Tomoh

Islamic Library

ENT
University of Khartoum
Faculty of Medicine
Academic Secretariat – Batch 88 (Qasawir)

Ahmed Siddig Mazin Ahmed

1
Table Of Contents:

1. TONSILITIS AND ADENOIDITIS..............................................3

2. Sinusitis.........................................................................................7
3. Acute ottitis media.........................................................................10
4. Chronic Otitis Media.....................................................................14
5. Upper airway obstruction..............................................................21
6. Epistaxis........................................................................................29
7. Nasopharyngeal Carcinoma..........................................................34
8. Vertigo...........................................................................................37
9. Fungal Rhinosinusitis....................................................................39
10. Hearing Loss (HL).......................................................................41

2
 TONSILITIS AND ADENOIDITIS
Lecture1:Dr. Nagat Abdalla
Tonslitis and adenoiditis are mainly diseases of children, although adults can be
affected.
Adenoiditis is not congenital, but can be acquired at age of 2 months. When child
reach 10-12 years, adenoids atrophy.

Anatomy of Tonsils:
Ring of Waldeyer is an aggregiation of lymphoid tissue arround the orifice of the
aerodigestive tract, it's composed of group of lymphoid tissue including:
1. Nasopharyngeal tonsil (=adenoid):
found in the roof & posterior wall of the nasopharynx.
2. Tubal tonsils:
found lateral to the adenoid at the orifice of the eustachian tube.
3. Palatine tonsils:
A capsulated aggregiation of lymphoid tissue, found in tonsillar fossa (in
lateral wall of oropharynx).
Bounded by:
o Anteriorly: anterior pillar of the tonsils
o Posteriorly: Posterior pillar of the tonsils.
o Base: pharyngeal muscle.
Palatine tonsil is crypted by 16-20 crypts, one of this crypts is large & known
as crypta magna. If acute tonsilitis is not probabaly treated, pus can
accumulate in the tonsillar crypts leading to chronic tonsilitis.
4. Lingual tonsils:
Found in posterior 1/3 of the tongue.

Types of Tonsilitis:
Acute tonsilitis
Chronic tonsiltis

ACUTE TONSILITIS
Acute inflammation of the tonsils occur commonly in children & transmitted by
droplet infections.

Causative organisms in children:

Viral:
 Adenovirus
 EBV
 HSV
Bacterial:
 Group A βHaemolyic streptococci
 Streptococcus pneumonae
 Haemophilus influenzae
 Anaerobic bacteria

3
Causative organism in adults:
Viral:
 Influenza and parainfluenza virus
 Adenovirus
 Enterovirus
 Rhinovirus

Bacterial:
 Group B Haemolyic streptococci
 Other types of streptococci
 Haemophillus influenzae
 Anaerobic bacteria

CLINICAL FEATURES OF ACUTE TONSILITIS:

Symptoms:
Pyrexia, malaise, headache.
Sorethraot & odenophagia (painful swallowing).
Abdominal pain & vomiting due to swallowing of postnasal discharge.
Change of voice due to odenophagia which restrict tongue movement.
Otalgia
Neck pain due to cervical lymphadenitis. (tonsils drains to jugulodigastric L.Ns).

Signs:
 Hyperemic tonsils
 follicular tonsilitis: Pus in the tonsillar crypts (seen as white follicles in the
tonsils). This a feature of acute tonsilitis.
 Membranous tonsilitis: when the ammount of secretion increase in tonsillar
crypts, a membrane is formed.

 i.e. Follicular tonsilitis & membranous tonsilitis are the degree of same pathology.

 Clinically we can differentaite between viral & bacterial tonsilitis:

 Viral tonsilitis: only redness
 Bacterial tonsilitis: swollen tonsils & white follicles.

DIFFERENTIAL DIAGNOSIS OF ACUTE TONSILITIS:

1. Acute diphteria:
 membranous tonsilitis: true membrane, when we remove it  no bleeding.
 Acute diphteria: pseudomembrane, when removed  bleeding
(Greenish membrane + patient is very toxic).
2. Infectious mononucleusis: (monospot test).
3. Scarlet fever
4. Acute leukemia: (CBC)
5. Agraulocytosis

TREATMENT OF ACUTE TONSILITIS:

Viral: self limiting, symptomatic treatment, analgesics, no antibiotics, local gargles.
Bacterial: Antibiotics, pencillin is the drug of choice, erythromycin in pencillin

4
 hypersensitive patients. Analgesics. Local gergles.

COMPLICATIONS OF TONSILITIS:
Local complications: infection from tonsil can spread to surounding structures
1. Respiratory obstruction: severe edema & swollen tonsils, this can lead to upper
airway obstruction.
2. Peritonsilllar abscess (quinsy): collection of pus in the peritonsillar space. Deviate
the tonsil to the other side.
3. Parapharyngeal abscess: extension of infection to the parapharyngeal space.
4. Mediastinitis.
5. Otitis media: spread through eustachian tube.

General complications:
1. Septecemia.
2. Acute rheumatic fever & glomerulonephritis:
 Occurs specially in A βhaemolytic streptococci.
 Immune reaction due to the similarity between streptococcal antigens to
the basement membrane of cardiac muscles & renal tubules.

CHRONIC TONSILITIS
 Chronic inflammation of the tonsils due to repeated attacks of acute tonsilitis.
 Occurs if:
 Low immunity
 Organism is highy virulent
 Treatment is inadequate: antibioics course is minimal 7 days

CLINICAL FEATURES OF CHRONIC TONSILITIS:

Local symptoms:
History of repeated attacks.
Sense of irritation in the throat.
Bad taste.
Kissing tonsils: when tonsils highy enlarge & meet each other, leading to difficulty in
swallowing and breathing.

General symptoms:
Anemia due to poor appetite.
Fatigue and arthritis due to absorbtion of toxic postnasal discharge.

Signs:
Inequity in the size of the tonsils.
Congestion of anterior pillar of the tonsil.
Intratonsillar abscess, calcification, & scaring
Pus oozing from the tonsillar crypts on pressure.
Enlarged cervical glands due to repeated attacks (jugulodigastric LNs)

TREATMENT OF CHRONIC TONSILITIS:

When symptoms are persisitent, tonsilectomy is indicated.

Tonsilictomy is indicated due to local manifestations:

5
 1. Recurrent attacks of acute tonsilitis; usually more than 5 attacks in one year, or
more than 8 attacks in 2 years.
2. One attack of quinsy.
3. Huge tonsils affecting eating & breathing (kissing tonsils)
4. Persistant jugulodigastric LNs enalrgement.
5. FB of the tonsil
6. Tumor of the tonsil

General indiactions of tonsillectomy:

Tonsilitis accting as a septic focus

Contraindiactionas of tonsillectomy:
1. Blood diseases (Heamophilia, factor VII deficinecy .. etc).
2. Acute attack: due to hyperemia & congestion  severe bleeding.
3. URTI: due to hyperemia & congestion  severe bleeding.
4. Epidemic of poliomyelitis: to prevent dissemenation of the disease.
5. Active systemic diseases: e.g. DM, TB, anemia (due to low immunity).
6. Cleft palate & bifid uvula: to prevent scaring of soft palate, because it will be
difficult to repair.

ADENOIDITIS:
Inflammation of subepithelial lymphoid tissues in the roof & posterior wall of the
nasopharynx, usually occuring in children between age of 2 months –
11 years (adenoid atrophy after 11 yaers).

CLINICAL FEATURES:
Nasal symptoms:
 Nasal obstruction: enlarge adenoid obstruct the poterior opening of the nose.
 Nasal discharge: due to infection

Aural symptoms:
due to eustachian tube obstruction & extension of infection to the middle ear:
 Recurrent acute otitis media
 Chronic otitis media
 Leading to conductive hearing loss

General symptoms:
Mental dullness or mental retardation due to conductive hearing loss.

TREATMENT OF ADENOIDITIS:
Adenoidectomy in cases of marked symptoms.

6
 Sinusitis
Lecture 2:Dr.Nagat Abdallah
Objectives:
 Discuss anatomy of paranasal sinuses.
 Acute sinusitis.
 chronic sinusitis.
Anatomy:-
 paranasal sinuses are : maxillary , ethmoidal , sphenoidal and frontal sinuses.
 paranasal sinuses drains into the lateral wall of the nose.
 paranasal sinuses are filled with air and any secretions are removed by cilliary
action to the nose.
Types of Sinusitis:
 Acute sinusitis.
 chronic sinusitis.

Acute sinusitis
Acute inflammation of the mucus membrane of the paranasal sinuses initiated by
impairment of normal drainage and of the sinuses.

Predisposing factors:
 Local factors:
1)viral infections.
2)Allergy.
3)Barotrauma or physical trauma.
Barotrauma occurs when there is obstruction of the osteum of the sinuses and change
in
Atmospheric pressure (deep sea , high altitude , ...etc) pressure inside the sinus
increase
In pressure leading to rupture of the sinus causing severe pain and headache.
4)Deviated nasal septum (DNS):
Nasal septum is normally slightly deviated , if there is gross deviation , this will lead
To accumulation of secretions inside the sinuses and development of infections.
5)Nasal polyps: usually caused by allergies.
6)Tumors of the nose.
7)Nasal packing for epistaxis.
8)Long standing NG tube.
9)Foreign body in the nose.
10)Extension of infection from the teeth : specially from upper teeth to the maxillary
sinuses.
 Systemic conditions:
1)Immotile cilia syndrome - No cilia movement - accumulation of secretions -
secondary infections.
2)Kartageneer’s syndrome:
-syndrome of sinusitis and bronchiectasis (no cilia movement).
3)Immunodeficiency : IgG suubclass and HIV.

