New ppt aom

Dr.Sudha Shahi
ENT HNS
Bir Hospital ,NAMS

TOPICS OF DISCUSSION:
1. HISTORY
2. INTRODUCTION
3. CLINICAL FEATURES
4. SIGNIFICANCE
5. ETIOPATHOGENESIS
6. STAGES OF AOM
7. DIAGNOSIS
8. MANAGEMENT
9. OUTCOME/NATURAL HISTORY
10. COMPLICATIONS
11. RECENT STUDIES

2. HISTORY OTITIS MEDIA:
 Had been a disease of immense importance in the history
associated with high complication rate,morbidity and mortality
 Disease of childhood
 Treatment in 8th century,water from wells named after various
saints
 Ancient studies of skulls in different populations ranging upto
8000 years old showed evidence of acute and chronic OM

 Hippocrates defined the term OM in 450 BC
 Valsalva described the eponymous manoevre in 1704 AD
 Toynebee’s realization of the significance of ET role in OM led
to the evolution of methods for ME ventilation via
catheterization of ET
 Politzer and his Politzer bag for insuffilation of ME through ET
without use of a catheter has been a hallmark
 Treatment in ancient times with herbs ,animal and mineral
substances as ear drops

 Tympanocentesis concept by Jena Riolan the Young
 Permanent opening by catgut , whale bone rods ,gold foil
 Reintroduction of the process by Schwartze which was made
more famous by Armstrong by use of ear tubes
 Nasopharyngeal irradiation in World War 2 continued its legacy
until the potential dangers of malignancy was sought out

1.INTRODUCTION:
 Defined clinicopathologically as inflammation of the middle ear
cleft of rapid onset ,associated with Middle ear effusion,
infective in origin and a varied collection of clinical signs and
symptoms.(SB)
 Viral or bacterial infection of the mucosal lining of the middle ear
and mastoid air cell system.(SB)
 Characterised by the rapid onset of signs and symptoms of
inflammation in the middle ear accompanied by Middle ear
effusion.(Cumming)
 Acute Inflammation of middle ear space which typically occurs
over several hours but must occur less than 6 weeks.(GC)

RECOMMENDATION 1:
 To diagnose acute otitis media the clinician should confirm a
history of acute onset, identify signs of middle-ear effusion
(MEE), and evaluate for the presence of signs and
symptoms of middle-ear inflammation.
A diagnosis of acute otitis media requires
 1) History of acute onset of signs and symptoms,
 2) The presence of MEE, and
 3) Signs and symptoms of middle-ear inflammation.

Elements of the definition of AOM are all of the following:
1. Recent, usually abrupt, onset of signs and symptoms of middle-
ear inflammation and MEE.
2. The presence of MEE that is indicated by any of the following:
a. Bulging of the tympanic membrane
b. Limited or absent mobility of the tympanic membrane
c. Air fluid level behind the tympanic membrane
d. Otorrhea
3. Signs or symptoms of middle-ear inflammation as indicated by
either
a. Distinct erythema of the tympanic membrane
b. OR b. Distinct otalgia (discomfort clearly referable to the ear[s] that results in
interference with or precludes normal activity or sleep)

 Synonymous with acute suppurative otitis media.
 Normally develops behind an intact tympanic membrane, but
may
include acute infections arising in the presence of ventilation
tubes or existing tympanic membrane perforations.
 (#Otomastoiditis )

Subgroups of AOM
A.Sporadic AOM:
Episodes isolated events
Occurring with upper respiratory tract infections.
B. Resistant AOM:
Symptoms and signs beyond 3 to 5 days of antibiotic treatment.
C. Persistent AOM:
Persistence or recurrence of symptoms and signs within 6 days of finishing a
course of antibiotics.
D. Recurrent AOM:
Either 3 or more episodes within a six-month period
Or ?at least 4 or 6 episodes within a 12 month period

Symptoms
 1/3rd without ear related symptoms(children)
Local :
 Rapid onset Otalgia
 Impaired hearing
 Otorrhoea
 Tinnitus

General:
 Fever (2/3rd absence of fever data from pediatric age group),
 Irritability /nocturnal agitation
 Coryzal symptoms
 GI symptoms
 Poor feeding*
 Ear pulling*
 Clumsiness*
 Excessive crying*
 *Specific for pediatric age group

Signs
 Toxic look
 Constant rubbing of ear*
 Erythema of the TM (18-19%)
 Bulging or fullness of the tympanic membrane
 Acute perforation of the TM with otorrhea
 Retracted TM
 Opacification
#Thus important to perform otoscopic examination
*Specific for pediatric age group

#Few facts to be considered
 2/3 rd are apyrexial
 1/3rd children with no ear related problems
 AOM usually develops 3-4 days after onset of coryzal symptoms
 Otlagia will subside within 2/3rd without treatment
 Symptomatic relief on 88%wihout treatment by day4-7
 Hearing loss might persist > 20 db for 1 months in over 30%
and 2 months in 20% children

#100 studies have been published so far and yet there seems to be
difficulty in clear diagnostic guidelines
 52.5% MEE,32.5% symptoms and signs of inflammation ,2.5% rapidity
of onset
 Multinational study diagnostic certainity under 1 only 58% ,73% over 31
months
 Accuracy of reporting of OME is ahead of AOM
#Otoscopy is an precise art and even trained observers are shown to
have only 85% accuracy

SPEECH AND LANGUAGE DEVELOPMENT
 It is difficult to separate the literature on AOM and OME outcomes.
 In children with OME, a significant effect seems to occur in the early
years of life on expressive language development, but not receptive
language.
 A small number of studies point to persisting effects on expressive
language in school-age children.
 Little evidence showing different cognitive development in school-age
children
 There are suggestions that poor behavioural traits may be more
common by school age, but more work is required before conclusions
are drawn

3.WHY IS IT SO IMPORTANT TO KNOW ?
 Worldwide a pediatric healthcare problem
 Most common reason to visit a hospital in pediatric age
group
 Incidence raised in the last few years
 Most common cause for acquired hearing loss in children
 Morbidity and mortality due to serious extracranial or
intracranial complications

 Most common indication for prescribing an antibiotic to
pediatric population (10 million/25% of all antibiotic
prescriptions) 50 % in preschoolers
 Most common reason for GA in children
 Above all,huge impact on QOL
 Huge economic burden ,estimated cost of around 5 billion
USD /year,family burden
 Antibiotic resistance

Relative risk for recurrent acute otitis media in children upto 2 years(Alho
et al.,1993)

Incidence in children:
Most children experience at least one episode ofAOM during childhoood
Cumulative incidence ranges from 19% to 62% by age of 1 year and 50% to
84% by 3 yrs of age
Peak incidence during 6 -12 months
Incidence decreases by age and by the age of 7
By 6 months ,20% have had 2 or more episodes
Three or more episode by 1,3,5,7 years in 10 to 19%,50%,65% and 75%
children respectivley
6 or more episodes in 39% children by age of 7

Cumulative incidence of first episode of acute otitis media.(From Casselbrant ML,
Mandel EM: Epidemiology. In Rosenfeld RM, Bluestone CD, editors: Evidence-based
otitis media, ed 2, Hamilton, Ontario, 2003, BC Decker, p 147.)

