tongue
depressor should be applied t the middle 1/3 of the tongue. Why?
 If applied to the posterior 1/3  induces a gag reflex.
 If applied to the anterior 1/3  the base the tongue bulges upwards 
obscures the view.

The structures seen by tongue depressor are:

 The palate ( hard palate, soft palate and uvula)
 Anterior and posterior pillars
 The tonsils
 The posterior oropharyngeal wall
‫الدكتور عداهم‬
The retro-pharyngeal space is a
connective tissue space.
 Lies behind the pharynx.
 Lies between the
buccpharyngeal fascia & the
prevertebral fascia.
 The two fasciae are attached
in the midline by a strong
median raphe  there is
right & left spaces.
 Each space contains one lymph node called the lymph node of Henle. These nodes drain
the
upper respiratory tract. They atrophy before the age of 5 years.
AETIOLOGY
1- Suppuration of the retro-pharyngeal nodes, secondary to upper respiratory
infection.
2- Infection after adenoidectomy.
AGE: Children, below the age of 5 years.
SYMPTOMS
1- General symptoms Fever, headache, anorexia and malaise.
2- Pharyngeal symptoms a) Severe unilateral sore throat and referred otalgia.
On pus formation  the pain becomes throbbing.
b) Severe dysphagia  the patient is unable to swallow even his own saliva  drooling
of saliva from his mouth.
c) Severe dyspnoea i.e. difficult breathing. Why? Because
 collection of pus behind the nasopharynx  nasal obstruction &
 collection of pus behind the hypopharynx  laryngeal obstruction and stridor.
SIGNS
1) General sign Fever.
2) Pharyngeal signs
A pharyngeal swelling pushes the posterior pharyngeal wall forwards.
The swelling is limited to one side of the midline; due to midline attachment of the
bucco-pharyngeal and pre-vertebral fasciae.
3) Cervical signs Torticollis i.e. forward flexion of the neck. Why? Because neck
extension  stretching of pre-vertebral muscles  pressure on the abscess 
increase of pain.
.
INVESTIGATIONS
Plain x-ray & CT scan Widening of the pre-vertebral space with normal
vertebral bodies.
COMPLICATIONS
1- Spread of infection to  the mediastinum  mediastinitis.
2- Rupture of the abscess into the pharynx  aspiration of pus 
broncho-pneumonia.
TREATMENT
1- Medical treatment Massive antibiotic therapy.
2- Surgical treatment a) Drainage of the abscess by an incision in the
posterior
pharyngeal wall, with the patient in Trendlenburg’s position i.e. the head
is lower than
the chest in order to avoid aspiration of pus.
b)Tracheostomy when necessary
DEFINITION
Herniation of the pharyngeal mucosa through
Killian’s dehiscence.
What is Killian’s dehiscence? A potentially
weak area on the posterior surface
of the pharynx  between the upper oblique
fibers ( i.e. thyro-pharyngeus ) and lower
transverse fibers ( i.e. crico-pharyngeus ) of the
inferior constrictor muscle.
INCIDENCE
Commonly elderly males.
PHYSIOLOGY
The crico-pharyngeal muscle acts as a sphincter ( the crico-pharyngeal sphincter ).
This sphincter is normally closed, except during the oesophageal stage of swallowing.
How? At the beginning of this stage  the upper thyro-pharyngeus muscle contracts
to push food down through the relaxed lower crico-pharyngeal muscle.
AETIOLOGY
Neuro-muscular incoordination during swallowing  failure of relaxation of
the crico-pharyngeal sphincter  increased intra-pharyngeal pressure  herniation
of the pharyngeal mucosa through the potentially weak area of Killian’s dehiscence.
SYMPTOMS
1- Gradual progressive dysphagia  more to solids. Why? As the
pouch enlarges 
it becomes more in line with the pharynx  food enters the
pouch 
exerts pressure on the oesophagus.
2- Regurgitation of undigested acid-free food.
3- Bad mouth odour ( halitosis )  due to fermentation of the
retained undigested food.
4- Mild loss of weight.
SIGNS
1- Cervical examination Cystic swelling, partially covered by the sterno-mastoid muscle,
usually on the left side. It increases in size after meals & empties on pressure 
producing a gargling sensation.
2- Flexible hypopharyngoscopy Shows the mouth of the pouch.
INVESTIGATIONS
1. Barium swallow Characteristic retort-shaped appearance.
2. Manometric studies Increased pressure in the crico
pharyngeal.
TREATMENT
1. Repeated endoscopic dilatation of the crico-pharyngeal
sphincter  temporary relief.
2. Endoscopic division of the partition between the pouch
and the pharynx.
