Barotrauma of the Ear

Tissue injury caused by failure to equalise pressure between a gas containing space and the ambient environment. Boyle law governs the process: gas volume varies inversely with pressure, and the greatest relative volume change occurs near the surface, which is why most diving injuries happen in the first 10 metres.

Three anatomical sites

External ear barotrauma, or barotitis externa, occurring when a tight hood, earplug or wax plug traps gas in the canal, producing a relative vacuum with canal wall haemorrhage and blistering.
Middle ear barotrauma, which is by far the commonest, occurring when the Eustachian tube fails to admit air during descent. The tube functions as a passive one way valve that vents easily on ascent but requires active opening on descent, which is why descent is the dangerous phase. At a differential of around 90 mmHg the tube locks shut and no amount of Valsalva will open it. Beyond 100 to 500 mmHg the drum ruptures.
Inner ear barotrauma, caused by forceful Valsalva against a blocked tube generating a sudden cerebrospinal fluid pressure wave transmitted through the cochlear aqueduct, or by implosive pressure transmitted through the round window, causing round or oval window membrane rupture, perilymph fistula or intralabyrinthine haemorrhage.

Teed classification of middle ear barotrauma

Grade 0: symptoms without otoscopic signs.
Grade 1: erythema and retraction of the drum.
Grade 2: erythema with mild haemorrhage within the drum.
Grade 3: gross haemorrhage throughout the drum.
Grade 4: dark blue haemotympanum with a middle ear effusion.
Grade 5: perforation with free blood in the canal.

Risk factors: upper respiratory infection, allergic rhinitis, sinusitis, nasal polyps, deviated septum, adenoid hypertrophy, smoking, rapid descent, inability to perform equalisation manoeuvres, and prior middle ear surgery.

Middle ear barotrauma

Pain and pressure during descent, initially relieved by successful equalisation and becoming severe when equalisation fails.
Conductive hearing loss and fullness.
Abrupt relief of pain with the onset of bleeding indicates perforation.
Bloodstained discharge.
Mild transient vertigo from asymmetric middle ear pressure or from cold water entering through a fresh perforation, producing a caloric response.

Inner ear barotrauma, which must be distinguished from middle ear injury

Sudden severe sensorineural hearing loss.
Loud tinnitus.
Severe persistent rotational vertigo with nausea and vomiting, lasting hours to days rather than seconds.
Symptoms often begin during a forceful Valsalva at depth rather than on descent alone.
This is an emergency requiring immediate specialist assessment.

Alternobaric vertigo

Transient vertigo during ascent caused by asymmetric middle ear pressure release between the two ears. It lasts seconds to minutes, resolves spontaneously, and is dangerous chiefly because of disorientation underwater.

Distinguishing inner ear barotrauma from inner ear decompression sickness, which is the critical decision in a diver:

Inner ear barotrauma typically occurs during descent, with difficulty equalising, often with signs of middle ear barotrauma on otoscopy, and after any dive profile including shallow dives.
Inner ear decompression sickness typically occurs during or shortly after ascent, after a deep or long dive, particularly with helium mixtures, without equalisation difficulty, and often with other decompression symptoms.
Recompression is the treatment for decompression sickness and is potentially harmful in barotrauma with a fistula. Where the distinction cannot be made, discuss urgently with a diving medicine specialist.

Otoscopy with Teed grading, documenting drum appearance, haemotympanum and perforation.
Pure tone audiometry with masked bone conduction, urgently, in every case with hearing loss. This is what separates a conductive middle ear injury from an inner ear injury.
Tympanometry once a perforation is excluded.
Fistula test where vertigo is present.
Full neurological and vestibular assessment with head impulse testing, nystagmus assessment and test of skew.
High resolution computed tomography of the temporal bone where inner ear injury, pneumolabyrinth or ossicular disruption is suspected. Air within the labyrinth is diagnostic of a fistula.
Magnetic resonance imaging where labyrinthine haemorrhage is suspected, showing high T1 signal within the labyrinth, or to exclude other causes.
A complete dive profile history including depth, duration, gas mixture, ascent rate and the timing of symptoms relative to descent and ascent.
Nasoendoscopy to identify the nasal or nasopharyngeal cause of the equalisation failure, once acute symptoms settle.