7
Pathogenesis:-
-Viral infection will lead lead to ostia blockage - sinus hypoxygenation and
stagnation of
Secretions - Mucus gland ciliary dysfunction - further thickening and retention of
sinus
Fluid - favourable enviroment for 2ndry bacterial infection.

Etiology of Sinusitis:
1- Streptococcus pneumoniae.
2- Haemophilus influenzae.
3- Staphylococcus aureus.
4- Streptococcus pyogens.
5- Maroxilla catarhalis.
6- Viruses.
7- Anaerobic bacteria: Bacteroids , Fusobacterium , anaerobic G+ve cocci.
8- Nasocomial sinusitis caused by G-ve bacteria:
Pseudomonas aerginosa , klebsiella pneumoniae , enterobacter , proteus.

Clinical feature of sinusitis:-

*Symptoms:-
1- Nasal obstruction (main symptom).
2- Mucopurulent nasal discharge.
3- Postnasal discharge : discharge passing backwaed to nasopharynx and spitted.
4- Headache and facial pain over affected sinus.
5- Referred pain to:
-Eye: specially in ethmoidal sinusitis.
-Teeth :specially in maxillary sinusitis.
-Ears : specially in maxillary sinusitis.
-Vertex: specially in sphenoidal sinusits.
*Signs:-
-Anterior rhinoscopy showed nasal congestion and nasal discharge.
-Endoscopy show discharge from ostia of affected sinus.
Diagnosis:
-Radiography show opacification or fluid level in sinus . Fig.
-Culture and sensitivity.
Treatment of acute sinusitis:
1- Antibiotics:
Amoxicillin or septrin.
2- Oral or topical decongestant : to open ostia of the sinus.(like antihistamine).
3- Mucolytics for mucus lysis.
4- Nasal saline irrigation for decrease of the drained mucus.
5- Steam inhalation : help in opening the sinus ostia (neublizer).

Chronic Sinusitis
persistent of the same symptoms of acute sinusitis beyond 8-12 weeks.
 Treatmen of chronic sinusitis:
 Complication of Sinusitis:-
- Complications occur when infection spread to surrounding structures.
Local complications:-
1- Mucocele:

8
 Long standing obstruction of the sinus ostia lead to entrapment of secretion inside
The sinuses and balooning of the sinuses causing mucocele.
2-Osteomylitis: direct extention of infection to surrounding bone.
Fig.Mucocele case , pushing eye laterally.

 Orbital complications:-
1- Orbital cellulitis.
2- Subperiosteal abcess.
3- Orbital abcess.
4- Cavernous sinus thrombosis extend through angular vein.
 Intracranial complications:-
1- Meningitis.
2- Epidural abcess.
3- Subdural abcess.
4- Brain abcess {in the frontal lobe mainly}
Note ; in otitis media , brain abcess occur in temporal lobe.

Fungal sinusitis
- special intity of sinusitis.
- caused by aspergillus species:
Aspergillus flavus in sudan.
Aspergillus fumigatus out side sudan.
- give a feature of nasal polyp.
- Inside the sinuses , we have muconium like or waxic like material.
- Infection can spread to surrounding structure (orbit and cranium).
- Fig. Polyp formed by fungal granuloma.
- It can extend to the orbit causing unilateral proptosis.
- Can extend intracranially causing intracranial fungal granuloma.

Diagnosis of fungal sinusitis:-

-Radiological diagnosis.
-Microscopy.
-Fungal culture.
Treatment of Fungal sinusitis:
- Treatment by surgery : either by Conventional method , or
Functional endoscopic sinus surgery:
Clear the fungal material using sinuscope.
- Give antifungal drugs after surgery:
Itraconazole in a dose of 200mg daily.
Treatment extend for 3 months with following the pt.
- Steroids are sometimes indicated.

9
 Acute ottitis media
Lecture (3): Dr.Osama.M.Khalid
Anatomy of the ear:
-ear anatomically is devided into: external, middle and inner ear.
-middle ear is a cavity filled with air, covered laterally by TM (tympanic membrane).
- contain ossicles
- normal tympanic membrane (=Drum) is transparent and mobile, with light reflex.
Otitis media:
- inflammation of the middle ear.
- 2 types:
1- otitis media with effusion (secondary otitis media)
filled with fluid
sterile, not purulent fluid
2- acute otitis media (suppurative OM)
@purulent infection by organism
Acute otitis media:-
-Rapid onset of signs and symptoms and disappearance of them in less than 3 weeks
-chronic otitis media is persistence of symptoms for more than 3 weeks
chronic suppurative: by definition there is tympanic membrane perforation
chronic secretory: more than 3 months, because its expected to resolve in this 3
months
Epidemiology of acute otitis media:-
-in children world wide it is the 2nd most common disease after respiratory tract
infection.
-in sudan malnutrition and diarrhoeal diseases are more common
-peak incidence in first 2 years, even more common in 6-12 months
-more common in males than females
-at age of 6 years, 90% of children have at least one episode of AOM
-Recurrent Otitis Media “ROM” must be associated with risk factor which we should
treat
-occurs more in winter because the first step in pathogenesis is obstruction of ET
eustachian tube
-Recurrent OM: more than 3 times in 6 months, or 4 or more in one year.
Causative agent of AOM:-
50%  Bacterial
50%  Viral
-clinically viral AOM is associated with general symptoms like: runny nose, cough,
fever.. etc but bacterial AOM is not associated with general symptoms.
-Bacterial causes:-
 Sreptococcus pneumoniae  35%
 Haemophilus influenzae  25%
 Maroxella catarrhalis  15%
Risk factors of AOM:-
-All risk factors affect ET function by oedema, congestion and obstruction:

10
1- URTI “upper respiratory tract infection”
2- Allergies: allergic rhinitis
3- craniofacial abnormalities: eg.cleft palate
Because ET is always open
4- Down syndrome: because of very narrow mouth and nasopharynx
5- passive smoking
6- over crowding
7- Adenoids: in children
8- Naso pharyngeal tumor: adult with secretory OM, or AOM, nasopharyngeal tumor
should be excluded.
Eustachian tube “ET” :-
-connects middle ear with nasopharynx. It opens in lateral wall of nasopharynx.
-it is usually closed, and opens during swallowing, yawning and sneezing
-has bony and cartilaginous part
-opening involves cartilaginous part, by the action of tensor veli muscle
-closure is a passive process
-why children have more risk of developing OM?
Because ET is shorter, more horisontal, and with wider
opening.
Functions of ET:
1- pressure regulation of middle ear (most important)
Barotrauma can occur in landing and under water
2- clearance of middle ear secretions.
pathogenesis of AOM:-
Begins mainly with ET dysfunction
-otitis media usually follows an URTI in which there is salpingitis with oedema of ET,
leading to blockage, leading to negative pressure in the middle ear.
- to neutralize this pressure middle ear secretions increase
-till now no bacteria, this is called OME “otitis media with effusion”.
-patient complain of: dull pain, blocked ear, and decreased hearing
-occur more commonly in children with adenoids
-stasis of these ME secretions can lead to infection and irritation
-ascending infections can lead directly to AOM through ET
-other factors: allergic rhinitis, nasal polyps, adenoidal hypertrophy
*causes of the closure of ET:
1- weak tensor veli muscle
2- inflammatory processes: rhinitis, acute tonsilitis …etc (most common)
3- Extrinsic:
@adenoid in children (common)
@nasopharyngeal tumor in adults
Symptoms of AOM:-
-severe pain: usually onset at night, continue for 12 hrs, then settles and decrease in
severity for 3-5 days.
- discharge relieve pain, because first there is bulging of TM leading to ischemic pain,
when small perforation of TM occurs, discharge set out and pain is relieved
-fever, vomiting, loss of appetite may occur
-the younger the child, the more severe is the symptoms
-occasionaly tinnitus, voice resonance, due to conductive deafness
-Irritability may be the only indication in infants

