E.N.T.Acute otitis media.(dr.hiwa)

Acute otitis media

Prepared by Dr. Hiwa As’adM.B.Ch.B

C.A.B.S(ENT H&N Surgery)

F.I.C.M.S (ENT)

Classification Otitis Media is classified into:

Suppurative :

* Acute suppurative otitis media.

* Chronic suppurative otitis media.

Non Suppurative :

* Acute non suppurative otitis media.

* Chronic non suppurative otitis media.

Adhesive :

* Adhesive otitis media.

* Tympanosclerosis

Specific :* Tuberculous otitis media.

* Syphilitic otitis media.

Acute otitis media

Definition :

Is an acute inflammatory reaction

involving the mucosal lining of the middle

ear cleft in the whole or part of its extent

from the eustachian tube to the mastoid

antrum and air cells .

Incidence The commonest otological condition in

childhood.

Nearly 50% in the first year of life.

Remain high in the first 5 year of life.

Relatively infrequent in teenagers.

More frequent in the colder months of the year when URTI are also more frequent.

More common in children from urban area.

Less common in adult.

Classification :

1. Acute catarrhal otitis media

2. Acute middle ear effusion

3. Acute suppurative otitis media

Acute catarrhal o.m. Usually occurs after URTI particularly sinusitis or

influenza.

Simple oedema of the Eust. Tube mucosa

prevents proper opening and closing .

Clinically:

Deafness and popping in the affected ear and a

feeling of pressure.

There is no pain.

Nasal & pharyngeal symptoms are those of an URTI.

Nasal obstruction with a mucopurlent nasal

discharge.

The pharynx may or may not congested.

T.M. :• Retracted.

• Colour is normal or slightly pink with a few

dilated vessles.

Audiometry:• Slight to moderate conductive deafness.

Examination reveals:

The condition normally resolves as the URTI

symptoms disappear.

Nasal decongestant such as Oxymetazoline

combined with oral decongestant.

Inflation of Eust. Tube once the acute nasal

symptoms have subsided by:

• Valsalva’s method.

• Politzerization.

• Eustachian tube catheterization.

Until the tube opens and the hearing returns.

Treatment:

Acute middle ear effusion

This may be considered as amore sever

variety of catarrhal otitis media where the

tube is either completely blocked or

blocked for a longer time.

Between 20% and 50% of children will

have an episode of otitis media with

effusion at some time between the ages of

3 and 10 years.

Aetiology

In children: Eust.tube malfunction

Adenoid hypertrophy

Unresolved acute

O.M.

Allergy

In adults: Idiopathic

Barotrauma

Radiotherapy

AIDS

Children AetiologyEust. Tube malfunction:

Children have poorer Eust.tube function

than adults.

Is a result of the frequently associated

mucosal oedema.

Adenoid hypertrophy:•The most commonly suggestive

mechanism being displacement of the

Eust.Tube orifice rather than its

obstruction.

•Adenoids constitute a reservoir of

infection.

Unresolved acute o.m.: Fluid can remain in the middle ear

following an episode of acute otitis

media, But only about 5% of patient will

have middle ear fluid after 12 weeks and

none will have any 8 months later.

Many children with acute otitis media with

effusion do not have a past history, But it is

suggested that in them there may have

been a sub-clinical infection.

Allergy: Atopic allergy in the form of asthma, rhinitis

and dermatitis has been calculated to

affect about 1/3 of children at some time in

the first 10 years of life when otitis media

with effusion is also common.

It could just be that they are more prone to

develop otitis media with effusion

, because of the Eust. Tube oedema

associated with their rhinitis.

Adult Aetiology

Idiopathic: It is important to consider a postnasal space

tumour although it is not a common cause except in Chinese, (they have a genetic predisposition to such tumours).

Barotrauma: On descent in an aeroplane, it can sometimes be

difficult to equalize the negative middle air pressure by autoinflation and, if negative pressure is prolonged, a mild serous transudate may result.

Nasopharyngeal carcinoma: 2/3 of patients with a nasopharyngeal tumour will

have otitis media with effusion, But it is incorrect to think that this is the only presenting symptom.

Radiotherapy: Cause fibrosis around the eustachian tube resulting

in its malfunction.

AIDS: Individuals with AIDS have a higher incidence, due

to an increased incidence of :• URTI.

• Lymphoid hypertrophy of the adenoids

• Nasopharyngeal tumours (very rare).

Symptoms: Hearing loss (conductive

,more sever).

Discomfort (sufficient to

require the use of mild

analgesics).

Tinnitus , a feeling of

blockage and imbalance

are not uncommon.

Eardrum:• is congested and often

there is a dark orange

hue to it.

• It may be retracted.

• Little or no movement on

pneumatic otoscopy,

Examination:

Similar lines of catarrhal otitis media.

Myringotomy: if the fluid and deafness persist.

Examination of the postnasal space: if nasopharyngeal tumour is suspected

Treatment:

Acute Suppurative o.m

It is an episode of inflammation of the middle ear cleft associated with pain, fever, hearing loss and sometimes discharge.

Types depend on :Virulence of infecting organism.

