Acute otitis media in children

• Acute otitis media (AOM) is an acute infection of the middle ear. It causes a middle ear effusion (MEE) together with signs and symptoms of acute infection, usually after a viral cold.
• The usual bacteria are Streptococcus pneumoniae, non-typeable Haemophilus influenzae and Moraxella catarrhalis. The short, more horizontal Eustachian tube of infants helps these organisms reach the middle ear.
• The diagnosis depends on otoscopy: bulging of the tympanic membrane (TM) with loss of its landmarks, with or without ear pain or fever. Pain relief is the first treatment for every child.
• Many episodes settle without antibiotics. Watchful waiting for 48 to 72 hours ^[3] is appropriate for most children over 6 months ^[3] without severe signs. Antibiotics (usually amoxicillin) are reserved for younger children with bilateral disease, for AOM with perforation and pus, and for severe or persistent illness.
• Complications such as mastoiditis and meningitis are rare but dangerous. Otitis media with effusion (OME) commonly follows AOM and is the main reason for tympanostomy (ventilation) tubes.

By the end of this page you should be able to:

1. Explain why infants are prone to AOM from Eustachian tube anatomy.
2. Name the three common bacteria and how a cold leads to infection.
3. Recognise AOM and distinguish it from OME and otitis externa.
4. Apply the diagnostic criteria and define severe AOM.
5. Manage pain, choose watchful waiting and prescribe amoxicillin with the correct dose, timing and second-line choice.
6. List the important complications and when to refer.
7. Describe when tympanostomy tubes are used.
8. Give evidence-based prevention advice on vaccines and breastfeeding.

Otitis media is an umbrella term. It covers AOM, OME (sometimes called "glue ear") and chronic suppurative otitis media. These conditions overlap: after almost every episode of AOM, effusion remains in the middle ear for a while, so AOM and OME are stages of the same disease rather than separate illnesses. AOM itself is further divided into:

• Uncomplicated AOM: a single episode in an otherwise healthy child.
• Severe AOM: moderate-to-severe ear pain, ear pain lasting at least 48 hours, or fever of 39 degrees C or higher. Severe AOM is more common when both ears are affected, although the relationship is not consistent. ^{[3] [1]}
• Recurrent AOM (rAOM): three or more separate episodes in 6 months, or four or more in 12 months with at least one episode in the preceding 6 months ^{[3] [4]}.

AOM is one of the most common reasons children see a doctor and one of the commonest reasons antibiotics are prescribed for children. A systematic review of the global burden estimated the average AOM incidence at 10.8 new episodes per 100 people per year ^[1], ranging from about 3.6 in central Europe to 43.4 in parts of sub-Saharan and central Africa ^[1], which shows how much the burden varies with economic conditions. The total annual number of new AOM episodes is estimated at 709 million ^[1], with half (51%) occurring in children under 5 years of age ^[1]. Incidence is highest in children 1 to 4 years of age (61 new episodes per 100 children per year) and peaks in the first year of life (45.3 per 100) ^[1]. Over 60% of children under 3 years have at least one episode, and about a quarter have at least three ^[3].

OME is even more common because it is often silent: 80% of children have had at least one episode of OME by 10 years of age ^[1], and OME peaks at about 1 year of age. Attendance at day care, crowding and family history all raise risk.

AOM is usually uncomplicated in high-income countries, but an estimated 21,000 people die from complications of otitis media every year ^[1], mostly in low-income settings, and the global prevalence of hearing loss associated with otitis media is estimated at 30 (range 0.7 to 95) per 10,000 people ^[1]. Clinically diagnosed AOM in high-income countries has declined since the mid-1990s, attributed to stricter diagnostic criteria, more careful antibiotic use and pneumococcal vaccination, but it remains a leading cause of GP visits, antibiotic prescriptions and surgery in these countries.

AOM is almost always preceded by a viral upper respiratory infection. Viruses such as respiratory syncytial virus, rhinovirus, adenovirus, influenza and parainfluenza viruses infect the nasopharynx and Eustachian tube. They do the damage that allows bacteria to enter the middle ear; viruses alone cause AOM in only about 5% of cases ^[1].