11
-hearing loss occur if accumulation of fluid has taken place due to retraction of TM
due to negative pressure
-more fluid collection  more hearing loss
- Glue ear is chronic secretory OM
- Adhesive otitis media: adherent of TM with mucous membrane of middle ear,
leading to conductive deafness
physical examination:-
-the classic description of otitis media is a reddish, bulging TM due to accumulation
of fluid, with loss anatomic landmarks:
-Dull/absent light reflex
-Decrease mobility
Differential Diagnosis:-
1- Otitis Externa: Normal TM
2- curumen impaction:
-collection of wax
-like OME
But it occurs gradually and not preceeded with symptoms
3- Dental abscess: pain
4- foreign body FB of the ear canal
5- refered pain (parotid, tooth, and lymphadenitis)
6- Tonsilitis
Treatment of AOM:-
#Medical Treatment:
[1] Antibiotics:
Amoxicillin: 20-40 mg/kg/day, for 10-14 days, or
Augmentin: 45 mg/kg/day, tweice a day for 10-14 days (at least 10 days course)
[2] Analgesics:
NSAID regularly to decrease inflammation
[3] Decongestants to relieve the ET obstruction, but they can lead to dryness and ET
obstruction
#Surgical Treatment:
*Myringotomy:
-involves puncturing the TM aspiration of middle ear fluid to relieve pressure
- only used if medical ttt failed
-Indications of Myringotomy:
1- very toxic appearing child
2- failed treatment regimen with suppurative complications (see Below)
3- immunosuppressed patients
4- New born infants in which the usual pathogen may not be the cause
Complications of otitis media:
1- Glue ear in case of OME leading to conductive deafness
2- chronic otitis media with perforation of TM
3- Mastoiditis
4- Labyrinthitis
5- Meningitis
6- Neck abscess
7- intracranial sepsis
8- Facial nerve palsy
Recurrent episodes may lead to TM chronic perforation, otorrhea, cholesteatoma, and

12
permanent hearing loss.
Secondary OM [OME]:-
S &S (symptoms and signs):
1- blocked ear
2- decrease hearing
Management of OME:-
Wait and watch for 3 months
-Medical therapy: steroids, give systemic or local steroids (local is better to minimize
side effects)
-Valsalva maneuver to help opening of ET
-Surgical: Myringotomy + insert ventilation tube (Grommit tube)
Risk factors for AOM:
1- Inflammation: allergies, URTI
2- congenital: craniofacial abnormalities
3- Carcinomas: NPC (naso pharyngeal carcinoma).
4- others: passive smoking.

13
 Chronic Otitis Media
Lecture4:Dr.Siddig Alsayed Kardman

Anatomy:-
-Attic area : is the area in middle ear between maleus and incus, has close proximity
to middle cranial fossa.
-Tympanic membrane consist of pars flaccida and pars tensa.

Otitis Media is defined as:

-an inflammation of the middle ear cleft( i.e., the Middle Ear ,Eustachian Tube and
Mastoid Air Cells).
Natural History of Otitis Media:
Upper respiratory tract infection or mucosal congestion leads to Eustachian tube
obstruction leading to stasis, effusion and multiplication of bacteria.
Two fades:
1-Spontaneous resolution with drainage via the eustachian tubes.or
2-perforation of the tympanic membrane.
Effusion may remain if tube still obstructed.

Otitis Media Classification:

-Classified according to:
1- Duration of disease (Acute, subacute, chronic).
2-Quality of effusion (Serous, mucoid, purulent (suppurative))
-Serous : Otitis media with effusion.(O.M.E)
-Mucoid , Purulent : suppurative O.M. (S.O.M)
Note : S.O.M means suppuurative O.M.(not secretory O.M)
3-Tympanic membrane appearance.

Epidemiology:
-Thre population group according to W.H.O:
 Low prevelance : 0.5% : USA , UK.
 Middle prevelance : 2-7% : Nigeria , Sudan.
 High prevelance : more than 7% India.
-Morbidity : patient suffer from recurrent discharge , in children can lead to cognitive
problems.
-Mortality : related mainly to intracranial complications.
-occurs mainly with middle ear infection persist and cause significant hearing loss and
damage to middle ear.Usually involve a perforation of the TM.
Deafness

Ear discharge (otorrhea). T.M. perforation

Chronic Otitis Media

Official Definition of Chronic O.M:

COM: unresolved inflammatory process of the middle ear cleft associated with

14
TM perforation, otorrhea and hearing loss.

ETIOLOGICAL FACTORS:
1-Dysfunction of Eustachian tube.
2-Chronic inflammation in nose and pharynx.
3-Dysfunction of immune system..

Chronic Suppurative Otitis Media:

Microbiology:
1-mixed
2-P. aeruginosa %60-40
3-S. aureus %20-10
4-Diphtheroids
5-Klebsiella
6-OTHER ANAEROBES

Pathology :
-Middle ear mucosa is lined by secretory epithelium forming gland like structure.
-Hyalinization or Tympanosclerosis.
A healing response ,It is formed by fused collagenous fibers.
It is hardened by the deposition of calcium and phosphate crystals.
Conductive hearing loss is associated with masses restricting ossicular mobility

Ossicular erosion is frequent in C.O.M:

-Infection process per se
-Necrosis following vascular thrombosis
-It most commonly affect the lenticular process of the incus and head of the stapes
Fig. Perforation , eroded ossicles and tympanosclerosis.

Chronic Otitis Media - Types:

1-Tubotympanic disease.: related to ET and T.M.(Safe type).
2-Atticoantral disease: related to Attic and Mastoid antrum. (Unsafe disease).

Tubotympanic disease: (safe disease)

-The infection is limited to the mucosa and the anteroinferior part of the
middle ear cleft, hence the name. This disease does not have any risk of bone
erosion.

Clinical features of tubotympanic disease:-

-Deafness ( conductive type )/Hearing impairment.
-Discharge ( characteristic).
-Central perforation.
-Patency of Eustachian tube.
-Nidus of infection in U.R.T.I.
-Immune status of patient .
-Aerobic and Anaerobic
-Active Tubo Tympanic C.S.O.M.(with discharge).
-Inactive Tubo Tympanic C.S.O.M.(dry ear).
History of Tubotympanic disease:
- patient present with Long standing, unilateral or bilateral, painless otorrhoea,

15
deafness
Discharge profuse , mucoid, mucopurulent, Non odorous.
-Follow U.R.T.I. and entry of water.

How to assess the patient?

Main basis to assess activity , type , extent
1. Inspection ,( otoscopy , E.U.M.(examination under microscope) )
Mucoid discharge , Perforation (central) in Pars Tensa.
Pale mucosa (rarely polyp)
2. Pus for c/s(culture and sensitivity).
3.Audiological assessment
 Voice test
 Tuning fork test.
 Pure tone audiogram.
Fig. Conductive hearing impairment in Pure tone audiogram.
Hearing loss:
-Air conduction threshold is within 40 dB means TM proferation with intact ossicular
chain.
-If air-bone gap is more than 40 dB is associated with discontinuity of ossicular chain.

Treatment of Tubotympanic disease:

-Aural toilet
-Cotton buds
-Suction and cleaning
-Antibiotics
Topical antibiotics
Systemic antibiotics
-Surgical treatment
1.Management of precipitating disease(Adenoid ,DNS , Nasal polyps).
2. Aural polypectom.
3.Reconstruction tympanoplasty.(from the temporalis fascia).
Fig. Perforated T.M with intact ossicles no pattches of tympanosclerosis.
Fig. Kidney shape perforation with intact. Fig. Intact ossicles with central perforation.
Fig. Left with anterior perforation with intact ossicles and tympanosclerosis.
Fig. Eroded handle of maleus.

Atticoantral disease ( unsafe disease)

-Fatal intra-cranial and extra-cranial complications can occur.
-Disease spreads by erosion of the bony wall of the attic.
-Cholesteatoma may occur.
-Commonly seen in sclerosed mastoid cavities.
-Deafness ( mixed type ).
-Discharge ( characteristic)
-Attic perforation in pars flaccida.
-Osteitis
-Aerobic and Anaerobic organismas.
-Cholesteatoma.

History of Atticoantral disease:

-Long standing, unilateral or bilateral,

16
-Discharge: scanty , intermittent with characteristic fouly smell .
-Dizziness, if discharge spread to middle ear.
-symptoms of complications.

*Main basis to assess extent and anticipate complications :-

1. Inspection ,( otoscopy , E.U.M.)
PARS FLACCIDA perforation .
2. Audiological assessment.(hearing impairment).
3. Radiological assessment.

Cholesteatoma:
-Keyword in unsafe C.S.O.M
-Cystlike, expanding lesions of the temporal bone, lined by stratified epithelium.
-containing desquamated keratin and purulent material.
-Extend from attic perforation and invasion of mastoid air cells.
Classification :
1-Congenital cholesteatoma.
2-Acquired cholesteatoma.
Note: cholesteatoma doesn’t contain cholestrol , and it is not a tumor.
Four theories:
1-Pocket retraction: dysfunction of Eustachian tube.
2-Epithelial migration: to the edge of a peripheral perforation.
3-Implantation Inward growth of the surface epithelium follows papillary
proliferation of the germinative layer of the pars flaccida.
4-Metaplasia from pseudostratified ciliated columnar epithelium.
Treatment of Atticoantral disease:
- always surgical treatment
Eradication of the disease and cholesteatoma with Mastoidectomy/Attictomy.
-Management of complications if present.
Fig. Perforation is difficult to see can be missed.
Fig. Perforation or retraction pocket.
Fig. Cholesteatoma in form of polyp.
Fig. Subtotal perforation.
Fig Cholesteatoma is not a tumor , but act like a tumor because it cause
Destruction and can reach middle cranial fossa.
RADIOLOGICAL ASSESSMENT :.
- CT-scan.
- can do mastoid x-ray, but it gives lesser information.
Fig. Cholesteatoma in CT-scan.
Fig. Cholesteatoma with intracranial extension.
-Indications for image study:
1-Uncontrollable aural discharge.
2-Complications such as facial paralysis, labyrinthitis(vertigo).
-When central nervous stystem involvement is suspected, MRI should be considered.
-Coronal CT scan is the best.