Incidence taken in 6 developed countries in adult
population
16 % 0f total adult patients seen out of which
 6% 15-24years
 7% 25-44 years
 3% 45 years or Older
 M=F
 Frequency more common in AIDS if triple therapy is
unavailable

Relationship with otitis media with effusion
 In attempting to identify the aetiological factors that might
be responsible for acute otitis media. it is often difficult to
do so because many authors fail to distinguish between
acute otitis media and otitis media with effusion.
 While accepting that they may be the two ends of a
continuous spectrum. there is no doubt that they are two
clinically distinct conditions that affect two different age
spectra

5.ETIOPATHOGENESIS
a) URTI
b) Allergy
c) ET dysfunction
d) Hydrops Ex vacuo
e) Genetic
f) Immune related
g) Syndromic association

a)Upper respiratory tract infection
,
Viral Bacterial Fungal
Rhinovirus,
Rsv,
Adenovirus,
Influenza,
Parainfluenza,
Enterovirus
H.Influenzae
Strep pneumoniae,
Moraxella catarrhalis
Group A strep,
Staph aureus,
Alloiococcus otitidis
E.Coli
Enterococcus
Pseudomonas
*Mycoplasma
Chlamydia
,Corynebacterium,
Mycobacterium Tuberculosis
Clostridium tetani
Aspergillus
Candida

BACTERIOLOGY OF MIDDLE EAR ASPIRATES FROM ADULTS AND WITH ACUTE
OTITIS MEDIA

 Similar findings were seen in naspharyngeal carriage studies
 Similarly MIC50 and MIC 90 for amoxicillin also seemed to
shoot up after
 Those with tympanostomy tubes also had similar findings
 Finally owing to the fact of changing bacteriology , Prevnar 13
vaccine was approved in 2010 instead of 7 valent and included
strains 1,3,5,6A,7F and 19A in addition ot PCV7 strains
 But a continued surveillance is yet the need of the

 Before 2000 Strep Pneumonia was the most common cause of AOM
followed by H.Influenzae , M.catarahhalis, Staph aureus
 PCV7 vaccine in 2000 ,decrease of 7.8 to 6% RR reduction
 Study by Rochester in 2001-2003 vs1995 ot 2001 there was
reduction in persistent AOM and failures by 24%.
 H.Influenzae emerged as the major pathogen and S.Pneumoniae
serotypes non vaccine
 Interestingly after 2000 studies revealed rather increase in the
incidence of AOM from 12 %in 1999 to 32% in 2002 and more in
those who received more than one dose of vaccine

 Biofilms
 Sessile communities of interacting bacteria attached to a
surface.
 They are encased in a protective matrix of
exopolysaccharides rather than living in a motile
“planktonic” or free-floating state.
 The reduced metabolic rate ofbacteria in the biofilm
renders them resistant to antimicrobial treatment.
 The bacterial community relies on a complex intracellular
communication system that provides for organized
growth characteristics known as “quorum sensing.”

 Recent animal and human studies have suggested that
biofilms can also be isolated from the middleear.
 Post and coworkers, using polymerase chain reaction
(PCR) methodology, found evidence of bacteria in 48%
of culture negative MEE specimens from children
undergoing tympanostomy tube insertion for chronic
OME.
 Biofilms also have been identified in the nasopharynx
of children with otitis media, and it was suggested
that the biofilm may act as a reservoir for
bacterial pathogens resistant to antibiotics.

Three potential routes are described:
1. Eustachian tube,
2. Tympanic membrane perforations or grommets,
3. Haematogenous.

b) Allergic conditions
Atopy
Nasal congestion
ET edema
Dysfunction
negative ME pressure
compromised ventillation
Mast cells and IgE antibody
Inflammatory mediators
ET Obstruction
Transudation of fluid in ME space

c)Eustachian tube
 Three main functions:
 Pressure regulation(Ventillation)
 Protection
 Clearance

 Pressure regulation
 Levator veli palati
 Tensor veli palati
 Impaired due to functional or anatomic obstruction

Physiological impairment in children
Shorter wider more horizontal ET in children makes it difficult
to
equalize an artificially induced negative middle ear pressure as
compared to adults
#Pressure chamber study

 The more horizontal position of the tube in children might allow
easier access for bacteria.
 Combined with poor tubal function which allows children to
create a high negative middle ear pressure by sniffing
 The fact that acute otitis media is more frequent in children
with Down's syndrome and those With cleft palates would
support some role for eustachian tube dysfunction.

 Protection
 At rest ET remains closed protecting it from the nasopharyngeal
secretions and sound pressure and reflux of secretions from
nasopharynx
 Gas cushion in mastoid and intact middle ear

 Clearance:
 Mucociliary action of the middle ear and ET
 Pumping action of ET during closure

INTERESTING STUDIES ABOUT ET DYSFUNCTION
Bipedalism and Big Brain
Loss of Facial Prognathism (Facial Flattening)
Speech ,cooking
Change in Palate Morphology Related to Eustachian Tube
Function

e) Genetic
 A meta analysis of risk factors has shown that when one family
member had AOM the risk increased for other family members
(relative risk 2.63).
 Racial differences are well described with increases in
American Indians, Eskimos and Australian Aboriginals.
 Poor economic status, may contribute to the increased risks
in these groups.
 Evidence comes from twin studies

 Many immune related mechanisms, which are likely to
have a genetic basis, have been proposed.
 Certain human leukocyte antigen (HLA) classes have
been shown to be significantly associated with increased
risk of AOM
 Maternal blood group A is reported to an independent risk
factor (relative risk 2.82).
 Atopy has also been associated with increased risk of
developing AOM.

f)Immune factors
 Number of specific associations suggest that certain defective
or immature pathways may predispose toinfection.
 Low levels of IgG2 subclasses have been reported in several
studies to be more common in otitisprone children.
 Those with IgG2 deficiency were shown to be three times more
likely to develop post-ventilation tube insertion otorrhoea for
example.
 Delayed maturation of anti-pneumococcal antibodies appear to
predispose to AOM.

 Defective complement-dependent opsonization has been
associated with recurrent AOM and diarrhoea in infancy.
 Low concentrations of mannose-binding protein which acts
as an opsonin
 Defect with over 20 percent of children with recurrent AOM
 Important in infancy

 Aberrant expression of critical cytokines, such as TNF and ILs
resulting in suboptimal host defence, has been postulated as a
cause for persistent infection.
 Expression of mucin genes (MUC5B )
 Advanced disease associated with low CD4 counts does seem
to be associated with an increased incidence of AOM in HIV

g)Environmental factors
 The day-care attendance outside the home.(RR 2.45 vs1.59
home)
 The incidence of AOM appears to follow that of seasonal
upper respiratory tract infections (URTI) in the winter months.
 Breastfeeding for three months is protective (rr, 0.87).
 Use of a pacifier (dummy) carries a relative risk of 1.45.

 Poor socioeconomic status associated with poor housing
and overcrowding has been reported to be associated with
AOM (overcrowding: rr, 5.55 in a Greenlandic population, for
example). Passive smoke exposure from parental smoking is
weakly associated (rr, 1.0-1.6).
 There is more limited evidence to support the role of dietary
factors, in particular cow's milk allergy, in predisposing to
AOM.

