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ACUTE OTITIS MEDIA
1.Acute suppurative otitis media
Inflammation of the middle ear , the area between the tympanic
membrane and the inner ear by pyogenic organism less than 3 weeks.
Aetiology :
It is more common especially in infants and children of lower socio-economic
group. Typically, the disease follows viral infection of upper respiratory tract
but soon the pyogenic organisms invade the middle ear.
Predisposing factors: anythings that interferes with normal function
of Eustachian tube predisposes to middle ear infection
- recurrent attacks of common cold , URTI .
-infection of tonsils and adenoids .
-chronic rhinitis and sinusitis .
-nasal allergy .
-Associated conditions: cleft palate, Down syndrome.
Route of infection:
• Eustachian tube: most common route . Eustachian tube in infant and
children is shorter , wider and more horizontal , breast or bottle feeding
may force fluid into middle ear .
Swimming and diving can also force water to middle ear.
• External auditory canal : Traumatic perforation of TM.
• Blood born: uncommon route .
Bacteriology:
- Streptococcus pneumonia
- Haemophilus influenza
- Moraxella catarrhalis
. Pathophysiology:
The patient has an antecedent event (viral URI or allergy) → the event
results in Congestion of the respiratory mucosa → obstruction causes
negative pressure followed by Accumulation of secretions → these
secretions accumulate in the middle ear space → viruses and bacteria
that Colonize the upper respiratory tract can reach the middle ear via
aspiration, reflux → microbial growth in the middle ear secretions may
result in suppuration.
Clinical Features
Symptoms:
Diminished hearing
ear pain may disturb sleep and is of throbbing in nature.
Tinnitus
child runs high degree of fever and is restless accompanied by vomiting
and convulsions
Otorrhea
Signe:
Tympanic membrane is retracted
Erythematic tympanic membrane
handle of malleus assuming a more horizontal position.
prominence of lateral process of malleus and loss of light reflex.
conductive deafness.
TREATMENT
• Antibacterial therapy
- Amoxicillin or Augmentin
• Decongestant nasal drop
- Ephedrine nose drops
• Oral nasal decongestants.
- Pseudoephedrine
• Analgesics and antipyretics.
• Dry local heat.
• Myringotomy
- It is incising the drum to evacuate pus and is indicated when
(i) drum is bulging and there is acute pain
(ii) there is an incomplete resolution despite antibiotics when drum remains full with persistent
conductive deafness
(iii)there is persistent effusion beyond 12 weeks
2.OTITIS MEDIA WITH EFFUSION
This is an insidious condition characterized by accumulation of non-purulent
effusion in the middle ear cleft.
often the effusion is thick and viscid but sometimes it may be thin and serous.
The fluid is nearly sterile. The condition is commonly seen in school-going
children.
Pathogenesis
Two main mechanisms are thought to be responsible:
1. Malfunctioning of Eustachian tube. Eustachian tube fails to aerate the middle
ear and is also unable to drain the fluid.
2. Increased secretory activity of middle ear mucosa. Biopsies of middle ear
mucosa in these cases have confirmed increase in number of mucus or seroussecreting cells.
Aetiology
1- Malfunctioning of eustachian tube :
A- Adenoid hyperplasia
b-chronic rhinitis and sinusitis
c-chronic tonsilitis
d-benign and malignant tumours of nasopharynx
e-palatal defect eg: cleft palate
2- allergy
3-unresolved otitis media
4-viral infection
Clinical Features
Symptoms: The disease affects children of 5- 8 years of age. The symptoms include:
(1) Hearing loss.
(2 Delayed and defective speech. Because of hearing loss, development of speech is delayed or
defective.
(3) Mild earaches.
• Clinical assessment:
• O/E:
• Otoscopic findings: Tympanic membrane is often dull and opaque with loss of light reflex.
-It may appear yellow, grey or bluish in color.
• -Thin leash of blood vessels may be seen along the handle of malleus or at the periphery of
tympanic membrane and differs from marked congestion of acute suppurative otitis media.