Differential diagnosis of C.S.O.M:

1-Tuberculous otitis media
Hematogenous route.
Multiple perforation and fetid.

17
 Creamy aural discharge.
Active pulmonary disease.
2-Middle ear carcinoma
Middle age patient.
Long term otorrhea with blood.
Otalgia.
CT scan showed temporal bone destruction.

Complications of otitis media :

Intratemporal
1-Mastoiditis
2-Petrositis
3-Labyrinthitis
4-Facial paralysis
5-Labyrinthine fistula
Intracranial
1-Extradural abscess
2-Subdural abscess
3-Brain abscess
4-Meninigitis
5-Sinus thrombophilbitis
Extracranial
1-Retropharyngeal abscess
2-Parapharyngeal abscess
3-Lymphadentitis

Intra-cranial complications
1)Extradural abscess:
Clinical Picture
– Persistent headache on the side of otitismedia.
– Pulsating discharge.
– Fever
– Asymptomatic (discovered during surgery).
Diagnosis of extra dural abcess:
– CT scans reveal the abscess as well as the Middle ear pathology.
Treatment:
– Mastoidectomy and drainage of the abscess.

2)Subdural Abscess:
Definition
– Collection of pus between the dura and the arachnoid.
– It’s a rare pathology.
Clinical picture:
– Headache without signs of meningeal irritation.
– Convulsions.
– Focal neurological deficit (paralysis, loss of sensation, visual field defects).

3)Meningitis:
Definition

18
– Inflammation of meninges (pia & arachinoid).
Pathology:
– Occurs during acute exacerbation of chronic unsafe middle ear infection.
– Two forms:
• Circumscribed meningitis: no bacteria in CSF.
• Generalized meningitis: bacteria are present in CSF.
Diagnosis:
– Lumbar puncture is diagnostic.
Treatment:
– Treatment of the complication itself and control of ear infection:
• Specific antibiotics.
• Antipyretics and supportive measures.
• Mastoidectomy to control the ear infection.

4)Venous Sinus Thrombosis:

Clinical picture:
– Signs of blood invasion:
• (spiking) fever with rigors and chills .
• persistent fever (septicemia).
– Positive Greissinger’s sign which is edema and tenderness over the area of the
mastoid emissary vein.
– Signs of increased intracranial pressure:
headache, vomiting, and papilledema.
– When the clot exeends to the jugular vein, the vein will be felt in the neck as a
tender cord.
Treatment:
- Medical:
• Antibiotics and supportive treatment.
• Anticoagulants
- Surgical:
• Mastoidectomy with exposure of the affected sinus and the intra-sinus
abscess is drained.

5)Brain Abscess:
Definition:
– Localized suppuration in the brain substance.
– It is most lethal complication of suppurative otitis media.
Incidence:
-- 50% is otogenic brain abcess
– It is more common in males especially between 30 – 10 years of age.
Pathology:
– Site: Temporal lobe or • Less frequently, in the cerebellum. (more dangerous)

Intratemporal complications
1)Labyrinthine fistula :
communication between middle and inner ear
It is caused by erosion of boney labyrinth due to cholesteatoma
Lateral canal erosion is the most common location
Clinical picture :
Hearing loss

19
 Attack of vertigo mostly during straining ,sneezing and lifting heavy object
Positive fistula test
Diagnosis :
High index of suspicion
Long standing disease
fistula test
Ct scan of temporal bone
Treatment :
Mastoidectomy
2)Facial nerve paralysis:
-Congenital or acquired dehiscence of nerve canal
-It is possibly a result of the inflammatory response within the fallopian canal to
The infection
-Tympanic segment is the most commom site to be involved
Diagnosis :
-Clinical May occur in acute or chronic ottis media
-Ct scan
Treatment :
-Acute otitis media (cortical mastoidectomy
+ventilation tube)
-chronic otitis media with cholestetoma
( mastoidecomy ± facial nerve decompresion )
3)MASTOIDITIS:
Definition
• It is the inflammation of mucosal lining of antrum and mastoid air cells system.
Mastoiditis per se actually occurs with most infections of the middle ear. It is
not considered a complication until bone destruction occurs.
Clinical Features:
Symptoms:
Earache ,Fever ,Ear discharge
Signs:
Mastoid tenderness , Sagging of posterosuperior meatal wall ,TM perforation,
Swelling over mastoid ,Hearing loss.
TREATMENT:
Medical treatment:
− Hospitalize.
− Antibiotics.
− Analgesics.
Surgical treatment:
−Myringotomy.
− Cortical mastoidectomy.
Extracranial Extratemporal complications :
-Extension of infection to the neck
-Bezold abscess ( extension of infection from mastoid to Sternocleidomastoid
muscle.)

Quiz
Fig. Congenital cholesteatoma T.M is intact.
Fig. Chronic secretory otitis media.

20
 Upper airway obstruction
Lecture5:Dr.Siddig Alsayed Kardman

 Obstruction of the portion of the airways that is located above the thoracic inlet.
(from nasal obstruction till larynx and upper trachea.)
 The upper airway starts At the nostrils, extends through the nasal conchae to the
nasopharynx, over the uvula to the hypopharynx and larynx,or,At the lips,
extends through the oral cavity, over the tongue and below the hard and soft
palates, to the hypopharynx and larynx.
*Nose *Nasopharynx *Oropharynx *Larynx (supraglottis, glottis and
subglottis)
*Trachea (extra thoracic).

Calssification of UAO:
Acute or Chronic (decompensated airway).
Partial or Complete .
Congenital or Acquired.

Clinical Features:
Stridor:{Noisy breathing with effort}.
- Harsh sound produced by vibration of upper airway structure
- Indicates upper airway obstruction.
Hoarseness: Indicates involvement of vocal cords.
Respiratory distress / suprasternal retraction.
Cough.
Signs of hypoxemia:
- Anxiety
- Restlessness
- Tachycardia
- Pallor
- Cyanosis: late sign
- calm patient : end stage.
Etiology:
Infectious:
Croup ( Acute laryngotracheobronchitis ).
Acute epiglottitis.
Bacterial trachitis
Diphtheria.
Retropharyngeal abscess / peritonsillar. abscess.
Ludwig Angina
Non infectious:
Congenital maformations
Angioneuretic oedema.
Foreign body inhalation.
Caustic burn and trauma.
Neoplasms.

21
Neurological

Croup ( laryngotracheobronchitis )
Term applied to group of inflammatory conditions involving larynx , trachea and
characterized by Triad :
1)Inspiratory stridor.
2)Barking cough.
3)Hoarseness of voice +/_ resp.distress.
Etiology of Croup:
Usually viral in origin:-
- Parainfluenza virus (type 1)
- Influenza virus
- RSV , adenovirus , measles virus
Epidemiology of Croup:
It is the most common cause of Acute Airway Obstruction in children.
Age group 3m-3 years (peak 2years).
Affects boys more often than girls.
Peak occurrence is in fall and winter.
Clinical features:
Usually history of preceding URTI.
Gradual or sudden in onset.
Triad :
Inspiratory stridor

Brassy(barking) cough Hoarseness of voice +/_ resp.distress

Diagnosis:
It is clinically diagnosed
Neck x-ray and CBC all should be done in clinically stable pt .
- AP neck film : show a pencil tip or steeple sign of the subglottic trachea
Management of Croup:
- Some children improve spontaneously because of natural fluctuations in the
disease.
Steam inhalation.
Oxygen.
Adequate hydration.
Nebulization with Racemic epinephrine.
-Steroid:Used in
- moderate to severe croup
-A child who needs admission in ICU for croup management needs steroid.
-Preparations Dexamethasone or Nebulized Budesonide

ICU admission:
1)Signs of hypoxia
2)Severe distress with exhaustion
3)Decision about ventilation
*Most children with croup doesn't need hospitalization because symptoms typically
resolve within a few days.
Bacterial causes of acute airway obstruction:
Acute epiglottitis --- Hemophilus influenzae type B.

22
Bacterial tracheitis --- Staph Aureus
Cornybactrium diphtheria

Acute epiglottitis
-It is a rapidly progreesive bacterial infection causing acute inflammation and edema
of the epiglottis and adjacent structures : aryepiglottic folds and arytenoids.
-Also known as supraglottitis.
-It is life threatening condition may lead to sudden and complete airway obstruction.
-Age : 2-6 years ( peak at 3 year).Infant.
-older children and adult are rarely affected.
Causative agents :
- Hemophilus influenzae type B , pneumococci , staphylococci, streptococci
Clinical features :
Previously well child
Sudden onset , history is short, 4-12 hours of sore throat and high fever
4“D”
Distress ,Dysphagia , Dysphonia , Drooling of saliva.
may lead to death if complete airway obstruction.
Diagnosis:
-History
- clinical Presentation.
- Appearance of the child( swan neck appearance.(characteristic).
-Pharynx examination at this stage in ER is absolutely contraindicated.
-Next step = admission in ICU.
-Neck x-ray : Not the priority.
-Do not leave the patient unattended.
Fig. Swan neck , child subconciously try to open airway.
Fig. Swollen epiglottis.
Management:
Protection of the airways is the primary priority.
Quickly proceed with epiglottitis protocol.
It is better to initiate a “false” epiglottitis drill than to miss this disease.
Epiglottitis protocol:-
- Safe and supervised transfer to skilled hand
- Inform consultant Pediatrics, ENT, ICU, Anesthesia
- Don't attempt to examine throat in ER
- Keep patient as comfortable as possible:-
1-donot rush to the cannula.
2-comfortable : on his mother hands for example.
- Administering 100% O2
- Assembling at bedside CPR equipment including resuscitation bag and mask,
intubation equipment.
- Taking the pt. to OR
- Attempt IV line or sampling only after intubation in OR /or Tracheostomy.
*Diagnosis of Acute epiglottitis:
After epiglottitis protocol has been performed and pt has secure airways you can
do :
- blood culture : usually positive for HIB.
- CBC : WBC may be moderately elevated.

