Acute otitis media (AOM) is an inflammation of the middle ear caused by bacterial or viral infection. It is common in young children and causes symptoms like ear pain, fever, and hearing loss. While most cases clear up without treatment, antibiotics are usually prescribed to reduce symptoms and risk of complications. For recurrent cases, management involves identifying and addressing risk factors, medical or surgical prophylaxis including ventilation tubes, and vaccination when available. AOM poses a significant burden as it is one of the most frequent reasons children receive antibiotics.

1. Acute otitis media in children
AOM may be clinicopathologically as inflammation of the middle ear cleft of rapid onset, infective
origin, associated with a middle ear effusion & varied collection of clinical symptoms & signs. It is
synonymous with acute suppurative otitis media. It is normally behind an intact tympanic
membrane, but may include acute infections arising in the presence of ventilation tubes or existing
tympanic membrane perforations.
Subgroups of AOM
1. Sporadic episodic: episodes occurring as infrequent isolated events, typically occurring with
upper respiratory tract infections.
2. Resistant AOM: persistent of symptoms & signs of middle ear infection beyond three to five
days of antibiotic treatment.
3. Persistent AOM: persistence or recurrence of symptoms & signs of AOM within six days of
finishing a course of antibiotics.
4. Recurrent AOM: either three or more episodes of AOM occurring within six-month period ,
or at least four or six within a 12 month period.
Symptoms
1/3rd of children may have on related symptoms.2/3rd may be apyrexial.
Symptoms suggestive of AOM include rapid onset of otalgia, hearing loss, otorrhoea, fever, excessive
crying, irritability, coryzal symptoms, vomiting, poor feeding, ear-pulling & clumsiness.
AOM most commonly develops three to four days after the onset of corizal symptoms. The otalgia
will settle within 24 hours in 2/3rd of children without treatment.
The otorrhoea if present, is mucopurulent & may be blood-stained.
Symptomatic relief is obtained without treatment in 88% by day four to seven.
Hearing loss caused by the middle ear effusion, occurs early in the illness & may persist at greater
than 20db for one month in over 30% & two months in 20% of children.
Signs
The child may be unwell & may rub his or her ear.
The diagnosis is often confirmed, rightly or wrongly, by an attempt at otoscopic assessment of the
tympanic membrane. However, a poorly functioning otoscope, the moving target of a child’s head,
narrow ear canal of an infant, the natural redness of the tympanic membrane of screaming child,
wax, untrained eye, straining to interpret a two dimensional image, all combine to make otoscopy an
imprecise art.( trained observer 85% accuracy). Diagnosis is supported by otoscopic assessment of
tympanic membrane colour, position, & mobility.

2. In AOM the tympanic membrane is usually opaque. It is more commonly yellow or yellowish pink in
colour being red in only 18-19%.
The position of tympnanic membrane reliably predicts AOM only when it is bulging.
Hypomobility of the drum demonstrated by pneumatic otoscopy has been shown to aid diagnosis.
Investigations
Tympanometry may be used to establish the presence of a middle ear effusion.
Tympanocentesis & culture of middle ear effusion.
Full blood count
Immunoglobulin assay
D /D
Tonsillitis . teething ,temporomandibular joint disorders. URTI,
Aetiology
Mirobiological , anatomical & environmental factors combine with altered host defence mechanisms
to predispose to infection. Genetic predisposition to recurrent AOM is being increasingly cited in the
literature.
Infective agents
AOM is commonly associated with viral upper respiratory tract infections(60-90%). In decreasing
frequency include:
-respiratory syncytial virus;
-influenza A virus;
- parainfluenza viruses;
-human rhinovirus;
-adenoviruses.
The virus material may arrive either passively along tha eustachain tube along with other
nasopharyngeal secretions or may actively invade middle ear cleft possibly by haematogenous
spread.
Viral infection affects the Eustachian tube function> release of multiple inflammatory mediators
from cells> decrease the number of ciliated epithelial cells & increase mucus production>negative
middle ear pressure predispose to AOM.
Bacteria
1. H. influenza is the most common organism.