• -Tympanic membrane may show varying degree of retraction. Sometimes, it may appear full or
slightly bulging in its posterior part due to effusion. Province of lateral process, Decrease in
mobility of T.M has bulging contour “difficult to assessing ossicular land mark
• Hearing Tests
(1) Tuning fork:
• rinne:
 *air louder than bone “positive” (normal)
 *Bone louder than air “negative” (conductive hearing loss)
• tests show conductive hearing loss
• Weber:
 Sound heard in midline (normal)
 Sound heard in bad ear (conductive hearing loss)
 Sound heard in good ear (sensorineural hearing loss)
• tests show conductive hearing loss
(2) Audiology:
•PTA: to masseur hearing sensitivity by threshold levels of individual, the intensity as a function of
frequency.
Conductive: gap between air and bone by 10 dB
Sensorineural: the air and bone within each other 10 dB, and the threshold higher than 25 dB.
There is conductive hearing loss
•Tympanometry:
Type A: look like a teepee and indicate normal middle ear.
Type B: flat line, there’s fluid or infection behind eardrum.
Type C: teepee but shifted negatively, indicate negative pressure in middle ear space.
The test show type B.
(4) X-ray mastoids. There is clouding of air cells due to fluid.
Treatment
The aim of treatment is removal of fluid and prevention of its recurrence.
A. Medical
1. Decongestants.
2. Antiallergic measures.
3. Antibiotics.
B. Surgical
When fluid is thick and medical treatment alone does not help, fluid must
be surgically removed.
1. Myringotomy and aspiration of fluid.
2. Tympanotomy or cortical mastoidectomy.
3. Surgical treatment of causative factor.
CHRONIC OTITIS
MEDIA
Chronic suppurative otitis media with and without
cholesteatoma
csom
• CHRONIC SUPPURATIVE OTITIS MEDIA
IS A LONG STANDING INFECTION OF A
PART OR WHOLE OF THE MIDDLE EAR
CLEFT CHARACTERIZED BY:
• EAR DISCHARGE (OTORRHEA)
• PERMANENT PERFORATION OF
TYMPANIC MEMBRANE.
EPIDEMIOLOGY:
 Incidence is higher in developing countries
 Affects both sexes and all age groups
 Most important cause of hearing impairment in rural population
Diagnosis:
 Duration > 3 months despite treatment
 Discharge mucopurulent otorrhea
 Deafness Perforation /Ossicular chains
Etiology:
 Pseudomonas aeruginosa
 Staphylococcus aureus
 Proteus species
Pathogenesis:
 ET dysfunction
 Poor aeration
 Mucosal edema and ulceration
 Capillary proliferative
 Osteitis
TYPES
 Clinically it is divided into two types :
1. Tubotympanic
2. Atticoantral
Tubotympanic type (Safe)
SIMPLE PERFORATION
 INTERMITTENT NON OFFENSIVE NON
BLOODY EAR DISCHARGE
 ON EXAMINATION (CENTRAL
PERFORATION )
ATTICO-ANTRAL
(UNSAFE)
 Chronic ,Scanty, offensive and bloody ear discharge
On examination marginal perforation
 You may see cholesteatoma
Risk of complications is high
property
Tubotympanic
Atticoantral
Discharge
Profuse,mucoid, odourless
Scanty,purulent,
smelling
Perforation
Central
Marginal
Granulations
Uncommon
Common
Polyp
Pale
Red and fleshy
Cholesteatoma
Absent
Present
Complications
Rare
Common
Audiogram
Mild to moderate
conductive deafness
Conductive or mixed
deafness
foul
ADHESIVE OTITIS MEDIA
• FORMATION OF ADHESION IN THE MIDDLE EAR AFTER RE-INFECTION AND HEALING OF
CSOM OR OME.
• -VE PRESSURE IN THE TYMPANIC CAVITY.