5. STAGES OF ACUTE OTITIS MEDIA
a) Hyperemia
b) Exudation
c) Suppuration
d) Resolution or Complication

a)Hyperemia /tubal occlusion
 Earliest response to antigens
 Processing of the antigen by immunocompetent cells
 Oedema and hyperaemia ME mucosa ,all 3 layers of TM
 Eustachian tube blockade
Symptoms:
Deafness
Earache
Fever +/-
Signs.
 Hyperemia and edema of TM and middle ear
mucosa(all three layers )
 TM is retracted with handle of malleus assuming a
more horizontal position
 Prominence of lateral process of malleus
 Loss of light reflex.
 Tuning fork tests show conductive deafness.

b) Exudation /Stage of presuppuration.
 Surpasses hyperemia
 Immune factors are released to recruit cells and cytokines from
systemic circulation(IL2 ,Platelet endothelial cell adhesion
molecule-1 )
 Increased expression of ICAM within vein and venule
 Leaky vein and venules to inflammatory infiltrates
(Igs,PMN,Macrophages,T helper cells)
 Complex cascade of cytokine release (IL 1,6,8,TNF
alpha,Leukotriene B4)

Symptoms.
 Marked earache which may disturb
sleep and is of throbbing nature.
 Deafness *
 Tinnitus*
Usually, child runs high degree of
fever and is restless.
Signs .
Congestion of pars tensa.
Leash of blood vessels as cart-wheel
appearance.
Later, whole of tympanic membrane
including pars flaccida becomes
uniformly red.
Inflammatory exudate in middle ear
#Tuning fork tests will again show
conductive type of hearing loss
*Mostly complained by adults

c) Stage of suppuration.
 Bacterial infection must
 Destruction of bacteria via opsonisation and complement
cascade and purulent collection
 Pus in the middle ear and to some extent in mastoid air cells.
 Tympanic membrane starts bulging to the point of rupture.

Symptoms:
Earache excruciating
Deafness increases
High grade fever
Vomitting
Convlsions
# X-rays of mastoid will show
clouding of air cells because of
exudate.
Signs:
TM red and bulging with loss of
landmarks.
A Yellow spot may be seen on
the tympanic membrane where
rupture is imminent.
‘Nipple-like’protrusion of
tympanic membrane with a yellow
spot on its summit.
Tenderness may be elicited over
the mastoid antrum

d) Stage of resolution.
 Inflammatory process begins to resolve.
 If proper treatment is started early or if the infection was
mild, resolution may start even without rupture of tympanic
membrane

Symptoms.
 With evacuation of pus, earache is
relieved
Fever
Signs.
External auditory canal may contain
blood-tinged discharge which later
becomes mucopurulent.
Usually, a small perforation
Hyperaemia of tympanic membrane
begins to subside
Return to normal colour and
landmarks.

e) Stage of complication.
 If virulence of organism is high or resistance of patient poor
 Disease spreads beyond the confines of middle ear
 Ensuing complications.

1Child aged 2 months through 12 years with
uncomplicated AOM presents to office
2 The clinician access pain.
3 Is pain present?
5 Clinician recommends treatment to reduce pain.
10.Amoxicillin at a
dose of 80-90
10mg/kg/day is the
initial antibacterial of
choice for most
children
9Does the child have
fever >39C and/or
moderate or severe
otalgia
13.Go to box14
6 Is observation an
appropriate initial treatment
option? **
4Go to Box 6
8.Go to box14
7.Child is observed for 48 to
72 hours with assurance of
appropriate follow-up. 11.Child managed
appropriately with
antibacterial therapy See
Table 6
12Go to
box14
No
No
Yes
Yes
Yes
A diagnosis of acute otitis media requires:
1) history of acute onset of signs and
symptoms;
2) the presence of middle ear effusion;
3) signs and symptoms of middle ear
inflammation.

 14. Did patient respond to
initial treatment intervention
(either antibacterial treatment
or observation)?
17 Is diagnosis of
AOM confirmed
16 Clinician
reasses and
confirms
diagnosis of
AOM
18 Assess
for other
causes of
illness and
manage
appropratiely.
15.Patient
follow-up
as
appropriate
.
19.Clinician should initiate antibacterial
treatment for children initially managed
with observation or change antibacterial
treatment for patients initially managed
with antibacterial therapy. (See Table 6 in
clinical guideline)
Yes
No
Yes
No
** Criteria for antibacterial
treatment or observation in
children with non-severe
illness:†
1) < 6 mos: antibacterial
treatment
2) 6 mos to 2 years:
antibacterial treatment with
certain diagnosis or severe
illness or observation with
uncertain diagnosis and
nonsevere illness.
3) 2 years and older:
antibacterial treatment if severe
illness or observe with
nonsevere illness with certain
diagnosis; observation for
uncertain diagnosis.
Caregiver is informed and
agrees to the option of
observation. Caregiver is able
to monitor child and return
should condition worsen.
Systems are in place for ready
communication with the
clinician, re-evaluation, and
obtaining medication if
necessary.
Antibacterial
choice should be
based on the likely
pathogen(s)
present and on
clinical experience

6. DIAGNOSIS –
A large multinational study rated clinicians diagnostic certainty in
children under one year of age at only· 58 percent, rising to 73
percent in those over 31 months.
In diagnosing AOM, only 52.5 percent of the studies cited
middle ear effusions, 32.5 percent included symptoms and signs
of inflammation and 2.5 percent considered the rapidity of onset.

 The guidelines of the Dutch College of General Practitioners
for the diagnosis of acute otitis media (AOM) are as follows, and
apply to both children and adults
HISTORY –
Local symptoms
General symptoms
#Association of URTI prior to the illness should be established
which strengthens the diagnosis

PHYSICAL EXAMINATION –
 Both TM to be assessed properly
Based on a combination of the history and the image of the
tympanum:
 A normal tympanum is pearl grey and transparent, with a
clear light reﬂex.
 This ﬁnding excludes acute otitis media

 An injected tympanum can indicate early acute otitis media,
but can also be caused by crying or by a common cold.
 Compare
 An intensely red tympanum conﬁrms the diagnosis

 A bulging tympanum indicates the presence of liquid in the
middle ear under pressure.
 This feature also conﬁrms the diagnosis of acute otitis media;

 Perforation of the tympanum with otorrhea (within an acute
clinical picture) also conﬁrms the diagnosis of acute otitis media.
 Anamnestic *data play an increasingly important role, the more
so when the image of the tympanum is unclear or difﬁcult to
judge.

AOM SOS score
1. Ear pain
2. Ear tugging
3. Iritability
4. Decreased play
5. Decreased appetite
6. Difficulty sleeping
7. Fever
Symptoms were graded into total 13 point score where
0 = none for first 6 symtoms and absent for fever
1= A little for first 6 symptoms and Present for fever
2= A lot for first 6 symptoms
# in general those with score less than 1 were wihtout the disease and
those with the disease usually had score abve 3 .
It is also useful in grading the improvement of symptoms in
subsequent visits.
Some studies have even supported use of antibiotic only when
scores were above 5
But non specific

 IMMITTANCE TESTING(TYMPANOMETRY)
 Immittance testing is an excellent adjunct to the
assessment of middle ear status and the management
of otitis media.
 When otoscopic evaluation is inconclusive or difficult to
perform, tympanometry can be very useful in evaluating
ear disease in children older than 6 months of age.
 A flat or rounded pattern (TW >350 daPa) with a
small ear canal volume indicates MEE, whereas a flat
pattern with a large ear canal volume suggests a
perforation or a patent tympanostomy tube.