3. External excision of the pouch together with crico-pharyngeal
myotomy i.e. cutting
of the crico-pharyngeal sphincter to prevent recurrence
Direct hypopharyngoscopy
DEFINITION:
Direct visualization of the hypopharynx by an open rigid hypo-
pharyngoscope.
INDICATIONS:
A. Diagnostic:
1- To examine the hypo-pharynx.
2- To take a biopsy.
B. Therapeutic:
1- Removal of a hypo-pharyngeal foreign body.
2- Dilatation of the crico-pharyngeal sphincter  In case of pharyngeal pouch.
3- Excision of hypo-pharyngeal benign tumours.
CONTRA-INDICATIONS:
Cervical spine deformities as severe kyphosis
Plummer Vinson’s syndrome
( Paterson Brown Kelly syndrome- Chronic pharyngo-
esophagitis)
INCIDENCE: Commonly middle-aged females.
AETIOLOGY: Unknown. May be iron deficiency or vitamin deficiency.
PATHOLOGY: Atrophy of the pharyngeal, oesophageal and gastric mucosa.
SYMPTOM
Gradual progressive dysphagia.
SIGNS
1- General signs a) Pallor ( due to anaemia ).
b) Spoon-shaped nails ( koilonychia ).
c) Splenomegaly.
2- Pharyngeal signs
1) Angular stomatitis  fissured mouth angles.
2) Glossitis  smooth tongue due to loss of papillae.
3) Atrophic glazed mucosa of the hypopharynx and cervical oesophagus.
INVESTIGATIONS ‫مهمة‬
1- Blood picture Hypochromic anaemia.
2- Gastric secretion Achlorhydria due to atrophy of the gastric mucosa.
COMPLICATIONS
1- Submucosal fibrosis  web formation and stricture at pharyngo-oesophageal
junction.
2- Pre-cancerous  post-cricoid carcinoma and cancer oesophagus.
TREATMENT
1- Iron and vitamins supply.
2- Repeated endoscopic dilatation  when stenosis occurs.
3- Regular follow up  to detect post-cricoid carcinoma and cancer esophagus.
PERITONSILLAR ABSCESS ( Quinsy)
DEFINITION
Collection of pus in the peri-tonsillar space.
The peri-tonsillar space is a connective tissue space.
 Lies between the capsule of the tonsil and its bed ( which is formed of the superior
constrictor muscle of the pharynx ).
INCIDENCE
Age: Adults.
Side: Unilateral.
Site :Above and lateral to the tonsil.
AETIOLOGY
Acute tonsillitis. The infection passes outside the tonsil through crypta magna.
SYMPTOMS
1- General symptoms Fever, headache, anorexia and malaise.
2- Pharyngeal symptoms After an attack of acute tonsillitis  the patient develops
a) Severe unilateral sore throat and referred otalgia. On pus formation  the pain
becomes throbbing.
b) Severe dysphagia  the patient is unable to swallow even his own saliva  drooling
of saliva from his mouth.
c) Bad mouth odour ( halitosis ).
SIGNS
1- General sign High fever.
2- Pharyngeal signs
a) A pharyngeal swelling 
 in the soft palate, above and lateral to the tonsil,
 pushes the adjacent tonsil downwards and medially, pushes the uvula to the opposite
side & on pus formation  The swelling pits on blunt probing.
b) Trismus i.e. inability to open the mouth  due to spasm of the pterygoid muscle.
3- Cervical signs
a) Enlarged tender upper deep cervical lymph nodes.
b) Torticollis i.e. neck tilt to the diseased side  due to spasm of the neck muscles.
COMPLICATIONS
1- Spread of infection to
a) the para-pharyngeal space  par-pharyngeal abscess &
b) the larynx  laryngea edema.
2- Rupture of the abscess into the pharynx  aspiration of pus  broncho-pneumonia.
TREATMENT
1- Medical treatment When? Before pus formation i.e. in the stage of peri-tonsillar
cellulitis. How? Massive antibiotic therapy.
2- Surgical treatment :Drainage of the abscess. When? After pus formation i.e. in the
stage of peri-tonsillar abscess  as indicated by throbbing pain pitting oedema or
pointing abscess.
How?
 Anaesthesia: Commonly surface with the
patient sitting.
 The incision: Is performed with a guarded
scalpel or better a quinsy knife in one of ‫ مكان ال‬INCISION ‫مهم‬
points
1) Most pointing point.
2) Midway between the last upper molar
Tooth and base of the uvula
3) 1/2 cm lateral to the meeting point of two lines  a vertical
line along the anterior
pillar & a horizontal line along the base of the uvula.
 The drainage: Is performed by a quinsy forceps;using
Hilton’s method i.e. the forceps is
introduced closed  opened in the abscess  withdrawn out
open.
