Recurrent Acute Otitis Media

Three or more distinct episodes of acute otitis media within 6 months, or four or more within 12 months with at least one episode in the preceding 6 months, with complete resolution of signs and symptoms between episodes. The requirement for interval resolution distinguishes it from chronic otitis media with effusion punctuated by exacerbations.

Mechanisms

Persistent bacterial biofilm on middle ear mucosa and within adenoid tissue, which survives conventional antibiotic courses and reactivates with each viral illness.
Immature or dysfunctional Eustachian tube function.
Repeated viral upper respiratory infection acting as the trigger for each episode.
Impaired mucosal immunity and reduced antibody responses to polysaccharide antigens in some children.

Risk factors

First episode before 6 months of age, the strongest predictor.
Day care attendance and older siblings.
Absence of breastfeeding.
Tobacco smoke exposure.
Pacifier use beyond 6 months and supine bottle feeding.
Cleft palate, submucous cleft, Down syndrome and craniofacial anomalies.
Allergic rhinitis and adenoid hypertrophy.
Immunodeficiency, including immunoglobulin A deficiency, immunoglobulin G subclass deficiency and specific polysaccharide antibody deficiency.
Primary ciliary dyskinesia and cystic fibrosis.
Gastro oesophageal reflux, with a weaker association.

Repeated discrete episodes of otalgia, fever and irritability, each resolving with or without treatment.
Normal tympanic membranes and normal hearing between episodes in true recurrent disease. Persisting effusion between episodes indicates a combined picture and shifts management toward tube insertion.
Frequent antibiotic courses with rapid relapse after completion.
Parental exhaustion, sleep disruption and repeated school or work absence, which are legitimate parts of the surgical indication.

Features that require investigation beyond the ear

Concurrent recurrent sinopulmonary infection, chronic wet cough, bronchiectasis or failure to thrive, suggesting immunodeficiency or ciliary dysfunction.
Neonatal respiratory distress in a term infant, situs inversus and chronic rhinorrhoea from birth, suggesting primary ciliary dyskinesia.
Chronic nasal obstruction, mouth breathing, snoring and hyponasal speech, suggesting adenoid hypertrophy.
Feeding difficulty, nasal regurgitation, bifid uvula or a notched hard palate, suggesting submucous cleft.

The first step is to confirm that the episodes are real. Parental report substantially overestimates frequency, and diagnoses made without otoscopy or without an effusion are frequently upper respiratory infections with referred otalgia.

Review documented episodes with recorded otoscopic findings and treatment.
Otoscopy or microscopy plus tympanometry between episodes, to determine whether the ear returns to normal or retains an effusion.
Age appropriate audiometry.
Nasoendoscopy to assess adenoid size and the nasopharynx.
Examine the palate specifically for submucous cleft: bifid uvula, zona pellucida and a notched posterior hard palate.

Investigations for the child with severe or atypical disease

Full blood count with differential.
Serum immunoglobulins G, A and M with immunoglobulin G subclasses.
Specific antibody titres to tetanus, diphtheria and pneumococcal serotypes before and 4 weeks after booster immunisation, to detect specific antibody deficiency.
HIV testing.
Sweat chloride testing and cystic fibrosis genetics where there is chronic respiratory disease or failure to thrive.
Nasal nitric oxide screening and ciliary brush biopsy for primary ciliary dyskinesia.
Middle ear fluid culture at the time of tympanocentesis or tube insertion to guide targeted therapy.

Modifiable risk factor reduction, which is the least expensive intervention and is frequently omitted

Complete elimination of tobacco smoke exposure in the home and car.
Continue breastfeeding for at least 6 months where possible.
Feed upright rather than supine.
Discontinue the pacifier after 6 months.
Reduce day care exposure or change to a smaller setting where feasible.
Treat allergic rhinitis with an intranasal corticosteroid such as mometasone 50 micrograms per nostril once daily in children aged 3 to 11 years, or fluticasone furoate 27.5 micrograms per nostril once daily from 2 years.
Ensure complete pneumococcal conjugate vaccination and annual influenza vaccination. Influenza vaccination reduces episodes during the influenza season.

Management of individual episodes

Treat each episode as acute otitis media with adequate analgesia and, given the recurrent pattern, with high dose co amoxiclav 90 mg/kg per day of the amoxicillin component divided twice daily for 10 days rather than plain amoxicillin, because beta lactamase producing organisms predominate in this group.
Where a ventilation tube is in place, treat otorrhoea topically with ciprofloxacin 0.3 percent with dexamethasone 0.1 percent, 4 drops twice daily for 7 days, and reserve oral antibiotics for systemic illness or failure.