Middle ear barotrauma without perforation

Analgesia: paracetamol 1 g every 6 hours and ibuprofen 400 mg every 8 hours.
Topical decongestant: xylometazoline 0.1 percent, one to two sprays per nostril twice daily for a maximum of 5 days.
Oral decongestant: pseudoephedrine 60 mg three times daily for up to 5 days, avoided in hypertension, ischaemic heart disease, arrhythmia, hyperthyroidism, prostatic obstruction and narrow angle glaucoma.
Intranasal corticosteroid for 2 to 4 weeks where mucosal inflammation is the underlying problem.
Autoinflation with gentle Valsalva several times daily once the acute pain settles, not while the drum is acutely inflamed.
No flying or diving until the drum is normal and hearing has returned to baseline.
Most cases resolve within 1 to 2 weeks. Persistent effusion beyond 4 to 6 weeks may require myringotomy with a ventilation tube.

Perforation from barotrauma

Keep the ear dry, no drops unless contaminated.
Where water exposure occurred, particularly in fresh or contaminated water, use ciprofloxacin 0.3 percent with dexamethasone 0.1 percent drops, 4 drops twice daily for 7 days. Never aminoglycoside drops.
Around 80 to 90 percent heal spontaneously within 3 months.
Myringoplasty for persistent perforation, which is essential before returning to diving.

Inner ear barotrauma

Strict bed rest with the head elevated 30 to 45 degrees.
Avoid all straining: stool softeners, avoidance of nose blowing, no lifting, no Valsalva.
Corticosteroids as for sudden sensorineural hearing loss: prednisolone 1 mg/kg orally daily, maximum 60 to 80 mg, for 7 to 14 days with a taper, started as early as possible.
Intratympanic dexamethasone 24 mg/mL as adjunct or salvage.
Avoid recompression unless decompression sickness is the working diagnosis, since recompression with an unsealed fistula risks further injury. When both are possible and the presentation is ambiguous, treat as decompression sickness with hyperbaric therapy after specialist discussion, since untreated decompression sickness causes permanent neurological injury.
Exploratory tympanotomy with sealing of the round and oval windows using fat, fascia or perichondrium is indicated for progressive or non improving sensorineural hearing loss, persistent disabling vertigo, or radiological pneumolabyrinth. Timing is generally within days rather than weeks where hearing is deteriorating.
Vestibular sedatives for no more than 48 to 72 hours, then vestibular rehabilitation.
Permanent cessation of diving is generally advised after inner ear barotrauma with a confirmed fistula.

Prevention and fitness to dive or fly

Do not dive or fly with an upper respiratory infection, allergic exacerbation or sinusitis.
Descend slowly and equalise early and often, before pain develops, using gentle Valsalva, Toynbee, Frenzel or the Edmonds technique rather than a forceful late Valsalva.
Treat allergic rhinitis and chronic rhinosinusitis definitively.
Address anatomical nasal obstruction with septoplasty and turbinate reduction where recurrent barotrauma occurs.
Balloon Eustachian tuboplasty in professional divers and aircrew with recurrent baro challenge dysfunction.
Ventilation tubes are an absolute contraindication to diving, since water enters the middle ear directly. They are acceptable for flying.
Pressure equalising earplugs and prophylactic decongestants for air travel in susceptible passengers.
Advise against sleeping through descent, which is a common cause of aviation barotrauma.

Fitness to return

Return to diving requires a normal drum, normal hearing at baseline, demonstrable ability to equalise, and resolution of any inner ear symptoms. After inner ear barotrauma with fistula repair, return is generally not recommended. Formal diving medicine assessment should make this decision.

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

Chronic Otitis Externa

Persistent or relapsing inflammation of the external auditory canal skin lasting beyond three months, or four or more discrete episodes in a year. The dominant process is a dermatitis with epithelial dysfunction rather than the acute bacterial invasion seen in acute otitis externa, so pruritus replaces pain as the leading symptom and the therapeutic emphasis shifts from antibiotics to skin care and removal of the perpetuating cause.

Pathophysiology

Chronic inflammation destroys the pilosebaceous and ceruminous apparatus of the cartilaginous canal. Cerumen production falls, the canal loses its acidic hydrophobic film, and lateral epithelial migration fails. Keratin then accumulates medially instead of being cleared. Repeated inflammation drives fibroblast proliferation in the subepithelial layer, producing progressive soft tissue thickening and eventually cicatricial stenosis with a fibrous plug or a blind ending canal.

The perpetuating cycle is itch, scratch, epithelial breach, secondary bacterial or fungal colonisation, treatment with sensitising topical agents, contact dermatitis, and further itch. Breaking this cycle rather than sterilising the canal is the therapeutic objective.