Resistance & age.

Drainage &antibiotics.

Previous infection.

Pnumatization.

Also risk factor suspected :

*male gender,* bottle feeding,

* a sibling with OM,* and early occurrence of *OM. In addition to daycare,

PATHOPHYSIOLOGYHistorically, the pathophysiology of OM has been linked with abnormalities of

Eustachian tube function.The three classic functions of the Eustachian tube are aeriation, clearance, and

protection of the middle ear.Early studies suggested that obstruction of the tube(i.e., underaeriation) was the underlying problem.Newer work, however, has refined that concept to suggest thatAOM is the result of bacterial entry into the middle ear(i.e., failure of protection). This entry is due to an abnormally patent (or compliant) tube rather than an obstructed one. Tubal obstruction along with failure of clearance, which are common findings in

children with COME, may be secondary rather than primary processes. First, in usual cases of AOM, viralnasal infection precedes the ear infection. Second, pathogenic bacteria subsequently appear and are found in the

nasopharynges of 97% of patients with AOM, with correspondence to the organisms in the MEE in 69%.

Third, the adenoids of childrenwith recurrent AOM contain pathogenic bacteria is clinically significant.

Aetiology Spread of infection:

• Up the Eust.tube (most middle ear infections

probably occur as a result of ascending infection by this

route via submucosal lymphatics).

• Through a pre-existing perforation of

T.M.(this may be due to a previous infection or

trauma, may also enter through a ventilation tube).

• Blood-borne infection (middle ear effusions may

occur during some viral illnesses and predispose to

secondary bacterial infection).

Age:

(The peak incidence is 5-7 years).

Operation in nose and throat :

especially when a postnasal pack has been

retained for more than 24 hours

Specific abnormality ass. with acute O.M.:

Immunosuppression

Cleft palate.

Down’s syndrome.

The adenoid pad:

(a large adenoid pad or a small nasopharynximpede mucocilliary flow, and stagnant mucus allows growth of pathogens.

Causative agentsBacterial:

Pneumococcus

Haem. Influenza

Strep. Pyogenes

Staph. Aureus

Branhamella Catarrhalis

Viral:Adenovirus

Rhinovirus

divided into 3 phases:

Phase 1 :

acute salpingitis

Fullness in the ear

Deafness is conductive in type

Retraction of tympanic mm. in early

stage but it is transitory

Clinical features:

Phase 2 :

acute tympanitis

a) Before perforation:Deafness increases

Bubbling sounds are heard

Discomfort progresses

Moderate to sever earache

Constitutional disturbances

T.M : dilatation of bl.v around the handle of malleus and periphery of the mm. until the whole of it becomes red with gradual loss of landmarks as it thickens and bulges

otoscopy

Otorrhoea follows

rupture .It may be

serous, blood

stained, mucopurulent or

purulent

Relief of pain.

Mastoid tenderness if

present usually

disappears

b) After perforation:

Phase 3 : retention of pus in mastoid (acute mastoiditis)

rarely seen today

Pain developes in mastoid region

Tenderness can be elicited over the mastoid

antrum and/ or tip

Oedema .the posterosuperior wall of the deep

meatus sags from odema

Constitutional disturbances increases

Acute Suppurative o.m

Differential Dx: Furuncle or diffuse O.E.

Referred otalgia .

Postauricular adenitis.

Herpitic lesion of ear.

1. Antibiotics therapy

Treatment :

Amoxycilline is recommended for

treatment of acute o.m. and

prophylaxis.Amoxycilline -- Calvulante, Cifaroxime , Cefixime , Trimethoprim–sulfamethoxazole and the combination of erythromycin and sulfisoxazole are advised when:

Amoxycilline seems clinically

ineffective,or allergy

When B-lactamase-producing

bacteria are suspected

1-Use of a nasal decongestant to open the airway

may be helpful .

2-antihistamines should be avoided because their

atropine-like effect leads to drying of secretions.

3- The combination of an antihistamine and

decongestant was found not to affect the clearance

of MEE.

3-Topical decongestants may be used for

short periods .

4- Aural toilet : this followed by A.B. drops or wick

soaked with A.B.

Other medical treatment

Surgical treatment

Drainage (myringotomy )

in the following circumstances :

1.Persisting high fever

and sever pain

2. Marked bulging of the T.M

3.Unsatisfactory spontaneous

perforation

Surgical treatment

Cortical mastoidectomy Should be

performed when subperiosteal

abscess or other complications

appear.

Grommets will usually

stop recurrent acute o.m.

But sometimes only

change its character from

episodes of sever fever

and pain to episode of

recurrent ear discharge.

Surgical prophylaxis

Adenoidectomy:Has favorable result in the first

and second year of follow up

with a reduction in the incidence

of acute otitis media ,compared

with control.

Tonsillectomy:

It is unlikely that tonsillectomy

alone will reduce the incidence.