 The following set of criteria uses TW and
otoscopy to categorize middle ear status
TW <150 daPa= no OME
TW > 350 daPa= OME
TW 150 TO 350 daPa= presence or absence of OME is
determined by otoscopy

AUDIOMETRY
 MEE usually results in a mild to moderate conductive
hearing loss.
 Audiometry should be used to determine specific
management strategies, with a more aggressive approach
considered in children with significant hearing impairment.
 Behavioral audiometry
 Visual reinforcement audiometry
 Play audiometry
 Auditory brainstem response(ABR)
 Transient-evoked otoacoustic emissions

Guideline Definitions for Evidence-based Statements

7. MANAGEMENT
 Though the majority of patients receive antibiotics there is no
evidence to support their efﬁcacy.
 In an international case series of 386 adults, ‘recovery’ was
more frequent (92 percent; 68 of 74) in those that did not
receive antibiotics as opposed to those that did (75 percent;
235 of 312).
 Analgesis for otalgia would seem good practice, though this is
not supported by existing evidence.
???Controversial

Mgmt contd..
 Most children with AOM will get better quickly and without
treatment.
 A very small number may develop potentially serious
complications.
 Current debate questions whether and for whom treatment is
required, and the role of prophylactic strategies.

I. Conservative
II. Medical management
a. Antibiotics
b. Analgesics and antipyretic
c. Nasal or oral decongestants
d. Antihistamines
III. Surgical
IV. Others

I.CONSERVATIVE TREATMENT
 Most children will benefit from simple analgesics and anti-
pyrexials, in a quiet supportive environment.
 There is limited experimental animal evidence showing that
ibuprofen provides additional benefit by reducing mucosal
inflammation when taken in combination with amoxicillin.

 RECOMMENDATION 3 A*
 Observation without use of antibacterial agents in a child with
uncomplicated AOM is an option for selected children based on
diagnostic certainty, age, illness severity, and assurance of follow-up.
 Observation is an appropriate option only when follow-up can be
ensured and antibacterial agents started if symptoms persist or worsen.
 Nonsevere illness is mild otalgia and fever <39oC in the past 24 hours.
 Severe illness is moderate to severe otalgia or fever 39oC. A certain
diagnosis of acute otitis media meets all 3 criteria: 1) rapid onset, 2)
signs of middle-ear effusion, and 3) signs and symptoms of middleear
inflammation.

Criteria for initial Antibacterial Agent treatment or observation in children with
Acute otitis media
Age; Certain Diagnosis Uncertain Diagnosis
<6 mo Antibacterial therapy Antibacterial therapy
6 mo–2 y Antibacterial therapy Antibacterial therapy if
severe illness; observation
option* if non-severe
illness
>2 y Antibacterial therapy if
severe illnessobservation
option* if non-severe
illness
Observation option*

Comparative AOM Outcomes for Initial Observation Versus Antibacterial Agent

III. MEDICAL TREATMENT
a.Antibiotics
 Uncertainty over usage between countries
 Good evidence-base for children over 2 years of age but not
below 2
 Should be given to a child failing to improve after two to three
days of 'watchful waiting‘ if not given previously
 ‘Irregular' illness course.
 ‘High risk' children, defined by the Dutch
 Under the age of two years suffering a recurrent episode of
AOM.

Tt contd..
o A recent metanalysis showed two-thirds of children recovered
within 24 hours of the start of treatment, 80 percent by days two
to seven, with or without antibiotics.
 Antibiotics lead to 5 percent fewer children overall having pain
between days two and seven.
 NNT is 17 to prevent one child experiencing pain during days
two to seven.
 No differences were found between those who received
antibiotics and those who did not( less data)

TT contd..
 On progression of disease or of symptoms. no differences
were found in complications of AOM.
 Side effects;risk of developing antibiotic resistant bacteria.
 The length of treatment
Short (five day) and long (ten day) courses of treatment were
compared.
Authors concluded that five days of treatment was appropriate
in infections in low risk children over two years of age without
recurrent AOM or tympanic membrane perforation.

Tt contd..
 Under two years of age evidence is weaker for short term
treatment
 Modest benefit from antibiotic treatment between six and 24
months of age (NNT= seven for one symptomatic at four)
 Most recommend treatment below two years of age.
 Those presenting with high temperatures andvomitting(NNT ~3)

ANTIBIOTIC
RECOMMENDATION 3B:
If a decision is made to treat with an antibacterial agent, the clinician should
prescribe amoxicillin for most children.
When amoxicillin is used, the dose should be 80 to 90 mg/kg/day. (This
option is based on extrapolation from microbiologic studies and expert
opinion, with a preponderance of benefit over risk.)

Antibiotic contd..
DOC:
 Amoxicillin 80 - 90mg/ kg/day in three divided doses
 Amoxicillin-clavulanate (90 mg/kg per day of amoxicillin
component, with 6.4 mg/kg per day of clavulanate in 2
divided doses) in patients who have severe illness and for
coverage for B-lactamase-positive Haemophilus influenzae
and Moraxella catarrhalis

 Alternatives:
 Ampicillin (50 mg/kg/day in four divided doses)
 Alternatives in patients with a history of a non-type I
allergic reaction to penicillins are cefdinir, cefpodoxime,
or cefuroxime
#The ototoxicity of topical antibiotic ear drops in these
cases is well recognized and dose dependent, therefore
prolonged treatment should be avoided.

 In cases of type I reactions, alternatives are azithromycin,
clarithromycin, erythromycin-sulfisoxazole, or sulfamethoxazole-
trimethoprim.
 Ceftriaxone (50mg/kg per day), given for 3 consecutive days,
either intravenously or intramuscularly, can be used in children
with
 vomiting, or in other situations that preclude administration of
oral antibacterial agents.

 AOM unresponsive to initial antibacterial therapy, a 3-day
course of ceftriaxone better than a 1-day regimen.
 Trimethoprim-sulfamethoxazole and erythromycin-sulfisoxazole
have traditionally been useful as first- and second-line therapy
for patients with AOM,
 Recent pneumococcal surveillance studies indicate that
resistance to these 2 combination agents is substantial..
 Thus 3-day course of parenteral ceftriaxone due to its superior
efficacy against S pneumoniae is choice of treatment.
 If still does not improve, tympanocentesis with Gram stain, culture, and
antibacterial agent sensitivity studies of the fluid is essentia

Tt contd..
 Antibacterial therapy must be continued for a minimum of
10 days, and followed till tympanic membrane regains
normal appearance and hearing returns to normal.
 Early discontinuance of therapy with relief of earache and
fever, or therapy given in inadequate doses may lead to
secretory otitis media and residual hearing loss.