• EARDRUM RETRACTS ONTO STRUCTURE WITHIN THE MIDDLE EAR.
MAY CAUSE MIDDLE EAR ATELECTASIS:
• RESULT OF DYSFUNCTION OF EUSTACHIAN TUBE.
• THE EAR DRUM BECOMES FLACCID.
• WILL CAUSE BONE EROSION AT IS JOINT.
• CAN BE TREATED WITH TYMPANOSTOMY.
CHOLESTEATOMA
• Normally, middle ear cleft is lined by different types of epithelium in
different regions: ciliated columnar in the anterior and inferior part,
cuboidal in the middle part and pavement-like in the attic. The middle
ear is nowhere lined by keratinizing squamous epithelium. It is the presence of latter type of epithelium in the middle ear or mastoid that
constitutes a cholesteatoma.
• In other words, cholesteatoma is a “skin in the wrong place.
• The term cho- lesteatoma is a misnomer because it neither contains
cholesterol crystals.
Essentially, cholesteatoma consists of two parts:
• (i) the matrix, which is made up of keratinizing squamous epithe- lium
resting on a thin stroma of fibrous tissues.
•(ii) a central white mass, consisting of keratin debris produced by the
matrix (Figure 11.1). For this reason, it has also been named epidermosis or
keratoma.
ORIGIN OF CHOLESTEATOMA
• Presence of congenital cell rests.
• Invagination of tympanic membrane from the attic or
posterosuperior part of pars tensa in the form of retrac- tion pockets
(Wittmaack’s theory). The outer surface of tympanic membrane is lined
by stratified squa- mous epithelium which after invagination forms the
matrix of cholesteatoma and lays down keratin in the pocket.
• Basal cell hyperplasia (Ruedi’s theory). The basal cells of germinal layer
of skin proliferate under the influ- ence of infection and lay down
keratinizing squamous epithelium.
• Epithelial invasion (Habermann’s theory). The epithelium from the meatus
or outer drum surface grows into the middle ear through a pre-existing
perforation especially of the marginal type where part of annulus
tympanicus has already been destroyed.
• Metaplasia (Sade’s theory). Middle ear mucosa, like respi- ratory
mucosa elsewhere, undergoes metaplasia due to repeated infections and
transforms into squamous epithelium.
CLASSIFICATION OF CHOLESTEATOMA
• 1. Congenital cholesteatoma. It arises from the embryonic epidermal cell
rests in the middle ear cleft or temporal bone. Congenital cholesteatoma
occurs at three important sites: middle ear, petrous apex and the
cerebellopontine angle, and produces symptomatology depending on its
location.
• A middle ear congenital cholesteatoma presents as a white mass behind an
intact tympanic membrane and causes con- ductive hearing loss. It may
sometimes be discovered on rou- tine examination of children or at the time
of myringotomy.
• It may also spontaneously rupture through the tympanic membrane and
present with a discharging ear indistinguish- able from a case of chronic
suppurative otitis media.
• 2. Primary acquired cholesteatoma . It is called primary as there is no
history of previous otitis media or a pre-existing perforation. Theories on its
genesis are:
• (a) Invagination of pars flaccida. Persistent negative pressure in the attic
causes a retraction pocket which accumu- lates keratin debris. When
infected, the keratin mass expands towards the middle ear. Thus, attic
perfora- tion is in fact the proximal end of an expanding invagi- nated sac.
• (b) Basal cell hyperplasia. There is proliferation of the basal layer of pars
flaccida induced by subclinical childhood infections. Expanding
cholesteatoma then breaks through pars flaccida forming an attic
perforation.
• (c) Squamous metaplasia. Normal pavement epithelium of attic undergoes
metaplasia, keratinizing squamous epi- thelium due to subclinical infections.
Such a change has also been demonstrated in cases of otitis media with
effusion.