3. 2. Pneumococcus;
3. Moraxella catarrhalis
4. Streptococcus pyogenes
5. Staphylococcus aureus
Routes of spread of infection
Three potential routes are described: the Eustachian tube, tympanic membrane perforation or
grommets, haematogenous.
Negative middle ear pressure may facilitate the movement of bacteria up the Eustachian tube.
Otitis –prone children have been shown to have significantly poorer active tubal function( muscular
opening function).
Pathogen entry through tympanic membrane perforation or ventilation tubes is most commonly
associated with water exposure.
Haematogenous route for viral infection.
Risk factors of AOM
1. Genetic factors : there is growing evidence that recurrent AOM is likely genetically
determined. It is likely many genes are involved & familial association.
2. Immune factors: low levels of IgG2 subclasses more prone in otitis media. Aberrant
expression of critical cytokines, such as tumour necrosis factors & interlukins, resulting in
suboptimal host defence, has been postulated as a cause for persistent infection.
3. Environment factors: the incidence of AOM appears to follow that of seasonal upper
respiratory tract infections in the winter months. Breast feeding for six months is protective(
use of pacifier/dummy carries a relative risk of infection, poor socioeconomic status
associated with poor housing, overcrowding, passive smoking exposure from parental
smoking. There is more limited evidence to support the role of dietary factors, in particular
cow’s milk allergy, in predisposing to AOM.
4. Syndromic associations:children with down’s syndrome/ Turner’s syndrome do suffer more
frequently episodes of AOM. It may be due to dysfunction of ET or secondary to subtle
immunological factors that predispose to infection. A direct association between iron
deficiency anaemia, & degree of anaemia & frequency of AOM has been reported.
Epidemiology
AOM is one of the most common illness of childhood. It is account for approximately 25% of all
prescriptions for children under ten years of age.
Incidence appears highest in the first year of life, more frequently the second six months of life &
then gradually reduces with increasing age.

4. Recurrent AOM has been reported in 5% of children under two years of age. An important indicator
of future problems is a first episode before nine months of age, these children have a one in four risk
of developing recurrent AOM.
In the first two years of life, AOM occurs bilaterally in 80% of cases. After six years of age, it is
unilateral in 86%.
Surgical treatment : has limited role in the treatment of an uncomplicated episode of AOM.
Myringotomy was practised in preantibiotic era. Myringotomy is reserved for severe pain or where
complication is present or suspected.
Management of acute episodes
Conservative treatment
Most children with AOM will get better quickly without treatment. Most children will benefit from
simple analgesics & antipyrexials, in a quiet supportive environment. Paracetamol & ibuprofen are
most commonly used in the UK. Ibuprofen provides additional benefit by reducing mucosal
inflammation when taken in combination with amoxicillin.
Antibiotics
Amoxicillin remain the first choice in most centres, but higher than previously recommended doses.
If drug-resistance pneumococci are common or penicillin –sensitive patients treated with macrolide.
For persistent or resistance episodes beta-lactamase producing organisms. Options include
amoxicillin-cluvulonate or cefuroxime axetil orally.
Antihistamine & decongestants
Use of oral or intranasal antihistamine &/ or decongestant concluded that their use could not be
supported.
Management of recurrent acute otitis media
Alternation of risk factors
- AOM increase with the number of children in a day care.
- Advice should include sitting a child semi-upright if bootle-fed,
- Avoiding passive smoking;
- Restricting use of pacifiers particularly after infancy, should be recommended for otitis-prone
children.
- Mother should be advised to continue breastfeeding for at least six months.
- Increasing intake of vitamin C intake & avoiding alcohol in the third trimester.
- The role of cow’s milk, still unclear.

5. Medical prophylaxis
In the management of recurrent AOM, on average eight months of antibiotic prophylaxis would be
needed to prevent one episode of AOM. This strategy may be preferred in the absence of effusions
between episodes of AOM. Sulfisoxazole do better than those treated with amoxicillin both being
used at half the therapeutic dosage. This is important as antibiotic prophylaxis may therefore be
most appropriate for children not ot prone OME, while ventilation tubes may be indicated for those
prone to OME.
Vaccination
Vaccination against viruses; influenza A vaccination is currently available, RSV & parainfluenza virus
are undergoing clinical trial.
Vaccination against streptococcus pneumonia, Haemophilus influenza & Moraxella catarrhalis is
made difficult by the low immumogenicity of the capsule for the bacteria.
Immunoglobulin : intravenous immunoglobulin(GB-0998) in IgG2-deficient infants has been shown
to be effective prophylaxis for AOM.
Surgical prophylais
Ventilation tube: failure of medical prophylaxis with recurrent otitis media & OME.
Adenoidectomy & adenotonsillectomy : there is little evidence to support adenotonsillectomy.
Adenoidectomy may be considered in those children who have failed medical therapy & ventilation
tube insertion. The presence of OME increases the benefit of adenoidectomy.
Outcome
The natural history of AOM, middle ear effusions,auditory functioning, & speech & language
development.
OME: OME of 63% two weeks after AOM, 40% at one month, 26% at three months.antibiotic did not
appear to have any effect.
Auditory functioning(hearing loss): one in three children will have an air-bone gap greater than 20db
at one month of infection, & one in five children at three months.
Best clinical practice
1. AOM is one of the commonest illnesses of childhood. Accurate diagnosis is notoriously
difficult. A high index of suspicion is required in the unwell child.
2. The clinician should distinguish between sporadic, resistant, persistent or recurrent AOM as
management strategies differ.
3. 2/3rd of the children recover within 24hours with or without treatment, so a period of
watchful waiting may be reasonable in uncomplicated AOM.
4. Pyrexia ( >350C), severe otalgia, vomiting, age under two years & high risk children have all
been used as indicators to be use antibiotics sooner rather than later.