3- Tonsillectomy operation
When? After 4 - 6 weeks. Why? To avoid recurrence of quinsy.
PARPHARYNGEAL ABSCES
DEFINITION
Collection of pus in the para-pharyngeal space.
 The para-pharyngeal space is a connective tissue space.
 Lies on the lateral side of the nasopharynx and oropharynx.
 Extends from the base of skull, to the level of hyoid bone.
 Limited laterally by the mandible superiorly and the sterno-mastoid muscle inferiorly.
 Contains the internal carotid artery, internal jugular vein, last four cranial nerves, deep
cervical lymph nodes and deep Lobe of the parotid gland.
AETIOLOGY
1) Acute tonsillitis, peritonsillar abscess and infection after tonsillectomy. The infection
passes through the superior constrictor muscle of the pharynx.
2) Infection of the last lower molar tooth.
SYMPTOMS
1) General symptoms Fever, headache, anorexia and malaise.
2) Pharyngeal symptoms
a)Severe unilateral sore throat and referred otalgia. On pus formation  the pain
becomes throbbing.
b) Severe dysphagia  the patient is unable to swallow even his own saliva  drooling
of saliva from his mouth.
SIGNS
1) General sign High fever.
2) Pharyngeal signs
 A pharyngeal swelling which pushes the lateral pharyngeal wall and tonsil medially.
 Trismus i.e. inability to open the mouth  due to spasm of the pterygoid muscle.
3) Cervical signs
 A unilateral diffuse tender swelling below & behind the angle of the mandible,

deep to the anterior border of the sternomastoid muscle.

 Torticollis i.e. neck tilt to the diseased side  due to spasm of the neck

muscles.
INVESTIGATIONS
CT scan Diagnostic.
COMPLICATIONS
1) Spread of infection to
a) the base of skull  meningitis,
b) the carotid sheath  thrombosis of internal jugular vein and rupture of
carotid artery, the mediastinum ( along the
carotid sheath )  mediastinitis & the larynx  laryngeal oedema.
2) Rupture of the abscess into the pharynx  aspiration of pus  broncho-
pneumonia.
TREATMENT
1) Medical treatment Massive antibiotic therapy.
2) Surgical treatment Drainage of the abscess by a vertical cervical incision
along
theanterior border of the sterno-mastoid muscle.
LUDWIG'S ANGINA

‫مهمة جداا‬
DEFINITION
 Bilateral diffuse cellulitis of the floor of the mouth Suppuration
seldom occurs.
 The floor of the mouth is a connective tissue space. It is divided by the mylo-hyoid
muscle to  submandibular and sublingual spaces.
AETIOLOGY
Infection of the floor of the mouth e.g. lower teeth ( commonest ), mandible,
tongue, submandibular or sublingual salivary gland.
SYMPTOMS
 General symptoms Fever, headache, anorexia and malaise.
 Local symptoms
a) Severe dysphagia. Why? Because the tongue is pushed upwards
and backwards  may obstruct the food passage.
b) Severe dyspnoea. Why? Because the tongue is pushed upwards and backwards 
may obstruct the air passage.
SIGNS
a) General signs: Fever.
b) Pharyngeal signs
A swelling in floor of the mouth  pushes the tongue upwards and
backwards. Trismus i.e. inability to open the mouth  due to spasm of the
pterygoid muscles.
c) Cervical signs \Tender indurated swelling of both submandibular
regions. Suppuration seldom occurs.
COMPLICATION
Spread of infection to  the larynx  laryngeal oedema ( common ).
TREATMENT
1) Medical treatment
 Massive antibiotic therapy. ‫ ال‬HOSPITALIZATION ‫مهم‬
 Bed rest, in the semi-sitting position  to avoid airway obstruction.
2) Surgical treatment
 Drainage by a horizontal cervical incision below the mandible.
 Usually there is no or little frank pus  because suppuration seldom
occurs.
 Tracheostomy when necessary
MONILIASIS
Moniliasis ( candidiasis or thrush )
AETIOLOGY
Causative organism Candida albicans.
Predisposing factors Debilitating diseases ( as AIDS, malignancy &
diabetes mellitus ) and prolonged use of systemic antibiotics or
steroids.
SYMPTOMS
1) General symptoms No fever.
2) Pharyngeal symptoms Mild sore throat.
SIGNS
1- General signs No fever.
2- Pharyngeal signs
a) Diffuse hyperaemia of the pharyngeal mucosa.
b) The oral and pharyngeal mucosa is covered with multiple small
milky white patches. Removal of these patches reveals superficial
mucosal ulcers.
3- Cervical signs No enlarged cervical lymph nodes.