The three dominant bacterial otopathogens are:

1. Streptococcus pneumoniae (pneumococcus)
2. non-typeable Haemophilus influenzae
3. Moraxella catarrhalis

Which one dominates varies with place and with pneumococcal vaccine use. In more severe AOM with a perforated eardrum and pus, Streptococcus pneumoniae remains the most frequent pathogen (26%) ^[3], followed by Haemophilus influenzae (18.8%) ^[3] and Staphylococcus aureus (12.3%) ^[3]. Mixed infections and biofilms are common, which helps explain why some infections persist and why syrups are sometimes needed.

The Eustachian tube of an infant is designed badly for its job, which is the central reason children get AOM. Compared with adults, the child's tube is:

• shorter (about 13 mm at birth versus about 35 mm in adults) ^[1];
• wider and more compliant ("floppy");
• more horizontal (about 10 degrees to the horizontal at birth versus about 45 degrees in adults) ^[1];
• lined with thicker, more folded mucosa and more lymphoid tissue, including the tubal tonsil and adenoids.

This shallow angle means gravity does little to drain secretions, and the tube's cartilage and the tensor veli palatini muscle are not yet efficient at opening it. On top of this, the cartilage is denser with less elastin, Ostmann's fat pad is relatively larger, and the skull base has not descended to pull the tube into its adult position. Consequently the tube opens less well during swallowing and yawning, secretions pool, and nasopharyngeal organisms travel easily into the middle ear.

The lining is ciliated respiratory epithelium that sweeps mucus away from the middle ear toward the nose. Viral colds damage this epithelium, cause swelling and mucus, and paralyse mucociliary clearance. Pressure then equalises poorly: nitrogen absorption by the middle ear mucosa draws a vacuum ^[1], which sucks bacteria and viruses in. Supine feeding ("bottle propping") and pacifier use (especially when nose breathing is blocked, the Toynbee phenomenon) worsen this.

Risk factors for AOM include: young age; male sex; a family history of otitis media; craniofacial anomalies such as cleft palate; adenoid hypertrophy; upper respiratory infections; atopy; immunodeficiency; and laryngopharyngeal reflux. Environmental factors include low socioeconomic conditions, tobacco smoke exposure, having older siblings, and day-care attendance. Malnutrition, contaminated water, overcrowding and poor access to healthcare increase the risk of chronicity and complications in lower-resource settings.

1. Colonisation. Bacteria (S. pneumoniae, non-typeable H. influenzae, M. catarrhalis) colonise the nasopharynx, often without symptoms.
2. Viral trigger. A cold infects the nasopharynx and Eustachian tube, causing oedema, mucus and loss of mucociliary clearance.
3. Tube dysfunction. The Eustachian tube fails to open and equalise pressure; negative pressure builds in the middle ear. ^[1]
4. Ascent. Organisms travel up the short, horizontal tube into the middle ear, or are aspirated with negative pressure.
5. Inflammation and effusion. Pus accumulates behind the eardrum. The TM bulges, becomes opaque or red, and mobility is lost.
6. Persistence. Biofilms in the middle ear help bacteria evade both antibiotics and host defences, so effusion often persists after symptoms settle.

Viral-bacterial co-infection increases inflammation and reduces antibiotic penetration, which is part of why antibiotics can seem disappointing even when the right drug is given.

Ear pain is the most consistent symptom, but only 50 to 60% of children with AOM complain of ear pain ^[1]. Young, preverbal children show ear pain as tugging, rubbing or holding the ear, excessive crying, poor feeding, sleep disturbance or new irritability. Other symptoms include fever, vomiting, reduced appetite and, after TM perforation, ear discharge.

Because these symptoms overlap with an uncomplicated cold, history alone is unreliable. Ear pain is more useful for AOM, while hearing loss points to OME. Fever and vomiting are common to both AOM and viral infections and do not separate them.

Look for fever and assess how well the child looks overall. The critical step is otoscopy, ideally with a pneumatic otoscope and good light. The clinician should record the colour, opacity, position and integrity of the TM. Cerumen obscuring the view must be removed first, otherwise AOM is easily overdiagnosed.

The five otoscopic findings that matter are:

1. Bulging of the TM, the single most consistent sign of AOM and the feature that best separates AOM from OME.
2. Loss of landmarks: the cone of light and the malleus handle become indistinct as the drum bulges.
3. Erythema (redness) of the drum, although a crying child's drum can look pink without infection.
4. Opacity or cloudiness, highly predictive of MEE even without acute infection.
5. Immobility on pneumatic otoscopy: a normal drum moves briskly; a drum with fluid behind it barely moves.

Occasionally there is spontaneous perforation with pus in the ear canal; this still counts as AOM and usually relieves pain abruptly.