6. 5. Broad spectrum antibiotics are not generally required as first-line therapy.
6. In otherwise healthy children over two years of age, five days of antibiotics is usually
adequate.
7. For resistance or persistence AOMs it should be noted that pneumococcal drug resistance
can usually be overcome by increased antibiotic doses, Haemophilus may be beta-lactum
antibiotics may be required.
8. Modifiable risk factors should be discussed with parents. These include nursery attendance,
parental smoking, breastfeeding, use of pacifiers.
9. In the management of recurrent AOM, on average eight months of antibiotic prophylaxis
would be needed to prevent one episode of AOM. This strategy may be preferred in the
absence of effusions between episodes of AOM.
10. Ventilation tube insertion reduces the number of episodes of AOM by over 50%. This option
may be preferred when effusions persist between episodes of AOM.
11. Additional adenoidectomy may further reduce the number of episodes of AOM.
12. Tbe benefit of tonsillectomy on episodes of AOM are not sufficient to warrant its use in the
management of recurrent AOM.
13. Vigilance should be maintained for complications of AOM , the most common symptoms
being persistent pyrexia & headache.
Acute mastoiditis
Four classes of mastoiditis are defined. During episodes of acute otitis medfia, infection &
inflammation may naturally extend into mastoid cavity & be visualised radiologically.
Infection may spread to the mastoid periosteum by emissary veins; acute mastoiditis with
periosteitis. At this stage no abscess is present but the post-auricular crease may be full, pinna may
be pushed forward & there may be mild swelling, erythaema & tenderness of the post-auricular
region.
When acute mastoid osteitis develops, the infection has begun to destroy the bone of the mastoid
air cells & subperiosteal abscess may develop. A sub periosteal abscess most commonly in the post-auricular
region. A zygomatic abscess may develop above or in front of the pinna. A bezold’s abscess
may result from perforation of the medial mastoid cortex, tracking down the sternomastiod to the
posterior triangle. Pus tracking down peritubal cells may result in a retropharyngeal or para
pharyngeal abscess.
Subacute mastoiditis, incompletely treated AOM after 10-14 days of infection. Sign may be absent,
but otalgia & fever persist.
Acute mastoiditis is a disease of childhood.
-28% to be in children less than one year of age.

7. - 38% in one to four years old
-21% in four to eight year;
-8% in 8-18 year;
-4% in those over 18years.
Higher incidence in younger children reflects the peak ages for AOM.
Traditional teaching is that acute mastoiditis is preceded by 10-14 days of middle ear symptoms. But
it may vary . Clearly antibiotics do not fully protect against mastoiditis.
Clinical features
Symptoms are of otalgia & irritability in most children. Pyrexia is less common in those treated with
antibiotics. Otorrhoea is present in only approximately 30%.
Red or bulging TM may be seen. A normal TM is reported in a variable proportion of patients does
not exclude the diagnosis & is believed to result from resolution of the mesotympanic infection
following antibiotic treatment while the osteitis in the mastoid progresses.
Retroauricular swelling is seen 80% of cases. & reto-auricular erythaema in 50-84%.
Terderness is typically sited over MacEwen’s triangle ( on palpation through the conchal bowl).
Sagging of the posterior wall of the external auditory canal , resulting from subperiosteal abscess
formation,. Few patients will have a full house.
Organism same as AOM. Streptococcus pneumonia, streptococcus pyogenes, pseudomonas
aeruginosa ,staphylococcus aureus, psuedomonsa aeruginosa are most common.
Investigations
Full blood count, C-reactive protein(CRP) & blood cultures are obtained.
CT scaning may show evidence of osteitis, abscess & intracranial complications.
D/D
AOM, furnculosis, otitis externa,
Treatment
Myringotomy with or without ventilation tube placement, culture of the aspirate & high dose of
antibiotic is the most commonly recommended initial treatment in acute mastoiditis.
Failure to improve, subperiosteal abscess formation or intracranial complications, abscess drainage
with or without cortical mastoidectomy.