Sequelae of A.S.O.M

1. Healing : May be complete with return of hearing to

normal

90% of perforations are closed by a scar

within one month( in dry ear ) which are

virtually invisible

Sometimes is closed

by a thin veil-like mm

Adhesive changesare not often seen after a single attack of acute SOM

. Open perforation :2 May be dry or moist

Their position is non-

marginal

Sometimes it is adherent

to the inner tympanic

wall for a portion of its

circumference

Residual deafness . 3

The degree of deafness is variable

Anterior smallperforation is lessdeafening than

larger central one

. Tympanosclerosis4

Are chalky patches

Not always indicative

of past infection

They are compatible

with normal hearing

Complications

Intracranial: Extradural

abscess

Lateral sinus thrombosis

Otitis hydrocephalus

Meningitis

Brain absces:• Temporal lobe

• Cerebellum

Subdural absces

Cortical thrombophlebitis

Extracranial:Mastoiditis

Acute

Masked

Chronic

Petrositis

Labyrinthitis

Facial N.

paralysis

Mastoiditis

Two forms of true mastoiditis with bone destruction can developed from the mastoiditis accompanying otitis media even under antibiotic treatment :

1. Acute mastoiditis : It is marked by purulent liquefaction of the bony septa of

the pneumatic system with external rupture to form a subperiosteal .

The coarse is rapid

Paresis of the facial nerve is possible

2. Chronic mastoiditis :

It is partly a productive inflammation

with obliteration of the spaces of the

pneumatic system by inflammatory

granulation tissue and partly a continuous

inflammatory breakdown of bone

The coarse is insidious and the symptoms

are initially mild

Acute mastoiditis

Arise from an acute otitis media by extension of

infection from mastoid antrum to the air cell and

therefore occurs in a cellular temporal bone.

In most cases of acute mastoiditis produces no

bone destruction but in sever infection there is

greater inflammatory reaction resulting in pus

formation, increased tension ,resorption of bone

with loss of trabeculation and empyema

Clinical features1. General :

Worsening of the general condition

Rise of temperature

2. Local :

Increasing pain in the ear

Reappearance or increase of the aural discharge which is creamy, odorless, and purulent

Deafness increases

Tenderness over the mastoid bone

Retroauricular swelling with protruding ear There is swelling of the zygomatic process with extension to the cheek

and eyelids in an extensively pneumatized bone .it is more common in children

Otoscopy :

Reveals either :

Intact pale but still thickened

T.M with circumscribed

inflammation inthe

posterosuperior quadrant of

T.M

Or perforated eardrum with

pulsating discharge

Narrowing of the EAM due to

sagging of the posterosuperior

wall

Investigation Polymorphonuclear leukocytosis

Markedly increased ESR

Radiographs in

schueller’ s view

show a decrease

in radiolucency due

to reduction of the

air content in the

pneumatic system,

hazinessand opacity

of the mastoid cells

Treatment The incidence of acute mastoiditis has been

greatly reduced due to advent of antibiotics

1. Medical treatment : Bed rest

Until pus from the ear is available for C & S

parenteral penicillin should be given in high

dose combined if necessary with other

Antibiotic.

Aural toilet ( if discharge present )

2. Surgical treatment :

cortical mastoid operation (schwartze’s operation ) is indicated in:

Worsening of general condition & increase of the ESR

Aural discharge for more than 2 weeksdespite efficient treatment

Onset of facial nerve paralysis

Sign of a periosteal collection

Symptoms of otogenic complications

Subperiosteal abscess

1.Postauricular abscess : Lies over the external surface of mastoid

and is the commonest especially in children

the auricle is displaced outwards, forwards

and downwards

The postauricular sulcus tends to retained

Pus has often

tracked outwards

through minute

vascular channels in

the suprameatal

traingle

. Zygomatic abscess2

Pus escaping from zygomatic cells near the

squama forms an abscess deep to the temporal

muscle makes a swelling above & in front of ear

3. Von bezold’s & citelli’s

abscess :perforation of the tip or inner surface of the

mastoid may give rise to an abscess in the

sternomastoid muscle (bezold’s) or in the digastric

traingle (citelli’s) abscess

4.Pharyngeal abscess

Pus tracking from peritubal cells may

form a retropharyngeal or

parapharyngeal abscess

Petrositis It is due to direct extension of infection

from the middle ear or mastoid

May occurs in acute or chronic form of otitis media in a pneumatized petrous bone

It may present as part of a mastoiditis, or may follow a cortical mastoidectomy for mastoiditis ,usually 2-3 weeks after

Clinical features Sever unilateral headache, spasmodic in type

May be retro-orbital ,supraorbital or temporal in

distribution

In the presence of acute O.M headache with

diplopia due to paralysis of abducent nerve(

Gradenigo’s syndrom)is almost diagnostic

Following mastoidectomy a sudden recurrence or

increase of discharge may suggest a petrositis

Diagnosis

1. Persistent otorrhoea following cortical

mastoidectomy

2. Clouding and

rarefaction of

pertous apical

cells on X-ray

( Stenver’s view)

3. CT scan

Treatment

In the early stage is that of associated otitis

media and mastoiditis

Analgesic

As a rule mastoidectomy is indicated

searching for the presence of fistula leading

to petrous apex

Radical mastoidectomy for chronic cases

Thanks