Recommended Antibacterial Agents for Patients Who Are Being Treated Initially With Antibacterial Agents or Who
Have Failed 48 to 72 Hours of Observation or Have Failed Initial Management With Antibacterial Agents

Possible outcomes after the initiation of antimicrobial therapy:
(1) relief of the signs and symptoms of the acute infection at or
near the end of the course of treatment
(2) relief of the signs and symptoms, but persistence of MEE
for weeks or months after the treatment ends
(3) treatment failure or symptomatic failure
(4) Suppurative complication
(5) Spontaneous perforation of the TM
(6) Relapse within 3 to 4 weeks after the onset of the attack
(7) Symptomatic relief of the acute infection, but a recurrent
episode with or without persistent MEE

 RECOMMENDATION 4:
 If the patient fails to respond to the initial management option within 48 to 72
hours, the clinician must reassess the patient to confirm AOM and exclude
other causes of illness.
 If AOM is confirmed in the patient initially managed with observation, the
clinician should begin antibacterial therapy.
 If the patient was initially managed with an antibacterial agent(s), the clinician
should change the antibacterial agent(s). (This recommendation is based on
observational studies and a preponderance of benefit over risk.)

b.Antihistamines and/or decongestants
A metanalysis of the use of oral or intranasal **antihistamines and/or
*decongestants concluded that their use could not be supported
While combining the two treatments was shown to slightly reduce
AOM at two weeks (NNT = 10.5) the result may have been biased by
the design of the studies.
*Ephedrine nose drops (1% in adults and 0.5% in children) or
oxymetazoline
 Relieve ET oedema and promote ventilation of middle ear
**Pseudoephedrine (Sudafed)
 30 mg twice daily or a combination of decongestant and
antihistamine

Tt contd..
c.Analgesics and antipyretics
*The management of AOM should include an assessment of
pain.
If pain is present, the clinician should recommend
treatment to reduce pain. (This is a strong recommendation
based on randomized, clinical trials with limitations and a
preponderance of benefit over risk.)
*Guidelines Recommendation 2a

III.SURGICAL TREATMENT
 Limited role in the treatment of an uncomplicated episode of
AOM.
 Myringotomy was in the pre-antibiotic era, continued until the
late 1980s in some countries as a first-line treatment for AOM.
 Studies now show that myringotomy plus antibiotics offers no
advantage over antibiotics alone.
 Myringotomy alone, worse outcome
 Myringotomy is reserved for ;severe cases ;to relieve severe
pain; when microbiology is strongly required

## Myringotomy
 It is incising the drum to evacuate pus and is indicated
when
 (i) Drum is bulging and there is acute pain,
 (ii) Incomplete resolution despite antibiotics when drum
remains full with persistent conductive deafness
 (iii) Persistent effusion beyond 12 weeks.
All cases of acute suppurative otitis media should be carefully
followed till drum membrane returns to its normal appearance
and conductive deafness disappears

TT contd…
IV.Others
# Ear toilet.
 If there is discharge in the ear, it is dry-mopped with
sterile cotton buds and a wick moistened with antibiotic
may be inserted.
# Dry local heat
 Helps to relieve pain.

 RECOMMENDATION 5:
Clinicians should encourage the prevention of AOM through
reduction of risk factors. (This recommendation is based on
strong observational studies and a preponderance of benefits
over risks.)
#TREATMENT OF RECURRENT AOM

TT OF RECURRENT AOM CONTD…
Alteration of risk factors
 Reassurance of the benign natural of AOM
 Advice for day care centre
 Feeding the child(breast milk or bottled feeding)
 Avoiding smoke inhalation.
 Restricting the use of pacifiers.(otitis prone)
 Maternal factors
 The role of food allergies, in particular cow's milk, is still
unclear.

MEDICAL PROPHYLAXIS
 Considered only for recurrent AOM.
 Broad-spectrum is required.
 Risks for the development of resistant organisms increase,
adverse drug reactions may occur and active disease may
be masked.
 Studies of prophylaxis of recurrent AOM invariably treat
each individual recurrence with additional antibiotics.
 Trials therefore compare antibiotic prophylaxis versus
placebo between acute episodes.

 Over 50 percent of children having no treatment between
attacks will not suffer a further episode in the following six
months.
 Only one in eight continues to suffer recurrent AOM (i.e.
three or more episodes) during the trials, if treated only for
acute episodes.
 Reduction of approximately 1.5 episodes per 12 months of
antibiotic treatment given, above that expected from the
natural history.
 So one child would need eight months of treatment to
avoid one episode of AOM.

Tt of reccurent AOM contd..
Sulfisoxazole vs amoxicillin
 Recommendations are for six months of treatment through the
winter months in children who do not have background OME.
 This is important as antibiotic prophylaxis may therefore be
most appropriate for children not prone to OME, while
ventilation tubes may be indicated for those prone to OME.
 Place for its use in the management of high-risk children with
recurrent AOM, despite the absence of specifically targeted
studies.

Xylitol
 Xylitol also k/a burch sugar curbs bacterial growth
 Studies in daycare nurseries using chewing gum or syrup have
suggested reductions of 30-40 percent in the occurrence of AOM.
 It is ineffective if used in acute upper respiratory infections.
 Given the very large quantities that must be consumed, and potential
concerns over the safety of such consumption, its use cannot yet be
recommended.
##Findings from the studies suggested that xylitol-containing gum was superior to
xylitol syrup for preventing middle ear infections in healthy children.
There was no difference between xylitol-containing gum and xylitol lozenges in
preventing middle ear infections
Not effective in already acquired ear infections

Vaccination
 Vaccination against viruses Since 60-90 percent of episodes
are initially associated with viral infections (see above under
Viruses) viral vaccination seems the most logical first step.
 AOM secondary to infection by the measles virus is now
relatively uncommon in industrialized countries

 Influenza A vaccination is currently the only commercially
available preparation for the prophylaxis of viral upper
respiratory infections.
 RSV vaccines are undergoing clinical trials
 Parainfluenza virus vaccines have been evaluated in
animals and need to target types 1, 2 and 3 viruses. Limited
human studies demonstrate relative safety and
immunogenicity, but efficacy studies are not available.29

Vaccination against bacteria
 Vaccination against Streptococcus pneumoniae, nontypeable
Haemophilus influenzae and Moraxella catarrhalis is made
difficult by the low immunogenicity of the polysaccharide
capsule
 Success against Haemophilus influenzae type using a
polysaccharide-protein conjugated vaccine provides one
potential solution.
 Streptococcus pneumoniae 90 serotypes (anticapsular
antibodies can help)


Vaccination contd..
 A heptavalent conjugated vaccine (Prevenar, WyethLederle
Vaccines) highly effective in preventing invasive
pneumococcal disease
 Immunization at two, four, six and 12, and in one study
also 15 months of age.

 Trials are under way to see if immunizing the mother in the
third trimester of pregnancy is effective.
 Immunization after two years of age is with 23-valent
pneumococcal polysaccharide vaccine.
 Whilst vaccination is recommended in certain 'at risk'
children, its place in the management of AOM is not yet
clear.
 Non-typeable Haemophilus influenzae vaccines are being
developed.
 Moraxella catarrhalis vaccine research is at a preclinical
stage, but products are under development.