• 3. Secondary acquired cholesteatoma. In these cases, there is already a preexisting perforation in pars tensa. This is often associated with posterosuperior
marginal perforation or sometimes large central perforation. Theories on its
gen- esis include:
• (a) Migration of squamous epithelium. Keratinizing squa- mous epithelium of
external auditory canal or outer surface of tympanic membrane migrates
through the perforation into the middle ear. Perforations, involv- ing tympanic
annulus as in acute necrotizing otitis media, are more likely to allow in-growth
of squamous epithelium.
• (b) Metaplasia. Middle ear mucosa undergoes metaplasia due to repeated
infections of middle ear through the pre-existing perforation.
EXPANSION OF CHOLESTEATOMA AND
DESTRUCTION OF BONE
• Once cholesteatoma enters the middle ear cleft, it invades the surrounding structures, first
by following the path of least resistance, and then by enzymatic bone destruction .
• An attic cholesteatoma may extend backwards into the aditus, antrum and mastoid;
downwards into the mesotympanum; medially, it may surround the incus and/or head of
malleus.
• Cholesteatoma has the property to destroy bone. It may cause destruction of ear ossicles,
erosion of bony labyrinth, canal of facial nerve, sinus plate or tegmen tympani and thus
cause several complications. Bone destruction by cho- lesteatoma has been attributed to
various enzymes such as collagenase, acid phosphatase and proteolytic enzymes, liberated by osteoclasts and mononuclear inflammatory cells, seen in association with
cholesteatoma. The earlier theory that cholesteatoma causes destruction of bone by
pressure necrosis is not accepted these days.
FORMATION OF ACQUIRED
CHOLESTEATOMA
SYMPTOMS OF CHOLESTEATOMA
• Hearing loss.
• Discharge from the ear with or without an odor.
• Tinnitus.
• Dizziness
• Fullness or pressure in ear.
• Facial weakness or paralysis
HOW IS CHOLESTEATOMA
DIAGNOSED?
• Physical examination of the ear with an otoscope. The dead skin tissue
can sometimes be seen through the eardrum.
• A CT scan and audiology evaluation may also be necessary to
determine the size and extent of damage of the cholesteatoma.
TREATMENT:
• Initial treatment involve cleaning of the ear , antibiotics and ear drops to
treat any infection.
• A. Ototopical medications:
• Antibiotic only otic drops:
• Floxin.
• Antibiotic with steroid otic drops:
• Ciprodex
• Cipro HC
SURGICAL PROCEDURES FOR
CHOLESTEATOMA
Cholesteatoma Surgery
Mastoidectomy:
 Canal wall up
 Canal wall down
•Tympanoplasty.
•Tympanomastoidectomy.
Ossiculoplasty.
CAN CHOLESTEATOMA CAUSE LASTING
PROBLEMS?
• If left untreated, cholesteatomas can become large and infected. It can
spread to the inner ear and brain.
• This can lead to permanent hearing loss , dizziness , facial paralysis ,
brain abscess , or meningitis.
COMPLICATIONS OF OTITIS MEDIA
1.Impaired hearing.
2. Speech or developmental delays.
3.Spread of infection.
4.Tearing of the eardrum.
5.Cholesteatoma
COMPLICATIONS OF OTITIS MEDIA
1.Impaired hearing.
2. Speech or developmental delays.
3.Spread of infection.
4.Tearing of the eardrum.
5.Cholesteatoma
COMPLICATIONS
3.Spread of infection:
• Intratemporal (Within the Confines of Temporal Bone)
1. Mastoiditis
2. Petrositis
3. Facial nerve paralysis
4. Labyrinthitis
• Intracranial
1.extradural abscess
2.subdural abscess
3.mningitis
4.Brain abscess
5.Otitic hydrocephalus
6.Lateral sinus thrombosis
REFERENCES :
• Diseases of Ear, Nose and throat ( PL Dhingra) 6th edition.
• http://emedicine.medscape.com/article/994656treatment?src=refgatesrc1
• http://www.mayoclinic.org/diseases-conditions/earinfections/symptoms-causes/dxc-20199484