Tympanic Membrane Perforation

A defect in the tympanic membrane, classified by cause, site, size and duration. Each of these determines both the likelihood of spontaneous healing and the risk of long term sequelae.

Anatomy relevant to outcome

The pars tensa has three layers: outer squamous epithelium, middle fibrous lamina propria with radial and circular collagen, and inner mucosa. Healing depends on the fibrous layer and on migration of squamous epithelium across the defect. The pars flaccida lacks an organised fibrous layer and is where retraction and cholesteatoma originate. The blood supply runs along the malleus handle and the annulus, which is why anterior and marginal perforations, remote from this supply, heal less reliably.

Classification

By site: central perforations of the pars tensa leave a rim of drum around the defect and carry a low cholesteatoma risk. Marginal perforations reach the annulus and attic defects involve the pars flaccida; both allow squamous epithelial ingrowth and are associated with cholesteatoma.
By size: expressed as a percentage of the pars tensa. Small perforations under 25 percent produce a loss of 10 to 20 dB, subtotal perforations 30 to 40 dB.
By duration: acute until 3 months, chronic thereafter.

Aetiology

Infective: acute otitis media, chronic suppurative otitis media, necrotising otitis externa, myringitis.
Direct trauma: cotton buds, hairpins, hot slag or welding sparks, foreign bodies.
Barotrauma and blast injury: slap to the ear, explosion, diving, flying with Eustachian dysfunction.
Water: diving, water skiing, forceful irrigation.
Temporal bone fracture, particularly longitudinal fractures.
Iatrogenic: grommet extrusion, aural irrigation, surgical.

Mechanism of hearing loss

Conductive loss arises from reduced effective vibrating area and, when the perforation is large, from loss of the round window baffle so that sound reaches both windows in phase and cancels. Loss beyond 40 to 45 dB implies ossicular discontinuity or fixation rather than perforation alone, since a perforation alone rarely exceeds this.

Sudden sharp pain at the moment of injury, followed by relief, in traumatic perforation.
In perforation complicating acute otitis media, severe pain resolves abruptly as pus escapes.
Conductive hearing loss proportional to size and site, greater with posterior perforations that expose the round window.
Bloodstained discharge in trauma, mucopurulent discharge in infection.
Tinnitus.
Vertigo, which is a significant finding. Transient vertigo may follow the injury, but persistent vertigo indicates perilymphatic fistula, stapes subluxation or labyrinthine injury.
Water intolerance with pain and discharge on swimming or showering.

Signs

The defect on otoscopy, described by site, size, and whether the edges are everted, inverted or rolled.
Blood clot at the margin in fresh trauma.
Ossicular chain visible through large perforations. Inspect the long process of the incus and the stapes.
Tuning forks: Rinne negative in the affected ear and Weber lateralising to the affected side confirm a conductive loss.

Red flags

Sensorineural hearing loss, persistent vertigo, or nystagmus, indicating inner ear injury.
Facial nerve weakness, indicating temporal bone fracture or middle ear injury.
Cerebrospinal fluid otorrhoea.
Marginal or attic defect with keratin or granulation, indicating cholesteatoma.

Microscopy is superior to otoscopy for defining the margins and detecting keratin ingrowth. Do not irrigate the ear to obtain a view.
Pure tone audiometry with masking is mandatory in all traumatic perforations and before any surgery. It documents the conductive gap and, critically, detects sensorineural loss.
Tympanometry shows a flat trace with an abnormally high canal volume, confirming perforation when the drum cannot be seen.
Fistula test in patients with vertigo.
Computed tomography of the temporal bone for suspected temporal bone fracture, ossicular disruption, cholesteatoma, sensorineural loss, vertigo or facial palsy.
Diffusion weighted magnetic resonance imaging with non echoplanar sequences when cholesteatoma behind an intact area or in the attic is suspected.
Culture of discharge when the perforation is infected.

Differential considerations

Retraction pocket or a very atrophic, transparent neomembrane can be mistaken for a perforation. Pneumatic otoscopy and tympanometry distinguish them.
Chronic suppurative otitis media with a central perforation versus attic cholesteatoma with keratin, granulation and foul discharge.