Vaccination contd…
 Special attention should be drawn to children with, or awaiting,
cochlear implants.
 Concern has been raised about a number of cases of
meningitis.
 Whether it is implant related or inner ear abnormalities is
unclear.
 All such children are recommended to have the heptavalent
pneumococcal vaccine before two years and the 23-valent
pneumococcal polysaccharide vaccine at the age of two or
over
 Hib conjugate vaccine is recommended for all children up to

Obstacles
 Wide range of causative organisms, both bacterial and viral,
 Varied serotypes
 Technical difficulties in producing an effective immune
response
 Immune response before six months of age
 Parental resistance to multiple vaccination
 Possibility that the successfully targeted pathogens will
simply be replaced by others

Immunoglobulins
 Intramuscular pooled gamma-globulin in otitis-prone children has
been shown not to reduce the incidence of AOM.
 However, in a Japanese study, intravenous immunoglobulin (GB-
0998) in IgG2-deficient infants has been shown to be an effective
prophylaxis for AOM
Benign commensals
 Spraying benign commensals (alpha streptococci) into the nose to
recolonize the nasopharynx following antibiotics might reduce
AOM by inhibiting the growth of pathogenic bacteria.

Ventilation tubes
 A recent metanalysis found relative decrease in episodes of
AOM of 56 percent.
 The effect occurred mostly in the period when the tubes
were in place.
 Seventy-nine percent were reported to have an improved
quality of life.
Side effects
Recurrent otorrhoea in 7 percent and chronic otorrhoea in 4
percent;incidence of tympanosclerosis and focal areas of
tympanic membrane atrophy

 Antibiotic prophylaxis with amoxicillin vs tubes vs placebo.
 The amoxicillin group had a significant reduction in episodes
of AOM.
 The tube and placebo group did not.
 However, when AOM occurred in the placebo group, it was
more distressing than when otorrhoea occurred with AOM in the
group with tubes in place.
 May be considered for children with recurrent AOM, but no
persistent effusion, in whom medical strategies have failed. or
following failure of, medical prophylaxis in the child with
recurrent AOM and persistent OME.

SURGICAL PROPHYLAXIS
 There are relatively few trials addressing surgical prophylaxis.
 Surgery may reduce problems of antibiotic resistance and also
treat subsequent OME.

Adenoidectomy and adenotonsillectomy
 The limited evidence-base for best practice is most striking
when considering adenoidectomy.
 Two papers are particularly worth discussing
 The first concluded that adenoidectomy may be beneficial in
children who had previously had ventilation tube insertion and
suffered subsequent AOM.
AOM was reduced by 31 percent relative to the control group in
a two-year follow up (or 0.32 episodes per child-year), and subjects spent 42
percent less time with OME.
o Need for further tubes was reduced by 50 percent.

 Their second trial was of children who had not previously had
ventilation tube insertion.
 Modest reduction in the number of episodes of AOM was
recorded in the first year after surgery from 2.1 to 1.4 following
adenotonsillectomy , but not adenoidectomy.
 In summary,adenoidectomy may be considered in those who
have failed medical therapy ,further AOM following ventilation
tube insertion.

OUTCOMES OF AOM/ NATURAL HISTORY

OUTCOMES OF AOM
 An episode of acute otitis media may resolve rapidly with or without
antibiotics;
 It may prove resistant to first-line antibiotics;
 It may persist or recur shortly after a course of antibiotics has
finished;
 It may subsequently recur;
 It may progress to tympanic membrane perforation or other
complication of infection.
 Here we consider the medium- and long-term consequences of
infection: the natural history of AOM, middle ear effusions, auditory
functioning and speech and language development.

NATURAL HISTORY
SPONTANEOUS REGRESSION
 Without antibiotic treatment, symptomatic relief from pain and
fever occurs in approximately 60 percent of children within 24
hours of diagnosis, in over 80 percent by day two to three, and
88 percent by days four to seven.
 Only 73 percent reach the stage of complete resolution by day
seven to fourteen.
 For recurrent AOM the prognosis is also generally favourable.
Following study entry, and with only acute episodes treated,
recurrence rates fell to 0.13 episodes per child per month in
the subsequent 6-24 months.

 Other work has shown that even in early recurrences of
infection three to four weeks after a previous episode, a new
organism is usually involved.
 Caution should be attached to these findings.
 Though pooled numbers are large, high risk children and
those with baseline OME were generally excluded.

MIDDLE EAR EFFUSIONS
 Middle ear effusions are an important outcome of AOM. Data
show rates of OME of 63 percent two weeks after AOM,
 Forty percent at one month
 Twenty six percent at three months.
 Antibiotics did not appear to have any effect.

AUDITORY FUNCTIONING
 Approximately one in three children will have an air-bone gap
greater than 20 dB at one month after infection
 One in five at three months
 Limited evidence to suggest that AOM may reduce long-term
audiometric thresholds.
 Several studies reported small but significant loss of very high
frequency hearing (11-16 kHz) in those with many episodes of
AOM owing to disturbed ME mechanisms
 The significance for auditory functioning as the child grows
older is not established

The Pediatric Infectious Disease Journal: May 2000

#EXTRACRANIAL
#TYMPANIC MEMBRANE
 Tympanic membrane perforation is considered a commonest
complication of AOM.
 Reported in ~10 percent of episodes.
 Perforation is associated with a purulent or bloody otorrhoea
and immediate relief of pain.
 Typically occurs in the posterior half of the pars tensa, and is
associated with loss of the fibrous middle layer of the drum.
 This may predispose to future posterior retraction pockets.

Four outcomes.
 First: In most cases the perforation heals spontaneously and the infection
resolves.
 Second :The infection may resolve, but the perforation persists.
 Third :The perforation and otorrhoea may persist, manifesting as chronic
suppurative otitis media. 'Chronicity' is generally deemed to have occurred by
three months.
 Fourth :A further complication may arise.
#The long-term outcomes were assessed in a cohort of otitis-prone children followed up from 3 to 14 years of age.
By the end of the study 7 percent had collapse of the posterior superior tympanic membrane, chronic suppurative otitis media, or
central perforation.
 Scarring or tympanosclerosis was present in 27 percent,

#ACUTE MASTOIDITIS
Four classes.
 During acute episodes infection and inflammation may naturally
extend into the mastoid cavity, and be visualized radiologically but
not associated with the typical signs.
 Acute mastoiditis with periosteitis. (Infection spread to the
mastoid periosteum by emissary veins)
No abscess but the post-auricular crease may be full; the pinna
pushed forward and there may be mild swelling, erythema and
tenderness of the post-aural region.
 When acute mastoid osteitis develops, the infection has begun
to destroy the bone of the mastoid air cells and a subperiosteal
abscess may develop.

 A subperiosteal abscess develops most commonly in the post-
auricular region; zygomatic abscess;Bezold's abscess;
Retropharyngeal or parapharyngeal abscess
o A fourth stage may be reached, subacute ('masked') mastoiditis, in
incompletely treated AOM after 10-14 days of infection.
Signs may be absent, but otalgia and fever persist.
##In some developing countries rates of 5 percent are still quoted.
 In the 1970s it was estimated that 0.004 percent of cases of AOM
resulted in surgery for mastoiditis

Mastoiditis contd…
 The incidence is reported by several authors to be
increasing gradually again
 Disease of childhood.
 A large multicentre study found 28 percent to be in children
less than one year of age, 38 percent in one to four year
olds, 21 percent in four to eight year olds, 8 percent in 8-18
year olds and 4 percent in those over 18 years of age.
 This higher incidence in younger children reflects the peak
ages for AOM.