Aetiological categories that determine treatment

Chronic eczematous otitis externa: atopic dermatitis, seborrhoeic dermatitis, psoriasis, and irritant dermatitis. The canal is one site of a generalised skin disease and responds to dermatological rather than antimicrobial treatment.
Allergic contact dermatitis: neomycin is the commonest sensitiser, followed by framycetin, gentamicin, benzalkonium chloride, propylene glycol, parabens, quinolone vehicle components, hearing aid acrylates, nickel and rubber. Sensitisation rates to neomycin approach 15 percent among treated otological patients and rise with cumulative exposure.
Chronic bacterial infection: Pseudomonas aeruginosa, Staphylococcus aureus including methicillin resistant strains, and Proteus species, usually superimposed on abnormal skin.
Chronic fungal infection: Aspergillus niger, Aspergillus fumigatus and Candida albicans, commonly iatrogenic after prolonged antibacterial drops.
Secondary to chronic middle ear disease: recurrent mucopurulent discharge through a perforation or a mastoid cavity macerates canal skin and perpetuates inflammation. The canal will not settle until the middle ear is controlled.
Systemic and host factors: diabetes mellitus, HIV, chemotherapy, long term corticosteroids, chronic kidney disease with uraemic pruritus, iron deficiency, hypothyroidism, and previous temporal bone radiotherapy.
Granulomatous and neoplastic mimics: granulomatosis with polyangiitis, sarcoidosis, tuberculosis, Langerhans cell histiocytosis and squamous cell carcinoma present as chronic non resolving canal disease.

Natural history and clinically important sequelae

Untreated disease progresses through canal skin thickening to fibrous stenosis. Two end points matter clinically. The first is postinflammatory medial canal fibrosis, in which a fibrous plug forms against the tympanic membrane creating a false fundus, with conductive loss typically in the 30 to 50 dB range and trapped keratin behind it. The second is progressive lateral canal narrowing that traps debris and produces recurrent infection. Both require surgery once established, since fibrosis does not reverse with topical therapy.

Symptoms

Pruritus is the dominant and often the only symptom, characteristically worse at night and temporarily relieved by scratching or instrumentation, which perpetuates the disease.
Dryness and a sensation of blockage rather than severe pain. Significant otalgia in a chronically inflamed canal indicates an acute bacterial exacerbation, perichondritis, necrotising disease or malignancy.
Scant, thick, often malodorous discharge, sometimes only crusting on the pinna.
Progressive conductive hearing loss when stenosis or keratin retention develops.
Recurrent episodes with brief responses to successive courses of drops, then relapse within days of stopping.

Signs on otoscopy and microscopy

Dry, thickened, scaly or lichenified canal skin with absent cerumen and loss of canal hair.
Fissuring at the meatus and extension of eczematous change onto the concha, tragus and lobule when a dermatosis or contact allergy is responsible.
Narrowed canal with a fixed rather than oedematous appearance. Fibrotic narrowing does not indent under suction, unlike acute oedema.
Keratin plugs and desquamated debris medially, sometimes concealing the drum entirely.
Tympanic membrane thickening, myringitis, or a perforation revealing the middle ear as the driver.
Granulation tissue, polypoid change or a friable mass, none of which are features of simple chronic otitis externa.

Red flags

New or escalating deep pain, particularly nocturnal, in a diabetic or immunocompromised patient.
Bleeding on toilet, ulceration, a canal mass, or tissue that regrows after removal.
Facial nerve weakness or any other cranial neuropathy.
Unilateral disease with cervical lymphadenopathy, weight loss or a long smoking history.
Failure of a correctly delivered six week course of appropriate treatment.

Group specific patterns

Hearing aid users: recurrent maceration and contact dermatitis to mould acrylate, with disease confined to the mould contact area.
Atopic patients: bilateral disease with flexural eczema elsewhere and marked xerosis.
HIV positive patients: severe seborrhoeic pattern, extensive fungal disease, and higher risk of progression to necrotising otitis externa.
Elderly diabetics: attribute nothing to chronic otitis externa alone until skull base osteomyelitis has been excluded.
Patients with mastoid cavities: chronic canal and cavity dermatitis with keratin retention, requiring cavity toilet rather than escalating drops.

The diagnosis is clinical. Investigation is directed at identifying which of the aetiological categories applies, since the treatment differs completely between contact dermatitis, fungal disease, middle ear disease and neoplasm.