23
 - lateral neck radiograph : shows a thickened epiglottis ( thumb sign ).
Diagnosis confirmed by seeing an edematous cherry-red epiglottis on endoscopy.
Endoscopic examination should not be performed in advance of the epiglottitis
protocol.
The main components of Rx is :
- maintain adequate airways until inflammation and edema resolve often 36-72hrs
- Parentral Abx directed agiants HI assuming this is the cause : ceftriaxone or
cefotaxime
if not available may use chloramphenicol
- Duration of Rx : 7-10 days

Viral croup Acute Epiglottitis

(Subglottic) (Supraglottic)

Age 3m-3 yr 2-6 year

Preceding coryza Yes No

Stridor Loud quiet

Onset Over days Over hours

Toxicity no yes

Fever Low grade High grade

Drooling no yes

Voice Hoarse Muffled

Dysphasia no yes

Bacterial trachitis:
-It is uncommon infectious cause of acute UAO.
-pt may present with croup like symptoms.
-Etiology : Staph Aureus.
-On intubation: copious thick secretion ( pus).
-with appropriate airway support and Abx most pt . Improve within 5 days,

Other infectious causes of UAO

Diphtheria.
Retropharyngeal abscess / peritonsillar. abscess.
Ludwig Angina
Retropharyngeal Abscess:
-very dramatic scenario in paediatric ward.
-<3years.
-Sore throat (anorexia) for several days .
-Pyrexia, drooling, stridor.

24
*case: 3 year old child presented with sore throat , fever , anorexia , very ill for
several days parental antibiotics given with no improvement , pyrexia continue
despite antibiotic treatment(suggesting abcess somewhere).
Patient later present with drooling of saliva , stridor and UAO.
- if not treated patient will die.
-Diagnosis:
Lateral view X-ray: prevertebral space increased.
- treatment: Surgical drainage.(ultimate and only treatment).
-Antibiotics ??? With anaesthesia
Why retropharyngeal abcess is before 3 years?
Because after 3 years the lymph node of Rouvier regress(retropharyngeal LNs).
Ludwig Angina:
- collection of pus below the tongue.
- double tongue sign .
- very serious condition - need drainage.
Peritonsilar Abcess (Quinsy).

Non Infectious Causes of UAO

1)Foreign body inhalation:-
Essentials of diagnosis:
Acute onset of cyanosis and choking
*Inability to cough or vocalize (complete obstruction)
*Drooling with stridor (partial obstruction)
Risk age group: 6months-4 years of age.
First-aid for a choking baby:
*Infant <1 year of age: According to AAP and AHA.
*Place the infant face down over rescue arm with head position below the trunk. Five
back slaps are delivered rapidly between infant’s scapula with the heel of hand.
* Children >1 year of age ,Abdominal thrust ( Heimlich maneuver ) ,5 thrusts , Repeat
if not successful and call for help.
*If FB is directly visualized in the mouth, it can be removed by forceps.
*F.B. in trachea or lower airway: Endoscopy removal
Sometimes emergency tracheostomy is needed.
2)Congenital causes of upper airway obstruction:-
*c/f :
- cyclic cyanosis(congenital bilateral choanal atresia).
- abnormal cry(cri du chat syndrome).
- choking (tracheoesophageal fistula).
- stridor , recession ,Laryngeal cyst , web , laryngomalacia(wisling sound).
- vocal cord paralysis , craniofacial malformation , neck mass .
Fig. Flexible laryngoscopy showing omega shape uvula is characteristic of
laryngomalacia.
Fig. Cystic hygroma (very characteristic).
Fig. Bilateral choanal atresia after surgery.
Fig. Laryngeal web.
Fig. Congenital subglottic haemangioma.
Fig. Subglottic stenosis.

25
3)Angioneuratic edema:
-Hair dye poisoning in sudan
-PPD (para-phenylene diamene poisoning).
-Accidental: (children) .
-suicidal :(women).
-homicidal: (men).

Systems poisoning:-
- CNS : convulsion.
- CVS : Arrythmia.
- musculoskeletal: rhabdomylysis.
- kidney : Acute renal failure which is reversible.
non dose dependent : Angioneurotic edema.
Dose dependant : other systems.
Lethal dose = 10 mg.
Diffrential diagnosis:
Complement deficiency c1 estrase inhibitor deficency ( familial).
Fig. Angioneurotic edema , tracheostomy tube.
Neoplastic causes:
{Benign, Malignant } { larynx ,Pharynx and thyroid}
Fig. Juvenile Respiratory papillomatosis , showing warty shape growth in the vocal
cord.
Fig. CA larynx.
4)Neurological causes :
Recurrent Laryngeal nerve or vagus
IATROGENIC .
CVA .
Fig. Bilateral vocal cord palsy adductal palsy , can’t adduct.
Management of obstructed airway:
MEDICAL OR SURGICAL
Intubation Vs. Tracheostomy
Intubation Tracheostomy
Short term condition Chronic condition
Condition allowing Ttube to Failed intubation
pass “when you think of it”
Fig. Oropharyngeal airway , very useful in bilateral choanal atresia.
Factors that make intubation difficult:
1-Stiff Neck.
2-Trismus.
3-Long sharp teeth, crowns.
4-Bulky tongue.
5-Severe bleeding preventing visualisation (nose, maxilla and teeth, pharynx, lung,
GI).
6-Any space occupying lesion in pharynx or larynx.
Fig. Endotracheal tube.
Fig. Laryngoscope.
Fig. Laryngeal mask.
Fig. Laryngeal mask in place.

26
Surgical Measurements :
Cricothyroidetomy.
Tracheotomy (not tracheostomy..)
(incision) (ring)

Tracheotomy Indications :
1.Bypass upper airway obstruction.
2. In mechanical ventilation.
3. Pulmonary toilet and eliminate dead space.
4.Major head and neck surgery.
5. Severe sleep apnoea.
Fig. Tracheostomy tube.
Cricothyroidetomy:
-Simple , quick ,few instrument .
-avoid In children and subglottic pathology.
Anatomy:
Trachea lies in midline of the neck extending from cricoid cartilage (C6) superiorly to
the tracheal bifurcation at the level of sternal angle (T5).
Comprises 16-20 C shaped cartilage rings.
Length 10-12cm.
Diameter 15-20mm.
Technique:
-Operating room: Light , instruments, assistance ,Anaesthesia ?
-Position .(full extension).
-Incision and land marks.
-Retraction and dissection.
-Anterior jugular and isthmus .
-Incision between 2nd and 3rd tracheal rings
-Bjork flap or resect ring (… not in children).
-Insert tube .
-Tie or stitch to neck.

Types of tracheostomy tubes:

Nonmetal/metal
Cuff/uncuff
Fenestrated/unfenestrated
Short term/long term tubes
Single/double lumen tubes
Fig. Portex tracheostomy.
Fig. Obturator, inner cannula , outer cannula.
Fig. Fenestrated.
Fig. Speech valve.
Fig. 3 limb tracheal dilator.
Fig. Tracheal dilator + Tracheal look.

Emergency tracheotomy:
-Vertical incision.
-Bleeding ignored till airway secured.
Pediatric tracheotomy:

27
-Avoid emergency tracheotomy.
-No flap or ring excision.
-Use guide suture.
-Use broncoscope or intubation first.
Postoperative Care:
-Suction.
-Humidification.
-Cleaning the inner tube .
-Chest physiotherapy.
-Change after 3-5 days.
-Home care.
Decanulation:
-After disease process resolved.
-Can change tube to smaller size.
-Fenestrated tube.
-If tolerate occlusion 24 hrs. remove it.
-Dependency in children.

Early complications:
-Infection
-Hemorrhage
-Subcutaneous emphysema
-Pneumomediastinum
-Pneumothorax
-Tracheoesophageal fistula
-Recurrent laryngeal nerve injury
-Tube displacement

Delayed complications:
-Tracheal-innominate artery fistula
-Tracheal stenosis
-Delayed tracheoesophageal fistula
-Tracheocutaneous fistula

28
 Epistaxis
Lecture(6): Dr.Osama.M.Khalid

Bleeding from the nose or oral cavity.

ENT emergency.

Anatomy and Physiology:

-nasal vestibule.
-nasal cavity proper.
-nose is rich in vascularity.
-Why bleeding from nose?
1-vascular runs immediately under the mucosa.(no squamous
layer).
2-arteriovenous anastomosis.
3-blood supply comes directly from ICA&ECA with very high pressure.
Anatomy of lateral nasal wall:
Superior
Middle
Inferior
Blood supply to the nose:
ECA
1-sphenopalatine artery.(most common site of bleeding).
2-greater palatine artery.
3-ascending pharyngeal artery.
4-posterior nasal artery.
5-superior labial artery.
ICA
1-anterior ethmoidal artery.
2-posterior ethmoidal artery.