 Traditional teaching was that acute mastoiditis is preceded by 10-14
days of middle ear symptoms.
 However short length of middle ear symptoms prior to presentation
is noteworthy.
 In one study approximately 32 percent had one to two days
symptoms, 34 percent had three to six days, 26 percent seven to
fourteen days and 8 percent over 14 days.
 Antibiotics do not fully protect against mastoiditis.
 Symptoms are of otalgia and irritability in most children.
 Pyrexia is less common in those treated with antibiotics. Otorrhoea is
present in only approximately 30 percent.

Findings:
 Red or bulging tympanic membrane.
 A normal drum is reported in a very variable proportion of
cases, thus does not exclude the diagnosis believed to
result from resolution of the mesotympanic infection following
antibiotic treatment, while the osteitis in the mastoid
progresses.
 Retro-auricular swelling ~ 80 percent
 Retro-auricular erythema ~50-84 percent (less in previously
treated children).
 Tenderness is typically sited over MacEwen's triangle (on
palpation through the conchal bowl).

Contd..
 Pinna protrusion in two-thirds of cases.
 Sagging of the posterior wall of the external auditory canal, should
be looked for, but is quoted as an uncommon finding.
 Around 20 percent of samples do not grow bacteria.
 Streptococcus pneumoniae, Streptococcus pyogenes,
Pseudomonas aeruginosa and Staphylococcus aureus are the most
commonly reported.
 Haemophilus influenzae is less commonly reported, and Moraxella
catarrhalis, Proteus mirabilis and Gram-negative anaerobes rarely.

Investigation:
 CBC,
 C-reactive protein (CRP)
 Blood cultures.
 CT scan of the mastoid ;when intracranial complications are
present or suspected (though MRI may be more helpful in
identifying specific intracranial pathology), when
mastoidectomy is to be performed and in those not
improving on antibiotic treatment.
 May show evidence of osteitis, abscesses and intracranial
complications.

 Differential diagnosis includes
 AOM,
 Otitis externa,
 Furunculosis
 Reactive lymphadenopathy.
 Rarely, undiagnosed cholesteatoma, Wegener's
granulomatosis, leukaemia and histiocytosis may first
present with AOM, hence tissue should be sent for
histology if mastoidectomy is performed.

Treatment:
 Myringotomy with or without ventilation tube
 Culture of the aspirate and high-dose intravenous recommended
initial treatment in acute mastoiditis.
 Failure to improve, subperiosteal abscess formation (10-30%) or
development of complications indicates need for abscess drainage
with or without cortical mastoidectomy.
 A most important message is that intracranial complications from
acute mastoiditis develop in 6-17 percent of cases, and many of these
may develop during hospitalization.
 Although acute mastoiditis may be less common than in the past, its
severe complications still occur.

#PETROSITIS
 Infection may extend to the petrous apex.
 The classic features of Gradenigo's triad (VI nerve palsy,
severe pain in the trigeminal nerve distribution and middle
ear infection) are not always present
 Patients commonly present with other intracranial
complications.
 Recent papers recommend high-dose broad spectrum
antibiotics and a variety of mastoidectomy, from cortical to
radical, though drainage of the petrous apex is no longer felt
necessary.

#FACIAL NERVE PALSY
 In the pre-antibiotic era, it was estimated 0.5 percent of episodes of
AOM ,it is now quoted at 0.005 percent.
 Most are related to bacterial infection than viral
 Approximately 4/5 children present with a partial paralysis.
 The case series in the literature report that approximately 80 percent
of palsies respond well to ventilation tube insertion and intravenous
antibiotics.
 The remainder undergo cortical mastoidectomy.

 Advice is conflicting about when and in whom mastoidectomy is
required and the role of facial nerve decompression.
 As recovery is generally so good, a more conservative approach
without facial nerve decompression seems appropriate.
 Most children achieve rapid restoration of normal facial function,
with a mean time to complete recovery of four months.
 Those with a total paralysis at presentation have a recovery
stretching over many months.
 Sixth nerve palsy in the absence of petrositis has also been
reported.
 It is speculated this may stem from phlebitis spreading along the
inferior petrosal sinus from the lateral sinus.

#LABYRINTHITIS
 Round window permeability and preformed channels
during acute infection are important
 Particular concern arises in children with congenital inner ear
abnormalities and those with cochlear implants.
 Three types of labyrinthitis are recognized.
 Perilabyrinthitis is not associated with AOM.

 Serous labyrinthitis is inflammation of the labyrinth without
pus formation, and is characterized by recovery of auditory
and vestibular function.
 Suppurative labyrinthitis may result from spread of infection
from the mastoid or middle ear. Severe vertigo, nausea,
vomiting, nystagmus and permanent hearing loss result.
#Treatment of cases presented in the literature ranges from
ventilation tube insertion and aggressive antibiotic use, to
tympanomastoidectomy and cochleotomy.
 Intracranial

#EXTERNAL OTITIS /INFECTIOUS ECZEMATOID
EXTERNAL OTITIS
AOM with perforation and otorrhea or chronic suppurative OM
can cause an infection of the external auditory canal termed.
An infection in the mastoid may also erode the bone of the ear
canal or the postauricular area, resulting in dermatitis. The skin
of the ear canal is erythematous, edematous and filled with
purulent drainage, and yellow-crusted plaques may be present.

#HEARING LOSS.
 Can be conductive, sensorineural or both.
 Transient or permanent.
 Fluctuating or persistent conductive hearing loss is present in most
children who have MEE caused by AOM.
 Average loss of 27 dB, but the loss can be as much as 60 dB.
 Usually returns to normal however, might be permanent as a result of
recurrent acute or chronic inflammation due to adhesive OM or
ossicular discontinuity or fixation.
 Delay or impairment of speech, language and cognition in young
children,

#VESTIBULAR, BALANCE AND MOTOR DYSFUNCTIONS
 Balance problems, such as clumsiness.
 Vestibular system adversely affected.
 Tests of motor proficiency demonstrated to be abnormal in
children when MEE is present or a low grade labyrinthitis
 Residual effect of OM on the labyrinth
(ML Casselbrant, unpublished data, 1999).

#INTRACRANIAL
 In the pre-antibiotic era, intracranial complications of AOM were
more common and mortality rates of over 75 percent are
presented.
 Published mortality rates from intracranial complications now
average approximately 5 percent in industrialized countries.
 Persistent headache and fever are the most common early
symptoms of an intracranial complication.
 In half of cases there may be signs only of AOM and not
mastoiditis.
 Frequently two or more complications coexist.
 Early diagnosis is important for improving outcomes.

Seven classical intracranial suppurative complications of AOM
are described.
1. Meningitis
2. Extradural abscess
3. Subdural empyema
4. Focal otitic encephalitis
5. Sinus thrombosis
6. Brain abscess
7. Otitic hydrocephalus

 1.Meningitis
 Commonest intracranial complication of AOM~54-91 percent of
cases.
#One of the largest recent studies found no association between bacterial
meningitis and AOM, while another found an antecedent history of AOM in
29%
 Possible associations with congenital inner earmalformations
such as cochlear dysplasia, cochlear implants
 Younger children, average age two years, are most commonly
infected.