Bedside assessment

Microscopic examination with microsuction is essential and doubles as treatment. Debris must be removed before the canal can be assessed.
Determine tympanic membrane integrity and look specifically for an attic or marginal perforation, granulation and cholesteatoma.
Examine the pinna, concha, scalp, face, elbows, knees and nails for psoriasis, seborrhoeic dermatitis or atopic eczema. Nail pitting and scalp scaling redirect management entirely.
Ask precisely which topical preparations have been used, for how long, and whether symptoms worsened during use. Deterioration on drops is the signature of contact allergy.

Investigations

Bacterial and fungal swab from the medial canal under direct vision after debris removal, particularly before committing to prolonged therapy.
Patch testing when contact allergy is suspected, testing neomycin, framycetin, gentamicin, benzalkonium chloride, propylene glycol, fragrance mix, colophony and acrylates. This is the only reliable way to identify the culprit and to guide safe lifelong prescribing.
Pure tone audiometry with masking in any patient with hearing loss or canal narrowing, to quantify the conductive component and detect a coexisting sensorineural loss before any surgery is contemplated.
Capillary glucose and HbA1c, HIV testing where risk exists, and full blood count. Consider ferritin and thyroid function when generalised pruritus is present.
High resolution computed tomography of the temporal bone when stenosis is established and surgery is contemplated, when bone erosion or sequestration is suspected, or when there is any concern about neoplasm or osteomyelitis. It defines the length and calibre of the stenotic segment, the state of the middle ear and mastoid, the position of the facial nerve and the presence of retained keratin medial to the obstruction.
Magnetic resonance imaging with diffusion weighted sequences when soft tissue behind a stenosis needs characterisation or when skull base involvement is suspected.
Biopsy is mandatory for granulation tissue, any mass, ulceration that fails to heal, and disease unresponsive to six weeks of correct therapy. Send tissue for histology, mycobacterial culture and fungal culture. Add antineutrophil cytoplasmic antibody testing when granulomatosis with polyangiitis is considered.

Differential diagnosis and the discriminating feature

Keratosis obturans: bilateral, younger patients, associated with bronchiectasis and chronic rhinosinusitis, severe pain and conductive loss, a dense keratin plug that widens the bony canal circumferentially without focal bone erosion, and an intact underlying epithelium.
External auditory canal cholesteatoma: usually unilateral, older patients, dull or absent pain, focal erosion of the inferior or posterior canal wall with bone sequestration and localised keratin invasion.
Otomycosis: visible hyphae or conidiophores, intense itch, recent antibacterial drop use.
Allergic contact dermatitis: weeping erythema extending onto the concha and postauricular skin, worsening with each course of drops.
Psoriasis and seborrhoeic dermatitis: silvery scale or greasy yellow scale with disease at other typical sites.
Chronic suppurative otitis media: mucoid discharge and a tympanic defect. Canal changes are secondary.
Squamous cell carcinoma of the canal: bleeding, friable tissue, deep pain, facial weakness, and disease that recurs immediately after removal. Any of these mandate biopsy.
Necrotising otitis externa: granulation at the bony cartilaginous junction, disproportionate pain, raised erythrocyte sedimentation rate, diabetic or immunocompromised host.

Treatment succeeds when the perpetuating cause is removed and the canal skin is restored. It fails when successive courses of antibiotic drops are prescribed for what is fundamentally a dermatological or mechanical problem.

Core measures for every patient

Absolute prohibition of cotton buds, hairpins, keys and any self instrumentation. Explain that scratching is the engine of the disease.
Water precautions: a petroleum jelly coated cotton ball or a fitted swim plug for showering, no swimming during active treatment, and thorough drying of the meatus by tilting the head rather than by inserting anything.
Scheduled microsuction. In canals that retain keratin, three to six monthly toilet under the microscope prevents relapse more reliably than any drop.
Withdrawal of all aminoglycoside containing preparations if there has been repeated exposure, pending patch testing.
Emollient care of the pinna and concha, and treatment of the underlying dermatosis at other body sites.

Topical corticosteroids

The mainstay in eczematous, psoriatic and contact dermatitis related disease.

Betamethasone valerate 0.1 percent drops, 2 to 3 drops twice daily for 7 to 14 days, then tapered to alternate days and then twice weekly for maintenance.
Clobetasol propionate 0.05 percent ointment applied on a ribbon gauze wick for hypertrophic or lichenified canal skin, changed daily for 5 to 7 days, then substituted with a less potent preparation.
Hydrocortisone 1 percent cream for the concha, meatus and lobule, twice daily for up to 2 weeks.
Prednisolone or dexamethasone containing drops without an antibiotic component are preferable when previous sensitisation is suspected.
Continuous potent corticosteroid beyond two weeks causes canal skin atrophy, telangiectasia and fungal overgrowth. Move to intermittent weekend dosing for maintenance rather than daily use.