Important anastomosis in the nose:

1-anterior anastomosis = kisselbach’s plexus/little area:-
Found at the anteroinferior part of the nasal septum.
Most common site for epistaxis in both adult and children.
Consist of the following arteries:
1-anterior ethmoidal (branch of ophthalmic)
2-superior labial (branch of facial)
3-sphenopaltine (branch of internal maxillary)
4-greater palatine (branch of internal maxillary)

2-posterior anastomosis = woodruff plexus:

usually occur in adults
Consist of the following arteries:
1-pharyngeal artery.
2-posterior nasal artery of sphenopalatine artery.
More difficult to be controlled.

29
Epistaxis is classified into:
Anterior epistaxis {nose}
Posterior epistaxis {oral cavity}
Combined {nose+oral} in severe epistaxis.
*Anterior epistaxis:
Bleeding through nose
Usually in young patients
Usually septal
Most common (>90%)
Typically less severe
*Posterior epistaxis:-
Bleeding through oral cavity.
Usually due to uncontrolled HTN.
Usually from woodruff’s area.
More serious.
Etiology of epistaxis:
Local factors:
1-Vascular
2-Infectious/inflammatory.
3-Trauma (most common).
4-Iatrogenic.
5-Neoplasm.
6-foreign bodies specially in children.
Systemic factor:
1-vascular.
2-infection/inflammation.
3-coagulopathy.

Local factors
Infection/inflammation:
-any cause of inflammation in nasal mucosa.
-Rhinitis/Sinusitis:
Allergic (most common in sudan)
Bacterial.
Fungal.
Viral.
-Rhinitis: inflammatory / Sinusitis : infection.
-why epistaxis occurs in rhinitis/sinusitis?
1-hyperemia.
2- mucosa in chronic rhinitis
Which easily rupture due to sneezing or nasal picking.

Trauma:-
1)nasal picking:
-common in females and children.
-can be:
Habitual or itching
-can lead to:

30
 Epistaxis or septal perforation.(fig)
2)nose blowing/sneezing:
3)nasal fracture.
4)insertion of nasogastric tube or nasotracheal tube.
5)trauma to sinuses , Orbit , middle ear or base of skull.
6)barotrauma: restive pressure on sinuses >edema>bleeding.
Fig. Nasal fracture with septal hematoma , can lead to venous
Sinus thrombosis in cavernous sinus (are value less).

Iatrogenic:
-functional endoscopic sinus surgery.(FESS)
-Rhinoplasty : correction of the nose.
-nasal reconstruction.

Neoplasm:
+)juvenile nasopharyngeal angiofibroma.
-male , teen age.
-15 years old male presented with recurrent epistaxis.
-nowdays called naspharyngeal angiofibroma , because
It is now affecting old ages.
-management: surgery , embolization , therapy,
-diagnosis : MRI or MRA.
-biopsy is contraindicated.
-commonest benign neoplasm.
+)Inverted papilloma:
-Benign tumor.
-males in 50’s with unilateral obstruction and epistaxis.
+)Malignancy:-
-nose, nasopharynx , paranasal sinuses.
-commonest: Nasopharyngeal carcinoma.
-patient presenting with epistaxis ,look for the
nasopharynx even if you find a bleeding site.
Fig.inverted papilloma.
Fig.posterior rhinoscopy of nasopharynx.
Fig.closer view.
Foreign bodies:-
-self inflicted (pedi) vs traumatic foreign body.
-in children.
-most dangerous foreign body is (watch battery) because it
destroy nose concae and nasal septum in one hour
and can lead to tracheoeosophageal fistula.
Septal perforation:
-chemicals , infections (TB , leprosy, etc..)
*Chemicals:
-commonest is nasal sprays (should be directed to lateral wall
Of the nose not medial wall).
-Cocaine.

31
 Systemic Factors
Vascualr:
1-hypertension:
-most common.
-most difficult to manage (severe epistaxis).
2-Arteriosclerosis.
3-hereditery hemorrhagic telangectasias.
-uncommon in sudan.
-spots of blood in all the body. Fig.
Infection/Inflammation:
-fever increase blood flow.
-TB , syphilis.
-Wegner’s granulamatosis: epistaxis ,respiratory
And renal symptoms.
-SLE.
-Klazar.
Coagulapathies:
-Thrombocytopenia.
-platelet dysfunction.
Systemic disease (uremia).
Drug induced (NSAID, herbal supplement).
-Clotting factor deficiency:
Haemophilia.
Von williebrand’s disease.
Hepatic failure.
-Hematological malignancies.

Etiology and Age:-

1-children:
-commonest is F.B and nasal picking.
-1/3 with chronic bleeds have coagulation disorder.
2-Adults:
-trauma.
-idiopathic (with known bleeding site).
3-Middle age:
-tumors.
4-Old age:
-Hypertension.

#NPC should be excluded in all ages specially in recurrent epistaxis.

Initial management:
-ABC’s
-history and examination.
-prressure of the anterior part of the nose.

32
-after 5-10 min of pressure , epistaxis stop in 50-60%of cases.
-vital signs - need I.V fluids?
Physical examination:
Anterior rhinoscopy.
Endoscopic rhinoscopy.
If anterior part of bleeding is seen do cauterization by:
-chemical: AgNo3 better less painful and cover large area.
-electrical.

If failed : anterior nasal pack by gauze , remove it after

24hrs.
If failed : posterior nasal pack , remove it after
48hrs.
If failed : examination under GA , ligate the bleeding site
Or cauterize sphenopalatine , anterior
ethmoidal , or posterior ethmoidal.

Lab investigation:
- Hb , CBC , platelet , etc.
Radiological:
- mass
-angiofibroma treatment by surgery.

Non surgical treatments:

-discontinue medication.
-avoid nasal picking and treat itching.
-atopic rhinitis : use drugs to humidify nasal cavity.
-control HTN.

*recent modification of nasal packs: easy to apply , easy to

Remove and less painful.
*posterior nasal pack can lead to respiratory obstruction.
*don’t ask the patient to raise his head.
*don’t use adrenaline because:
-bleeding HTN lead to cerebrovascular accident.
-Rebound phenomenon.
*adrenaline can be used in elective surgery.

33
 Nasopharyngeal Carcinoma
Lecture(7)Dr.Nazik Elfadil
 Classification of Cervical Lymphnodes:
- Level 1 : Submental and Submandibular.
- Level 2 : Upper deep cervical LNs.
- Level 3 : Middle deep cervical LNs.
- Level 4 : Lower deep cervical LNs.
- Level 5 : Posterior triangle LNs.
- Level 6 : Pretracheal and Prelaryngeal LNs.
- Level 7 : Mediastinal LNs.

 Diffrential diagnosis to level 2 metastasis:(behind and below the mandible)

i. Nasopharynx.
ii. Palatine tonsil.
iii. Posterior 1/3 of the tongue.
iv. Piriform fossa.
v. Thyroid gland.

 Eustachian tube elevation isnan important anatomical land mark which lay just
behind and superior to eustachian tube .
Opening : Above and below is fossa of Rose muller which harbor more than 95%
Of NPC!.
 All the mucosa of the nasopharynx at birth is respiratory
epithelium(pseudostratified ciliated columnar epithelium with scattered goblet
cells ) , by adulthood , 60% of lining mucosa is metaplasized to squamous
epithelium:
 Squamous epithelium : posterior and lateral wall.
 Respiratory epithelium: Anterior wall.
95% of NPC is squamous cell type.
Anatomy Of Naspharynx:
- Nasopharynx is very rich in submucus lymphatics , so locoregional spread to local
LNs, is very common.(cheif presenting symptom).
- Submucus lymphatics of nasopharynx can cross the mid line (metastasis go to the
other side).
- It is a blind spot in skull base so it is difficult to be examined (late presentation).
- Has important relationships:(important in staging and management).
Roof : Skull base + sphenoid sinus + foramen lacerum.
Posterior : (C1, C2, cervical vertebrae + prevertebral muscles).
Laterally: parapharyngeal space.
- Seperated by styloid process into:
i- prestyloid compartment :(deep lobe of parotid gland
ii-post styloid.(lower 4th cranial nerve).
 Clinical cause and factors : The invasive and metastatic potential of NPC is
Responsible for the symptomatology.
Fig. Bilateral cervical LNs enlargment with technical cauterization.
NPC is the commonest Upper airway aerodigestive tract malignancy that give
Bilateral cervical lymphadenopathy.
 Nodal stations of NPC :
1) First nodal station.

34
 Lay at lateral wall of nasopharynx at the apex of fossa of Rosemuller
(non palpable clinically).
2) 2nd Nodal station :
Retropharyngeal group of LNs (not palpable clinically).
3) 3rd Nodal station :
Level 2 cervical lymph node - late but unfortunately the commonest presentation.
Fig. Old man with level 2 enlargment Diffrential diagnosis (see above).
Fig. Right sided ptosis : patient has ophthalmoplegia for 7 months due to
Neurological affection of extraocular muscles.
Orbital manifestation in NPC is due to :
i- NPC can spread to pterygopalatine fossa - infra orbital fissure and
Attack the orbit.
ii- NPC to skull base to sphenoid sinus to cavernous sinus lead to
ophthalmoplegia
3rd , 4th and 6th cranial nerves affection.