Appearances described in the source material are: a normal shiny, concave drum; a red, bulging drum in AOM; an opaque drum with a fluid level in OME; and a drum with a ventilation tube in place.

The main distinction is from the conditions in the table.

AOM is a clinical diagnosis; tests support it rather than make it.

• Otoscopy and pneumatic otoscopy are the primary tools. They have excellent accuracy for OME and good accuracy for AOM.
• Tympanometry objectively assesses drum mobility and middle ear function. A flat type B trace suggests effusion; a type C trace suggests negative pressure. Tympanometry is easier to perform than pneumatic otoscopy but has lower specificity (50 to 75% versus about 80%). ^[1]
• Acoustic reflectometry can be used by parents to screen for effusion.
• Audiometry is used for OME, not for acute infection, to quantify any conductive hearing loss.
• Tympanocentesis (needle aspiration of middle ear fluid) is rarely needed. It gives diagnostic certainty (especially to identify organisms) and rapid pain relief, but does not shorten effusion or prevent recurrence. Reserve it for treatment failure, severe or unusual cases, or research.
• Imaging (CT) is for suspected complications such as mastoiditis, not for uncomplicated AOM.

Two credible sources agree on the diagnostic criteria ^{[1] [4]}. AOM is diagnosed when MEE is present together with one of the following: moderate-to-severe bulging of the TM; mild bulging of the TM with recent (less than 48 hours) onset of ear pain or intense erythema of the TM; or acute ear discharge not caused by otitis externa. MEE is required for both AOM and OME; without MEE, neither diagnosis holds, which explains why AOM is widely overdiagnosed.

OME is diagnosed by one or more of: reduced TM mobility on pneumatic otoscopy; reduced mobility on tympanometry; an opaque drum; or a visible air-fluid level behind the drum.

Severity. The degree of bulging does not reflect AOM severity. Severe AOM is defined as having moderate-to-severe ear pain, ear pain for at least 48 hours, or a temperature of 39 degrees C or higher ^{[1] [3]}. A practical severity score (temperature, general condition, pain, drum redness and bulging; total 4 or more means severe) is available ^[3]. International approaches agree that the threshold for urgent treatment is a hot, very painful or systemically unwell child.

OME is the silent cousin of AOM: fluid in the middle ear behind an intact drum, without signs or symptoms of acute infection. After AOM, all children have OME for some time ^[1], and it can last for weeks or months. One attack often blends into the next, so parents and clinicians must not think of each illness as a fresh infection.

The hallmark is conductive hearing loss caused by impaired sound transmission. About half of affected children have hearing loss above 20 dB ^[5], and 5 to 10% above 50 dB ^[5]. Watch for hearing difficulty, speech delay, poor school performance, clumsiness and disturbed sleep. Severe or persistent OME can damage the drum (retraction pockets, tympanic atrophy) and, rarely, lead to cholesteatoma.

Management of OME is mostly watchful waiting:

• Many episodes resolve spontaneously, particularly when effusion has lasted less than 3 months ^[5].
• Antibiotics, corticosteroids, antihistamines, decongestants and mucolytics are not recommended; they rarely give lasting benefit.
• Autoinflation (the Politzer manoeuvre) may help older children.
• Tympanostomy (ventilation) tubes are the benchmark treatment ^[5] for persistent OME with a hearing loss of 25 to 40 dB ^[5] or drum damage, especially when there are speech, learning or developmental risks.

OME is diagnosed when effusion persists at consultations three months apart. Chronic OME means effusion lasting at least 3 months. OME should not be screened for in healthy asymptomatic children; screen at 12 to 18 months ^[1] only in children at increased risk (permanent hearing loss, speech or language delay, autism spectrum, craniofacial anomalies, cleft palate, developmental delay, or visual impairment). ^[5]

The framework below is a teaching approach to AOM; local guidelines and the child's circumstances always take precedence.

Pain assessment comes first. Offer regular doses of paracetamol (acetaminophen) or ibuprofen, using the correct dose for age or weight, maximum doses for severe pain. Anaesthetic/analgesic eardrops (phenazone with lidocaine) help pain and are an option when no immediate oral antibiotic is given and there is no perforation and no otorrhoea. Decongestants and antihistamines do not help.

Safety-net advice for families: an antibiotic is often not needed; seek help if symptoms worsen rapidly or significantly, do not start to improve after 3 days, or the child becomes generally unwell.