Antibiotic prophylaxis

Largely abandoned as routine practice. The effect is modest, preventing roughly one episode per child per year, and it drives resistance and colonisation with resistant organisms.
Where used in selected cases, such as during a winter season while awaiting surgery: amoxicillin 20 mg/kg orally once daily at night for 3 to 6 months. Review at intervals and stop if episodes continue.

Ventilation tube insertion

The principal surgical intervention.

Indicated for three episodes in 6 months or four in 12 months, particularly where there is an effusion present at the time of assessment, where complications have occurred, or where the child has craniofacial anomalies, immunodeficiency or an only hearing ear.
Reduces the frequency of episodes by approximately one to two per year and, importantly, converts subsequent episodes into painless otorrhoea treatable with topical drops rather than systemic antibiotics.
Short term tubes are appropriate for the first insertion.
Discuss the expected complications: otorrhoea in 10 to 25 percent, tympanosclerosis, blockage and a small risk of persistent perforation.

Adenoidectomy

Considered in children aged 4 years and above, in those requiring a second set of tubes, and in any child with significant nasal obstruction or chronic adenoiditis.
Removes the biofilm reservoir and mechanical obstruction of the tube.
Contraindicated in overt or submucous cleft palate and in velopharyngeal insufficiency.

Additional considerations

Tonsillectomy is not indicated for recurrent acute otitis media alone.
Immunoglobulin replacement is reserved for confirmed antibody deficiency under specialist immunology supervision.
Audiological review is essential, since repeated episodes may leave persistent conductive loss or unmask a sensorineural component.
Warn families of the features of mastoiditis and intracranial complication and provide clear escalation instructions, since the recurrent group has the greatest cumulative exposure to these risks.

Follow up

Review 6 to 8 weeks after tube insertion with otoscopy and audiometry, then 6 monthly until the tubes extrude and stability is confirmed. Most children outgrow the tendency by 6 to 7 years as the Eustachian tube matures and viral exposure declines.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Otomycosis

Fungal infection of the external auditory canal, usually a superficial colonisation of macerated keratin rather than tissue invasion, accounting for roughly 10 percent of all otitis externa and considerably more in humid tropical settings.

Aspergillus species cause 60 to 90 percent of cases, with Aspergillus niger predominant, followed by A. fumigatus and A. flavus.
Candida albicans and C. parapsilosis account for most of the remainder and produce a less visually obvious picture.
Mixed bacterial and fungal growth is common in previously treated canals.

The canal offers warm humid keratin, an ideal substrate. Disease follows loss of the acidic cerumen film and epithelial disruption. Prolonged antibacterial ear drops are the single most important iatrogenic cause, eliminating competing flora and providing a moist vehicle. Corticosteroid containing drops compound this by local immunosuppression.

Predisposing factors

Antibacterial or steroid ear drops used beyond 10 to 14 days.
Humid climate, swimming, occlusive hearing aids and earphones.
Self instrumentation with cotton buds.
Open mastoid cavity, which retains keratin and cannot self clean.
Diabetes mellitus, HIV, chemotherapy, long term corticosteroids.
Tympanic membrane perforation, which allows fungal colonisation of the middle ear mucosa.

Invasive disease is rare and confined to the immunocompromised, where Aspergillus penetrates the canal floor and produces fungal skull base osteomyelitis with a mortality far exceeding that of pseudomonal disease.

Pruritus dominates, typically intense and unrelieved by antibacterial drops.
Aural fullness and blockage from the mycelial and keratin mass.
Pain is mild to moderate. Severe deep pain suggests bacterial superinfection or invasive disease.
Otorrhoea is scant, thick and often described as damp rather than purulent.
Conductive hearing loss of 10 to 25 dB from obstruction.
Tinnitus and, occasionally, a sensation of movement within the canal.

Otoscopic appearances

Aspergillus niger: white cottony mycelial mat studded with black conidiophores, the classic wet blotting paper appearance.
Aspergillus fumigatus: greyish green mat. Aspergillus flavus: yellow green.
Candida: creamy white or greyish curd like material without visible hyphae, often only a soggy desquamating canal with no diagnostic morphology.
Underlying canal skin is erythematous and macerated. After removal of the mat the epithelium is denuded and may bleed.
Myringitis with a granular or thickened drum, and in up to 10 percent a tympanic membrane perforation caused by mycotic thrombosis of tympanic vessels.

Features that change the diagnosis

Severe nocturnal otalgia, granulation at the bony cartilaginous junction, or any cranial nerve deficit in a diabetic or immunocompromised patient indicates invasive fungal otitis externa.
Bleeding, a friable mass or non healing ulceration requires biopsy for carcinoma.

Diagnosis is made by microscopic otoscopy, and confirmation is only needed when the appearance is atypical, disease is refractory, or invasion is suspected.