TREATMENT
1. Local anti-fungal drugs as miconazole and nystatin.
2. Treatment of the cause.
RECURRENT APHTHOUS ULCERS (RAUs)
Recurrent aphthous ulcers
INCIDENCE
Commonest cause of oral and pharyngeal ulceration.
AETIOLOGY
Unknown. May be vitamin deficiency,
immunological disturbance or stress.
CLINICAL PICTURE
1- General manifestations Good
general condition.
2- Pharyngeal manifestations
 Recurrent single or multiple variable
sized painful oral and pharyngeal ulcers
which are surrounded with marked
hyperaemia.
 They heal spontaneously within 1 – 2 weeks.
TREATMENT
Local corticosteroids.
BEHCET'S DISEASE
Behcet’s disease
AETIOLOGY
Unknown. Most probably 
an auto-immune disease.
CLINICAL PICTURE
1) General manifestations
 Iridio-cyclitis.
 Genital ulcers.
 Progressive sensori
neural hearing loss.
2- Pharyngeal manifestations
 Recurrent multiple
small painful oral and
pharyngeal ulcers
which occur in
groups
ACQUIRD IMMUNODEFCIENCY SYNDROME (AIDS)
Acquired immuno-deficiency syndrome ( AIDS )
AETIOLOGY
Causative organism Human immuno-deficiency
virus ( HIV ).
CLINICAL PICTURE
1- General manifestations Poor general condition.
2- Pharyngeal manifestations
a. Hypertrophy of the pharyngeal tonsils.
b. Recurrent and severe candidiasis, viral pharyngitis and aphthous ulcers.
c. Hairy leukoplakia: White mucosal patches. It consists of localized
epithelial hyperplasia . The basement membrane remains intact.
d. Kaposi’s sarcoma: Red plaque or nodule. It is a malignan mesenchymal
tumour. It consists of aberrant slit like vascular spaces surrounded by
atypical spindle cells
3- Cervical manifestations Enlarged deep cervical lymph nodes.
INVESTIGATION
Enzyme-linked immuno-sorbent assay ( ELISA ) To detect antibodies to
HIV.
TREATMENT
The patient should be referred to a specialized hospital.
Larynx
LARYNGOMALACIA
LARYNGOMALACIA
Etiology: not known.
Signs
 Elongation of epiglottis (omega shaped)
 Arytenoids prolapse antero-medially on inspiration ,
 Shortening of the aryepiglottic folds,
 Inward collapse of the aryepiglottic folds (cuneiform
cartilages) on inspiration
The vocal folds, are normal.
Treatment:
- Most cases of laryngomalacia can be managed by
observation. The condition usually improves spontaneously
at the age of 2 years.
- Surgical management is indicated in rare instances.
- Tracheostomy is rarely needed for respirator
obstruction
Congenital laryngeal web
Congenital Web
PATHOLOGY
A fibrous band between the anterior parts of the two vocal folds.
SYMPTOMS
1) Weak hoarse cry.
2) Inspiratory stridor; if the web is large.
SIGNS
A white triangular band in the anterior part of the glottis.
TREATMENT
 Tracheostomy when necessary.
 Surgical excision of the web. How?
- Micro-laryngoscopic by surgical instruments or better laser surgery when
Thin.
- Through laryngofissure when thick.
Singer's nodule
Vocal ( singer’s ) nodules
AETIOLOGY
Abuse of voice.
INCIDENCE
More common in children & professional voice users as singers and teachers.
PATHOLOGY
Localized epithelial hyperplasia and / or sub-epithelial organized haematoma
 of the vocal fold.
SYMPTOMS: Hoarseness of voice
SIGNS
Bilateral small sessile smooth swellings. They occur at the junction of the
anterior 1/3 and posterior 2/3 of the vocal folds. Why? Because this is the site
of maximum contact of the vocal folds during phonation  maximum trauma.
TREATMENT
1) Voice therapy The treatment of choice. Usually successful.
2) Micro-laryngeal excision by surgical instruments or laser surgery, in case of
failure of voice therapy. It should be followed by voice therapy to avoid
recurrence
‫‪ THANK YOU‬مفكر انها‬
‫لساا‬
‫دي بقي مهمه الدكتور في الريكورد قال إنه عايز كل‬
‫واحده اسمها ايه بالظبط يعني دي مهمه اوي‬
‫دي بقي مهمه الدكتور في الريكورد قال إنه عايز كل‬
‫واحده اسمها ايه بالظبط يعني دي مهمه اوي‬
‫دي بقي مهمه الدكتور في الريكورد قال إنه عايز كل‬
‫واحده اسمها ايه بالظبط يعني دي مهمه اوي‬
‫ اختصار لل‬tracheastomy ‫كله‬
‫يا ناس يا اهل‬
‫البلد خلصنا فايل‬
‫االوسكى‬