AOM is usually self-limiting: symptoms last about 3 days (up to a week) ^[2], and most children improve within 3 days without antibiotics ^[2]. Antibiotics make little difference to pain at 24 hours ^[2]; after that, similar numbers improve on their own as develop antibiotic side effects (vomiting, diarrhoea, rash). Complications such as mastoiditis are rare with or without antibiotics ^[2]. ^[3]

Watchful waiting means observing the child for 48 to 72 hours ^[3], treating symptoms only, and reassessing. It can be considered in all children over 6 months when follow-up within 72 hours is possible and there are no significant comorbidities.

• Under 6 months ^[3]: immediate antibiotics (little safety data for waiting).
• 6 to 23 months with bilateral AOM: antibiotics are generally recommended.
• 6 to 23 months with mild unilateral AOM: watchful waiting is an option.
• 2 years and older: watchful waiting is recommended unless there are severe signs or risk factors.

Immediate antibiotics (or a back-up prescription) are appropriate when the child is systemically very unwell, has severe signs, or has risk factors such as significant heart, lung, kidney, liver or neuromuscular disease, immunodeficiency, cystic fibrosis or prematurity.

When a decision to treat with antibiotics is made, amoxicillin is the first-line drug, because it covers the common pathogens reliably and has a narrow spectrum. A beta-lactamase-resistant drug such as co-amoxiclav is used when the child has had amoxicillin recently, has concurrent purulent conjunctivitis, or has recurrent AOM unresponsive to amoxicillin.

For penicillin allergy, a macrolide is the usual alternative where appropriate, although macrolides have limited activity against H. influenzae and S. pneumoniae. Co-amoxiclav is the usual second-line agent if symptoms worsen after 2 to 3 days on first-line treatment.

Dosing differs by guideline. The United Kingdom (NICE) uses age bands: amoxicillin 125 mg three times a day from 1 to 11 months ^[2]; 250 mg three times a day from 1 to 4 years ^[2]; 500 mg three times a day from 5 to 17 years ^[2], all for 5 to 7 days ^[2]. An Italian intersociety consensus (2025) recommends high-dose amoxicillin 90 mg per kg per day ^[3] in three divided doses, for 5 days ^[3], though two daily doses may improve adherence. These differences reflect local practice; check the local formulary. Some schedules use a longer course for very young or severely unwell children.

Second-line treatment: co-amoxiclav (amoxicillin-clavulanate) is used when there is no response to amoxicillin after 48 to 72 hours, or when the child has received amoxicillin recently, has AOM with purulent conjunctivitis, or has recurrent AOM unresponsive to amoxicillin. For anaphylactic penicillin allergy or treatment failure, consult local microbiology. Intramuscular ceftriaxone is an alternative in some protocols when oral treatment is not possible.

Humidified air, decongestants and antihistamines do not change the outcome. Families should be told that completing the prescribed course and reviewing if not better in 48 to 72 hours is the safer path than stopping early.

Complications are rare but important to recognise early:

• Acute mastoiditis behind the ear, from spread to the mastoid air cells. Presents with post-auricular swelling, erythema, protruding ear and fever. Requires urgent hospital assessment, blood tests, possible imaging, and intravenous antibiotics; drainage if there is an abscess or subperiosteal collection.
• TM perforation occurs in about 2% of AOM episodes ^[3]. It usually heals spontaneously within weeks to months. Persistent perforation can lead to chronic ear problems.
• Hearing loss is usually conductive from persistent effusion; it can impair language and learning in chronic cases. Sensorineural loss is uncommon and suggests a different process.
• Intracranial complications such as meningitis, brain abscess, sinus thrombosis or facial nerve palsy are rare but life-threatening. All require urgent referral and hospital care.
• Recurrent AOM itself is a morbidity, causing repeated pain, sleep disturbance and antibiotic exposure.
• Chronic OME with long-term hearing loss is a quieter complication but common.

On mastoiditis in particular, antibiotic use reduces the risk from about 3.8 to 1.8 cases per 10,000 AOM episodes ^[3]; put another way, over 4,800 children with AOM would need antibiotics to prevent one case of mastoiditis ^[3].

Refer urgently for suspected mastoiditis or any intracranial complication, for AOM with severe systemic infection, and for children who are high-risk or immunocompromised. Any child with acute complications should be sent to hospital.