Microscopy with microsuction identifies the mycelial mat and clears the canal for assessment. This is both diagnostic and therapeutic.
Determine tympanic membrane integrity before prescribing, since this restricts the choice of preparation.
Potassium hydroxide 10 to 20 percent wet mount of debris shows septate hyphae branching at approximately 45 degrees with conidiophores in Aspergillus, or budding yeasts with pseudohyphae in Candida.
Culture on Sabouraud dextrose agar with chloramphenicol at 25 to 30 degrees Celsius, held 1 to 3 weeks. Send a parallel bacterial swab, since dual infection is frequent.
Capillary glucose and HbA1c in all cases, HIV testing where risk factors exist.
Computed tomography and magnetic resonance imaging with deep tissue biopsy when invasion is suspected. Serum galactomannan supports invasive aspergillosis but a normal result does not exclude localised temporal bone disease.

Differential diagnosis

Bacterial otitis externa: pain dominates over itch, diffuse oedema, no visible fungal elements.
Keratosis obturans: dense keratin plug, severe pain, widened bony canal, no hyphae.
Chronic suppurative otitis media with secondary fungal colonisation: mucoid discharge through a perforation; the middle ear is the primary problem.
Contact dermatitis to previously used drops: weeping eczematous change extending onto the concha without visible mycelium.
Squamous cell carcinoma: friable bleeding tissue that regrows after debridement.

Mechanical clearance is the treatment. Antifungal drops applied to an uncleaned canal fail because the mycelial mat is impenetrable.

Essential first steps

Repeated microsuction under the microscope until the canal is completely clear, then again at 7 and 14 days. In heavily loaded canals two or three sessions are needed.
Stop all antibacterial and corticosteroid drops immediately.
Strict water precautions for the full treatment period and 2 weeks beyond.
Remove hearing aids until epithelialisation is complete.

Topical antifungals with an intact tympanic membrane

Clotrimazole 1 percent solution, 2 to 3 drops three times daily for 14 to 21 days, continued at least 7 days beyond visible clearance. First line for Aspergillus and Candida.
Miconazole 2 percent cream applied to the canal on a ribbon gauze wick, changed daily for 5 to 7 days, useful when drops are poorly retained.
Nystatin 100000 units per mL, 3 drops three times daily for 14 days, effective against Candida but not Aspergillus.
Acetic acid 2 percent, 3 drops three times daily, restores canal acidity and is a reasonable low cost adjunct and maintenance agent.
Boric acid 4 percent powder insufflation or boric acid in alcohol is highly effective and cheap but is strictly contraindicated with a perforation and causes considerable stinging on abraded skin.
Tolnaftate 1 percent solution is an alternative where azoles are unavailable.

When the tympanic membrane is perforated

Avoid alcohol based preparations, boric acid and gentian violet.
Rely on repeated microsuction and clotrimazole cream applied to the canal wall rather than instilled solution reaching the middle ear.
Where middle ear fungal disease is established, oral therapy is preferable to instilling potentially cochleotoxic solutions.

Systemic therapy

Reserved for extensive disease, disease involving the middle ear or a mastoid cavity, failure of two adequate topical courses, and immunocompromised patients.
Itraconazole 200 mg orally once daily for 2 to 4 weeks, taken with food and an acidic drink for absorption. Monitor liver function. Avoid in heart failure due to negative inotropy. Numerous CYP3A4 interactions, notably with statins, warfarin, and calcium channel blockers.
Fluconazole 150 to 200 mg orally daily for Candida only.
Invasive fungal otitis externa: voriconazole 6 mg/kg intravenously twice daily for two doses, then 4 mg/kg twice daily, converting to 200 mg orally twice daily, for a minimum of 6 to 12 weeks, with therapeutic drug monitoring, visual disturbance counselling and liver function surveillance. Liposomal amphotericin B 3 to 5 mg/kg daily is the alternative. Surgical debridement and biopsy are required in this setting.

Failure to respond

Re examine rather than repeat the prescription. Look for residual mycelium in the anteroinferior recess, an unrecognised perforation, a mastoid cavity, uncontrolled diabetes, ongoing use of antibacterial drops, or an incorrect diagnosis.

Complications and follow up

Tympanic membrane perforation, which usually heals once the fungus is eradicated but may persist and require myringoplasty.
Granular myringitis and canal stenosis after repeated episodes.
Invasive temporal bone disease in the immunocompromised.
Review at 2 weeks with microscopy. For recurrent disease, maintain acetic acid 2 percent drops twice weekly and after water exposure, and arrange 6 monthly microsuction in hearing aid users and patients with mastoid cavities.

Recurrent Acute Otitis Media

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management