Fig. Level 2 enlargment , misdiagnosed as tuberculus cervical lymphadenopathy.

If you have negative ZN stain - clinical diagnosis of tuberculus cervical
Lymphadenitis- Theraputic trial of TB drugs - no improvement after 3 wks-
Revise the diagnosis.
Fig. Right abducent palsy (commonest single cranial nerve affected in NPC).
Fig. Right hypoglossal palsy : single/multiple.
Jugular foramen syndrome (Verret’s syndrome):
NPC spread to skull base - jugular foramen - attacks 9th 10th and 11th cranial
Nerves (palatine paralysis + laryngeal paralysis).
Fig. Trismus bad sign indicate spread of NPC to parapharyngeal space (Trigeminal
nerve or ptrygoid muscle).
Fig. Lady with level 2 , with surgical scar
Investigations : Fine needle aspiration (FNA).(Avoid surgical invasive biopsy).
Fine needle aspiration in >90% of cases it diffrentiate between:
1- benign.
2-malignant (metastasis or lymphoma).
*Excisional biopsy disadvantages:
i- create a route of spread of the disease.
ii- false impression of cure.
iii- limit options for surgical excisional treatment.

Signs and Symptoms:

- Cervical lymphadenopathy(60%).
- Epistaxis and naso respiratory symptoms(40%).
- Audiological symptoms:
Due to ET tube obstruction - O.M.E.
#Adult presenting with O.M.E this NPC till proved otherwise.
Tinnitus , otalgia and deafness (30%).
- neurological symptoms , haedache , cranial nerve palsies and
Horner’s syndrome .(20%)
- Metastasis which can be locoregional (paranasal sinus , parapharyngeal
Space , infratemporal fossa , Orbit , Parotid and cervical lymphadenopathy).
- Distal metastasis are not common in NPC.

35
 1-Bone.(50%).
2-Lung
3-Liver
Note: Cranial involvement is local.
Epidemiology of NPC:
*Risk Factors:
1)Virus : EBV.
2)Genetics.
3)Geographic distribution.
-Sudan is an intermediate risk for NPC.
-More in males due to:
4)Alcohol.
5)smoking.
-Has 2 peaks :
young peak 10-15 year {genetic predisposition}
Old peak 50-54 year {enviromental factor}
Nasopharyngeal examination:
1)Posterior Rhinoscopy : mirror examination of the nasopharynx(this is done
Under local or general anaesthesia it is the quickest way to assess the
Nasopharynx.
2)Rigid endoscopy : it allows close-up view of the nasopharynx and it
is recesses.
3)Flexible fibreroptic nasopharyngoscopy:
Most useful endoscopy for nasopharynx and upper.
Very easy , expensive and not available in all countries.
4)Examination under GA - Biopsy.
5)Biopsy of the lesion.
6)Radilogical investigations:
MRI is gold standard in radiology.
MRI offers an advantage over CT in the detection and localization of
head and neck tumors and the distiction of LNs from blood vessels.
Clinical staging of NPC:
- TNM satging.
- staging is important in management and prognosis.
Histological classification of NPC:
Type 1 : squamous cell carcinoma.(25%). Poor response to chemo/radio therapy.
Type 2 : non keratinizing carcinoma.(12%) good response.
Type 3 : undiffrentiated carcinoma.(60%) good response.
Treatment of NPC:
- Stage 1 treated by radiotherapy.
- Stage 2,3,4 chemotherapy.
Chemotherapy either:
1) new adjuvant chemotherapy.(chemotherapy followed by radiotherapy).
Making malignant cells more susceptible to radiotherapy.
2) concurrent chemotherapy.(both chemo/radio therapy at same time).
Advantages : give better disease control + better prognosis.
Disadvantage: side effect of both and ICU admission.
*Prognosis of NPC is highly dependent on histological classification and clincal
staging.
*Stage IV : Advance disease + poor prognosis.

36
 (see slides)

Vertigo
Lecture(8):Prof.HashimYagi
-VERTIGO IS AGRAY AREA IN MEDICINE .
ANATOMY OF THE INNER EAR :
-The vestibular apparatus is a part of the inner ear ; 3 semicircular
canals , utricle and saccule.
-Vestibular apparatus doesn't communicate with the middle ear.
(vertigo is Not a middle ear disease ).
-Macula is the functional part in the utricle and saccule.
-Copula is the functional part in the semicircular canals.
-Fluid :1-Endolymph
2- perilymph
Meniere's Disease
-it is hydrops of the membranous labyrinth (endolymph is secreted
in excess ).
-Idiopathic.
-There IS : vertigo , Tinitus , Deafness (sensorineural ).
-Noise can provoke it.
-Vomiting , palpitations.
Treatment :
-Decrease salt intake.
-Rehabilitation exercises.
-Vestibular sedatives.
-Surgery : saccus Endolymphaticus (surgical decompression).
-Remission do occur.

Balance:
-The vestibular apparatus is the master of movement !
-Falling during sleep = abnormal vestibular system
-Normal balance need ;
1. Vision
2. Healthy left inner ear
3. Healthy Right inner ear
4. Muscle function and sense
-If any problem in one of them you tend to fall.

Vestibular nystagmus :
-Why seen in the eye , because the eye you can see them as their
muscle functioning& Because the eye Muscles receive
information from the vestibular system.
It consists of 2 components :
1 . Quick component : the brain is trying to correct it (brain
component )
Brain : go this way !
Vestibular system : no this way please !
Brain : I said this way !
2.Slow component : vestibular system
-Nystagmus is a sign of Acute vestibular disease !

37
 Types :
1. Peripheral nystagmus ; benign disease . Horizontal with a
rotatory element.
2. Central nystagmus ; serious disease . Disorganised dissociated
up and down one eye right and the other is left.
3.other types :Gase nystagmus (physiological )
Railway nystagmus.

-Vertigo : is the sensation of the external world revolving.

-Vertigo is a disease of the vestibular apparatus.
-You feel the world is rotating or you are rotating.
-Vertigo is not the dizziness of heart block.
-The vestibular system has nothing to do with the loss of consciousness !
-Loss of consciousness is a higher centres disease.
-Double vision is an eye disease.
-Blurring of vision is a brain ischemia.
-Aura = epilepsy
Etiology
1. Trauma or ear operation.
2. Infectious (viral are the most common ).
3. Vestibular neuritis.
4. Benign paroxysmal positional vertigo ( happens in special
situations ).
5. Meniere's Disease.

Nb : How to differentiate between benign vertigo and malignant

vertigo ?
-Benign vertigo is fatigable ( disappear with many repetitions ).
-Malignant vertigo persists and doesn't disappear.
- vestibular sedatives are given in acute phase but for chronicity u
need vestibular rehabilitation ( Rise the functioning ).
Treatment of Central nystagmus :
-Poor prognosis , treatment is by treating the central cause
( tumor ? Vascular disease ? etc )
Treatment of peripheral nystagmus : good prognosis
Excersing ‫اﻟﺪراوﯾﺶ‬
For eye , neck , shoulder , whole body like basket ball player.

38
 Fungal Rhinosinusitis
Lecture(9):Dr.Nazik Elfadil

20% from population affected at some time of their life.

Prevalence roghly estimated as 900 million case world wide.
High incidence of fungal sinusitis in Sudan.
Commonest in Sudan Asp. flavus.
World wide increasment incidence due to HIV.
Commonest offending organism world wide is Asp Fumigatus.
Only those who are hypersensitive to the fungi devlop the disese.
Those who are not hypersensitive will be just carrier
To proof you have to find fungal hyphae and mucin.
Classification Is based on clinical, radiological,histological and mycology studies

Classification of Fungal Sinusitis:

Invasive Non Invasive
1-Chronic Invasive FS 1-Allergic Fungal sinusitis .

2-Chronic Granulomatous FS . 2-Fungal ball ( Fungal granuloma ) .

Sinus mycetoma,
3-Acute Fulminant FS.

Pointers to Fungal Sinusitis:

Clinical : Thick , Muddy Discharge .
CT(soft tissue window) : Metallic calcification (Foreign Body appearance) .
Management of Fungal sinusitis:
Medical treatment(specific+nonspecific) + Immunotherapy
Surgical treatment
Followup of Fungal sinusitis:
Frequent follow up
Recent Study:
23/44
Male:Female 1:2
Age : 14-62.
Presenting symptoms:
1-Nasal obstruction 91%.
2-proptosis 35%
3-Epiphron 8.7% (excessive lacrimation)nasolacrimal duct affection.
4-Anosmia or (hyposmia) 8.7%
5-Muddy Rhinorrhea 12%.
6-Lacrimal Dacryocystitis. 4.3%
7-facial swelling.
Involved sinus:
*Ethmoid 96% commonest site for fungal sinusitis in adults.
*Maxillary 41%.(commonest in ordinary or bacterial).
*Sphenoid 22%.
*Frontal 9%.