Tympanostomy tubes (TTs) are tiny plastic tubes inserted through the eardrum, usually under general anaesthesia, that ventilate the middle ear and drain fluid. They usually fall out after 6 to 12 months ^[5], some types last up to 14 months or longer ^[5]. ^[1]

Indications (main ones):

1. Persistent OME (at least 3 months) in a child with documented hearing loss (25 to 40 dB) or tympanic membrane damage, particularly with speech, learning, behavioural or developmental concerns.
2. Recurrent AOM with effusion at the time of assessment: rAOM is defined as three episodes in 6 months or four in 12 months (with at least one in the preceding 6 months on the AAP definition). Tubes are not recommended for rAOM when no effusion is present at assessment, except in at-risk or complicated children.
3. Selected at-risk groups: children under 6 months with antibiotic-refractory toxic AOM, multiple drug allergies, persistent infection despite enteral and parenteral antibiotics, prior complications (meningitis, facial nerve palsy, mastoiditis, abscess, labyrinthitis), immunodeficiency, or craniofacial abnormalities and severe language delay.

What tubes help with: faster hearing restoration, prevention of OME recurrence in the short term, prevention of cholesteatoma in chronic cases, and reduced AOM frequency in the first year after placement. What they do not do: they do not prevent all episodes long-term, they do not prevent progression to tympanic atrophy, and they do not always improve long-term language outcomes.

Complications include tube otorrhoea (3 to 50% early postoperatively, usually settles) ^[5], obstruction (median about 6.7%) ^[5], early extrusion (about 3.9%) ^[5], migration into the middle ear (0.5%) ^[5], persistent perforation (1 to 10%) ^[5], and myringosclerosis. Adenoidectomy can reduce recurrence, particularly in children over 4 years or with proven nasal obstruction, by improving Eustachian tube ventilation ^[5].

As with OME, guidelines recommend about a 3-month watchful waiting period before placing tubes for persistent effusion, unless high-risk.

Because OM is multifactorial, prevention works on several fronts. Vaccination against the main bacteria and against respiratory viruses has measurably reduced AOM.

• Pneumococcal conjugate vaccine (PCV). PCV7 (seven serotypes) reduced pneumococcal AOM by 29% ^[1], overall AOM by 6 to 7% ^[1], and ventilation tube use for recurrent OM by 20% ^[1]. PCV13, introduced a decade later, further reduced AOM, mastoiditis and tube insertions ^[1]. A caveat: PCV can shift nasopharyngeal carriage toward non-vaccine serotypes and non-typeable H. influenzae, and PCVs do not prevent OM once recurrent disease is already established ^[1].
• Influenza vaccine. Trivalent inactivated and live attenuated influenza vaccines reduce AOM during influenza seasons by preventing influenza infection ^[1], which precedes AOM in up to two-thirds of young children ^[1]. Recommendations for influenza vaccination in children vary by country; follow the local schedule. Effectiveness varies by how well the vaccine matches the circulating strain.
• Investigational vaccines against non-typeable H. influenzae and M. catarrhalis are in development; none is licensed yet.

Breastfeeding protects against otitis media ^[1]; families are encouraged to breastfeed exclusively where feasible, alongside avoidance of tobacco smoke exposure, reducing day-care crowding where practical, and treating adenoid hypertrophy when present.

Routine antibiotic prophylaxis is not recommended for recurrent AOM because of resistance. Tympanostomy tubes or watchful observation are preferred.

• Clinical diagnosis: Even without pneumatic otoscopy, a careful look with a bright otoscope and assessment of drum mobility by observation identifies most cases.
• Tympanometry is helpful but expensive; well-trained pneumatic otoscopy is almost as good.
• Pain relief with paracetamol or ibuprofen and reassurance must be available even where antibiotics and ENT services are not; most children improve without antibiotics.
• Refer early if a child is not better in 3 days, is systemically unwell, or has post-auricular swelling, severe pain, neck stiffness or neurological signs.
• Surgery (tubes, mastoidectomy, drainage) needs referral to an ENT centre.
• Hearing should be assessed locally and early for children with recurrent or persistent disease, because language development depends on it.
• Malnutrition and poor living conditions increase complications; fix what is fixable (nutrition, smoke exposure, breastfeeding support) alongside ear treatment.

Acute otitis externa; Otitis media with effusion (glue ear); Hearing impairment in children; Acute fever in children; Adenotonsillar disease; Meningitis in children. These topics are named in plain text; cross-links are added as MedGrasp publishes them.