Acute otitis media Prepared by Dr. Hiwa As’ad M.B.Ch.B C.A.B.S(ENT H&N Surgery) F.I.C.M.S (ENT)
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
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