Immediate management of a traumatic perforation

Keep the ear dry. No irrigation, no drops unless there is contamination or infection.
Do not prescribe aminoglycoside containing drops. Use ciprofloxacin 0.3 percent with dexamethasone 0.1 percent, 4 drops twice daily for 7 days, only when there is contaminated water exposure, a foreign body, or established infection.
Analgesia with paracetamol 1 g every 6 hours and ibuprofen 400 mg every 8 hours.
Everted or inrolled edges can be repositioned under the microscope in the first days, which improves healing rates. A paper patch or Steri strip patch may be applied.
Advise against nose blowing, and to sneeze with the mouth open.
Approximately 80 to 90 percent of traumatic perforations heal spontaneously. Small perforations close within 4 to 6 weeks and most of the remainder within 3 months.

Urgent referral within 24 to 48 hours

Persistent vertigo, nystagmus, or sensorineural hearing loss on audiogram, which raise the possibility of perilymphatic fistula or stapes footplate injury and may require exploratory tympanotomy within days.
Facial nerve palsy.
Penetrating injury with suspected ossicular disruption.
Cerebrospinal fluid leak.
Retained hot slag, which burns through the drum and into the middle ear and requires removal under anaesthesia.

Management of infected perforations

Aural toilet by microsuction is the priority.
Topical ciprofloxacin or ofloxacin drops, 4 to 5 drops twice daily for 10 to 14 days, are more effective than oral antibiotics.
Systemic antibiotics only for cellulitis, systemic illness or complications.

Surgical repair

Indications, once the perforation has persisted beyond 3 months and the ear is dry:

Recurrent infection or discharge on water exposure.
Conductive hearing loss impairing function, usually an air bone gap of 20 dB or more.
Water intolerance affecting occupation or recreation, including swimmers, divers and military personnel.
Requirement for a hearing aid mould in a discharging ear.
Marginal perforation with squamous ingrowth or a developing retraction pocket.
Prior to certain occupations and before cochlear implantation.

Techniques

Fat plug myringoplasty for small central perforations under 25 percent, with closure rates around 80 to 90 percent.
Temporalis fascia graft by underlay technique, the standard for moderate perforations, with closure of 85 to 95 percent.
Cartilage with perichondrium, preferably tragal or conchal, for large and subtotal perforations, anterior perforations, revision surgery, atelectatic ears and poor Eustachian tube function. It resists retraction and yields higher closure rates, with hearing outcomes comparable to fascia when the cartilage is thinned to 0.5 mm.
Approach may be transcanal, endaural or postauricular depending on the anterior canal wall overhang and perforation position.
Endoscopic transcanal repair avoids a postauricular incision and gives better visualisation of the anterior annulus.
Ossiculoplasty is performed at the same sitting when the chain is eroded, using incus interposition or a partial or total ossicular replacement prosthesis with a cartilage interface to prevent extrusion.

Timing in children

Defer repair until around 8 to 10 years where possible, since Eustachian tube function matures and upper respiratory infections become less frequent, improving success rates.
Requirements before surgery: a dry ear for at least 3 months, an assessment of the contralateral ear, and documented audiometry.
Earlier repair is justified for recurrent infection, an only hearing ear, or marginal perforation with cholesteatoma risk.

Postoperative care

Keep the ear dry for 6 weeks. Avoid nose blowing, straining, heavy lifting and air travel for 4 to 6 weeks.
Packing is removed at 2 to 3 weeks under the microscope.
Antibiotic drops for 7 to 10 days after pack removal.
Audiometry at 3 months.
Graft failure occurs in roughly 5 to 15 percent, usually from infection, Eustachian tube dysfunction, an unrecognised anterior residual perforation, or early water exposure.

Complications of the untreated perforation

Recurrent chronic suppurative otitis media.
Secondary acquired cholesteatoma from squamous migration into the middle ear, particularly with marginal defects and traumatic perforations where epithelium is implanted at the moment of injury. This is the reason all traumatic perforations that fail to heal require review rather than discharge.
Progressive conductive loss from ossicular erosion.
Tympanosclerosis and myringosclerosis.

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

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.

Tympanic Membrane Perforation

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management