 Studies focus almost exclusively on bacterial aetiologies.
 The rate of Haemophilus inJluenzae type B meningitis has dropped
dramatically since vaccination was introduced. Streptococcus
pneumoniae is the causal agent in a greater proportion because of this
reduction.
 A second intracranial complication should be looked for in any infant with
meningitis with IVIR scanning.
 Myringotomy may help to establish the infective agent if evidence has
not been obtained from lumbar puncture.
 Treatment is medical.
 If mastoid surgery is required, it is usual to try and wait for an
improvement in the medical condition of the child first if possible.

2.Extradural abscess
 Next commonest intracranial complication.
 It is more commonly associated with chronic disease.
 Pus collects between dura and bone, usually after bone erosion.
 If lying in the posterior fossa medial to the sigmoid sinus, it is
termed an extradural (epidural) abscess, if within the split of dura
enclosing the sigmoid sinus it is called a peri-sinus abscess.
 It may be discovered only at mastoidectomy, but may be suspected
in the patient with persistent headache and fever or severe otalgia.
 Treatment is surgical drainage.

3.Subdural empyema
Collection of pus between the dura and arachnoid membranes and
is termed a subdural empyema.
 It is rare.
 It develops by direct extension of infection or thrombophlebitis.
 In addition to headaches and pyrexia, focal neurological signs,
seizures and signs of meningeal irritation may be present. Surgical
drainage of the abscess through burr holes or craniectomy may be
indicated. Mastoidectomy may sometimes be required, though many
cases cited in the literature were treated medically.

4.Sigmoid sinus thrombosis
Most commonly results from erosion of the bone over the sinus from
mastoiditis and may also be associated with other complications.
occurs in association with otitis media alone in 43 percent of cases.
Infected thrombus develops within the sinus and may then extend
proximally and distally to the internal jugular vein and superior vena
cava, entering the systemic circulation and causing septicaemia.
In addition to headache and otorrhoea, a spiking pyrexia may develop
. Griesinger's sign positive.
MRI :High signal intensity in the sigmoid sinus on both T I-and T
Tweighted images and absent flow.

If caused only by otitis media, myringotomy and antibiotics
may suffice.
However, in the presence of mastoid infection, it is more usual
to perform a canal wall up mastoidectomy, needle the sinus to
assess blood flow and occasionally to remove infected
thrombus.
As persistent sepsis and distant thrombosis are uncommon, the
role of anticoagulation is unclear in the literature.
Serial imaging to look for propagation of thrombus has been
recommended.

5.Focal otitic encephalitis (cerebritis).
 Focal inflammation and oedema of brain tissue may occur
independent of, or in association with, any suppurative
complication of AOM.
 Intensive antibiotic treatment is required.

6.Brain abscess
More commonly associated with chronic ear disease but may
occur in association with AOM and its complications
Brain abscess forms a larger proportion of complications in
developing countries. It may develop in both the temporal lobe
and cerebellum. Persistent headaches are the commonest
symptom. Initial symptoms may be of encephalitis, but these
often settle as the abscess organizes over days or weeks.
Eventually, signs of raised intracranial pressure, focal neurology
and infection develop

 Investigations
CT imaging followed by lumbar puncture, if safe.
Neurosurgical drainage may be avoided but will be required
if the abscesses are expanding.
Brain abscesses carry a potentially high mortality rate,
although in industrialized countries the few large Brain
abscess secondary to AOM.
 Series now quote rates of below 10 percent.
 One large review found the mortality from otogenic causes,
at 3.8 percent, was much lower than from other causes.

7. Otitic hydrocephalus
 Manifesting as raised ICP in the absence of any space-
occupying lesion, and without obstruction to the flow of
cerebrospinal fluid (CSF). Benign intracranial hypertension
is a synonym.
 Headache is the predominant symptom.
 It is commonly associated with sigmoid or transverse sinus
thrombosis and so lVIRI is an important investigation.
 Lumbar puncture will show raised CSF pressure, but normal
CSF composition.
 A number of medical treatments may be tried and liaison with a
paediatric neurologist is recommended if child.

Discussion:
1. Patient comes in OPD with hx of ear discharge for 5 days .
2. Otoscopy reveal perforation ,recurrent hx of discharge present
but last episode 3 months back Dx?
3. Patient with hx of Mplasty 5 years back .Comes with perforation
with repeated ear discharge for past 6 months but with symptom
free period of 6 weeks or more ?Dx
4. Patient comes with hx of ear ache with discharge for 1 week .No
perforation visible and no granulation tissue .Congested
/macerated mucosa with discharge ?Dx

 Summary
 Recommendation: To diagnose acute otitis media the clinician
should confirm a history of acute onset, identify signs of middle-
ear effusion, and evaluate for the presence of signs and
symptoms of middle-ear inflammation.
 2. Strong recommendation: The management of AOM should
include an assessment of pain. If pain is present, the clinician
should recommend treatment to reduce pain.
 3A. Option: Observation without use of antibacterial agents in a
child with uncomplicated AOM is an option for selected children
based on diagnostic certainty, age, illness severity, and
assurance of follow-up.
 3B. Recommendation: If a decision is made to treat with an
antibacterial agent, the clinician should prescribe amoxicillin for
most children. Option: When amoxicillin is used, the dose should
be 80–90 mg/kg/day.
 4. Recommendation: If the patient fails to respond to the initial
management option within 48 to 72 hours, the clinician must
reassess the patient to co reassess the patient to confirm AOM
and exclude other causes of illness

 If AOM is confirmed in the patient initially managed with
observation, the clinician should begin antibacterial therapy. If
the patient was initially managed with an antibacterial agent, the
clinician should change the antibacterial agent.
 5. Recommendation: Clinicians should encourage the
prevention of AOM through reduction of risk factors.
 6. No recommendation: There is insufficient evidence to make a
recommendation regarding the use of CAM for AOM.

 References
 Shambaugh Jr GE. Surgery of the ear. WB Saunders Co Phila Lond. 1967.
 Browning GG. Aetiopathology of inflammatory conditions of the external and middle ear. Scott-Brown’s
Otolaryngol, 2010
 Paul W. Flint et.al Cummings otolaryngology head and neck surgery, 2015
 James B.Snow,P.aAhley Wackym, Ballenger’s otorhinolaryngology head and neck surgery ,CT,2009
 Rhinitis, sinusitis and otitis media in Kartagener's syndrome (primary ciliary dyskinesia)January 1983Clinical
Otolaryngology 7(6):373-80
 Diseases of ear, nose and throat & head and neck surgery 7th edition
 Cytokines in nasopharyngeal secretions; Evidence for defective IL-1b production in children with recurrent
episodes of acute otitis mediaSeptember 2008doi10.1111/j.1365-2249.1994.tb06101
 Clinical Practice Guideline for Diagnosis and Management of Acute Otitis Media in Children. Pediatric
Otorhinolaryngology Japan 2006;27;(1):71-107
 Grommets (ventilation tubes for recurrent acute otitis media,McDonald S, Langton Hewer CD, Nunez
DACochrane Database Syst Rev 2008 Oct 8;(4):CD004741. doi: 10.1002/14651858.CD004741.pub2. PMID:
18843668
 Bluestone CD. Impact of evolution on the eustachian tube. Laryngoscope 2008;118:522–7.

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