39
Case 1: 35 years old male farmer from Alnohod presented with Left proptosis +
supraorbital swelling. On examination there is limitation in left visual feild and left
supraorbital swelling
CT scan(gold standard investigation for nose and paranasal sinuses) finding : bilateral
ethmoid and left frontal opacity with skull base defect.
All sinuses are in clise anatomical relation to the orbit the ethmoid lie medial to the
orbit and seperated from it by very thin plate of bone named as lamina papreacia.
Serology using counter immunoelectrophoresis for aspergillus flavus was positive.
Biopsy : Fungal granuloma with considerable fibrosis.
It is non caeseating granuloma with foreign body or langhans type of giant cells
And some times we may even find vasculitis due to vascular invasion.
Treatment:
Went for FESS(functional endoscopic sinus surgery) and external
frontoethmoidectomy
Itraconazole 200mg p.d for 6month.
Case2: 19 years old lady student from khartoum(by the way fungal sinusitis is
common in lady than in gentle men presented with Right nasl obstruction with history
of muddy nasal discharge(discharge looks like mud greenish ,very suggestive of
fungal sinusitis) , the patient was not responding to nasal decongestant for 1 year.
Not asthmatic , not aspirin hypersensitive(we have association between aspirin allergy
and allergies such as asthma or allergic fungal sinusitis) , not responsive to ttt.
On examination Right nasal swelling(polyp),greenish sticky tenaceous discharge
(very characteristic of fungal rhinosinusitis) inside the nose.
CT findings: opaque Right maxillary , ethmoid( heterogenous) very charecteristic for
fungal sinusitis.
The patient went for FESS and histology reveals fungal hyphae and
eosinophils(presence of eosinophil signifie the presence of allergy or hypersensitivity)
Mycology by blood testing using counter immuno electrophoresis was for aspergillus
flavus. The patient was diagnosed as having alllergic fungal sinusitis.
No invasion ,No bone erosion (lamina paprecia is intact).
Post surgical management:
-prednisolone 5mg with tapering to stop.
-nasal spray for life.

* Metalic calcification in CT.(in soft tissue window).

Characteristic for fungal rhinosinusitis.
Mycology :
Collection in sterile container in noramal saline.
PAS (periodic acid schiff).
22/23 were histologically +ve.
Types of sinusits:
Allergic fungal sinusitis 65%.
-Topical steroids for life on &off systemic steroids.
Chronic invasive 22%
-FESS (Functional endoscopic sinus surgery).
Chronic invasive & granulmatous:
-Oral itraconazole for 6 months.(monitor LFT monthly).
-Caldwelluc operation.(clearence of hyphae via subcilliary approach).
-Meticulus follow up is important (recurrence rate is high).

40
 Hearing Loss (HL)
Lecture(10):Dr.Osama.M.Khalid.

-Receptors of hearing : organ of Corti (hair cells).

-hearing loss(deafness),range from mild , moderate to profound HL.

Types of hearing loss:

1-sensori neural HL (SNHL).
2-conductive HL (CHL).

Sensori neural HL
-Sensory : affect organ of corti (hair cells).
-Neural : vestibulo cochlear nerve.
-Result of damage to the inner ear.
-90% of HL in adults.
-generally permenant HL.
classified into:
a-cochlear (affect choclea).
B-retro cochlear (affect nerve).
-Senile SNHL.

Causes of SNHL:-
1)Congenital: syndromic & non syndromic:
*Syndromic:
a-Alport syndrome
HL+ Renal impairment (recurrent GN can lead to RF).
Male , teen age .
b-Pendred syndrome
HL + Goitre
Female , teen age
Pendredian protein deficiency (tyrosine transporter).
c-Usher’s syndrome
HL + Retinitis pigmentosa.(bilateral).
d-Waardenberg syndrome
HL
White forelook
Heterochromia iridium (blue eye)
Common in sudan.
e-Treacher-Collins syndrome
HL
Low set ear , eye .
Change in facial features.
*Non syndromic:
a-Inner ear malformation :
Absent or deformed cochlea
Absent nerve
b-Infectious:
Rubella , CMV (intrauterine).

41
2)Infections :-
-Maternal Rubella
-Congenital CMV
-Mumps
Severe hearing loss (unilateral).
-Measles
-Meningitis:
Lead to cochlear ossification that is why it is the most difficult cause of
SNHL to be treated.(treatment by immediate cochlear implant).
*Generally any febrile condition can lead to SNHL
Viral infection
Sudden SNHL , the only cause that can be treated by medication.
3)Drugs :-
a-Aminoglycosides like : streptomycin & gentamycin( irreversible HL).
b-Diuretics (reversible HL).
c-Quinine (irreversible HL).
4)Trauma :-
Temporal bone fracture that comes across cochlear nerve.
5)Noise induced HL :-
‫ اﻟﻌﺴﺎﻛﺮ‬، ‫ اﻟﻤﻄﺎرات‬، ‫ ﻋﻤﺎل اﻟﻤﺼﺎﻧﻊ‬، ‫ اﻟﺘﻠﻔﻮن‬، ‫اﻟﺤﻔﻼت‬
Maximum 80db / 8hrs , 120db/hour lead to deafness.
Temporary threshold shift ‫ﻣﺎ ﺑﯿﺴﻤﻊ ﺑﻌﺪ اﻟﺤﻔﻠﺔ‬
6)Age related HL :- (presbycusis)
Senile , depend on family and residence.
7)Acouistic Neuroma :-
Not acoustic nor Neuroma it is Vestibular Schwannoma in the internal auditory
meatus
Pressing the nerve.
8)Sudden SNHL :-
Theories (viral , Autoimmune)
Occurs in hours to 3 days.
Defect more than 30 db.
Patient usually present late.
Treated quickly by high dose of steroid.

Conductive Hearing Loss (CHL)

-Occurs when there is damage or blockage in the outer or middle ear preventing sound
From travelling normally through the ear canal to the inner ear.
Can often be corrected.

Causes of CHL :-
Affect ear pinna
1-Anotia (no auricle).
2-microtia (underdeveloped auricle).
Affect external ear : (blockage):
3-ear wax (most common cause of CHL).

42
 4-congenital blockage of external canal.
5-F.B (seads).
Affect T.M:
6-Thick T.M (tympanosclerosis for example).
7-perforated T.M:
Loss of fusion of ossicles and T.M in amplification of sounds.
Affect middle ear :-
8-O.M with effusion :(secretory O.M)
More common in children and can lead to adhesive O.M/glue ear.
9-Otosclerosis :
New bone growth in middle ear , the stapes is fixed.
It is common in female , it is common in sudan.

Perforated T.M:
-Degree of HL depend on site and size of perforation.
-posterior perforation more HL.
-larger perforation more HL.
-ossicular disruption more HL.

*If child is not cooperative when removing F.Bs from the ear do GA.
*Remember function of ear wax:
Trap F.Bs , Contain lysozymal enzymes and IgA , keep PH of external canal acidic.
Fig. Perforated ear drum
Fig. Ear wax
Fig secretory O.M

Hearing Assessment:-
-Done after clinical examination of the ear.
-Clinical hearing assessment using tuning fork.

*Rinne’s Test:
Comparison between air conduction and bone conduction.
i-positive Rinne’s test:
-normally air conduction should be better than bone conduction.
-positive Rinne’s test : air conduction better than bone conduction indicating either:
A-Normal hearing.
B-SNHL.
ii-negative Rinne’s test:
-bone conduction better than air conduction.
-Indicate CHL.
Weber’s test :-
Comparison between the two ears.
Put tunning fork on the forehead.
If patient hear by right ear better than left ear
Conductive HL in his right ear or his left ear is diseased.
If left ear conduction better normal.

Pure Tone Audiogram :

-Normal person up to 20 db.

43
-SNHL ‫اﻟﺨﻄﯿﻦ ﯾﻨﺰﻟﻮ ﻣﻊ ﺑﻌﺾ‬
Mild 25-35
Moderate 35-45
Severe 45-
-Conductive HL‫اﻟﺨﻄﯿﻦ ﺑﻌﯿﺪات ﻣﻦ ﺑﻌﺾ‬
-Mixed HL.‫ﺑﻌﯿﺪات ﻣﻦ ﺑﻌﺾ وﻧﺎزﻻت ﺗﺤﺖ‬
-4000 is diagnostic for noise induced HL.

Management of HL:
*Management of SNHL:
- use hearing aids
i-behind the ear.
ii-completely in the canal.
-If patient has severe SNHL completely in the canal hearing aid are not useful.
-Child with congenital hearing loss should be treated in the first 2 years.
-After 4-5 years no treatment is useful.
-Neonate with HL assessment after 3 month
1)hearing aid (before 2 years).
2)If failed cochlear implant.

cochlear implant are beneficial in :

i-pre lingual:
ii-post lingual:
-cochlear implant is very expensive.
-child may need speech therapy.

Neonates with high risk of HL:

i-preterm.
ii-low birth weight (less than 1.5 kg)
iii-developed kernicterus.
iv-family history of HL.
-cochlear implant are electronic device.

Management of CHL:-
According to the cause:
-remove ear wax
-open external canal surgically.
-Tympanoplasty.
-Ossiculoplasty.
-Bone Anchored Hearing Aid (BAHA)
Used specially in:
Canal atresia and Tracher-Collins syndrome.

44