Steroid sparing options

Tacrolimus 0.1 percent ointment applied thinly twice daily for 2 to 4 weeks, then twice weekly, is effective in chronic eczematous otitis externa where corticosteroid dependence or atrophy has developed. Warn about a burning sensation during the first few applications and avoid it on frankly infected skin.
Aluminium acetate 8 to 13 percent solution on a ribbon gauze wick, changed daily for 3 to 5 days, is highly effective in weeping, macerated and oedematous canals. It is astringent, antibacterial and free of sensitising antibiotic.
Acetic acid 2 percent drops, 3 drops two or three times daily, restore canal acidity and are suitable for long term intermittent maintenance in patients with intact drums.

Antimicrobials, used narrowly

Antibiotic drops are reserved for a documented acute bacterial exacerbation, not for chronic maintenance. Ciprofloxacin 0.3 percent with dexamethasone 0.1 percent, 4 drops twice daily for 7 days, is the preferred choice because it is safe with a perforation and carries lower sensitisation risk than aminoglycosides.
Confirmed fungal disease: repeated microsuction plus clotrimazole 1 percent solution, 2 to 3 drops three times daily for 14 days, continued for at least a week after visible clearance. Refractory or extensive disease in an immunocompromised patient may require oral itraconazole 200 mg daily for 2 to 4 weeks with liver function monitoring and review of CYP3A4 interactions.
Systemic antibiotics have no role in chronic otitis externa in the absence of cellulitis, perichondritis or suspected skull base osteomyelitis. When those are present, treat as for the corresponding condition with antipseudomonal cover such as ciprofloxacin 500 to 750 mg orally twice daily.

Controlling the itch scratch cycle

A sedating antihistamine at night breaks nocturnal excoriation. Hydroxyzine 25 mg orally at night, or chlorphenamine 4 mg orally at night, for a limited period. Avoid in the elderly where falls, confusion, urinary retention and narrow angle glaucoma are concerns, and warn about next day sedation and driving.
Treat scalp seborrhoeic dermatitis with ketoconazole 2 percent shampoo twice weekly, since untreated scalp disease reseeds the canal.
Nail care and short nails reduce the trauma of scratching.

Correcting the driver

Optimise glycaemic control in diabetes, since persistent hyperglycaemia both perpetuates the dermatitis and raises the risk of necrotising disease.
Start or optimise antiretroviral therapy in HIV infected patients with recurrent severe canal disease.
Address chronic suppurative otitis media definitively with tympanoplasty, mastoid surgery or cavity revision. Canal disease driven by discharge will not resolve while discharge continues.
Review hearing aid moulds. Switch to a vented, silicone or hypoallergenic mould, reduce daily wearing hours during flares, and clean the mould daily with alcohol free cleaner.

Surgical management

Surgery treats the mechanical consequences of chronic inflammation, not the inflammation itself. Operating on an actively infected canal produces graft failure and restenosis, so the canal must be quiescent first.

Indications

Cicatricial canal stenosis or medial canal fibrosis producing a conductive hearing loss, typically 25 to 30 dB or greater, or preventing adequate examination and toilet.
Recurrent infection due to retained debris behind a stenotic segment.
External auditory canal cholesteatoma with bone erosion or sequestration.
Keratosis obturans with recurrent impaction despite regular microsuction.
Diagnostic uncertainty requiring wide biopsy, or confirmed neoplasm.
Failure of at least six months of properly delivered medical therapy in the presence of fixed anatomical narrowing.

Canalplasty and meatoplasty

Postauricular approach with elevation of canal skin, complete excision of the fibrous plug and thickened subcutaneous tissue, and drilling of the bony canal to a uniformly wide calibre with removal of the anterior bulge and any exostoses.
Resurfacing with a split thickness skin graft of approximately 0.2 to 0.3 mm harvested from the upper arm or thigh, or with local canal skin flaps where sufficient healthy skin remains.
A generous conchal meatoplasty with excision of conchal cartilage is essential. Restenosis at the meatus is the commonest reason for failure.
Packing with antibiotic impregnated ribbon gauze or a silastic sheet for 2 to 3 weeks to hold the graft and prevent contraction.

Postoperative care

Remove packing at 2 to 3 weeks under the microscope, then commence ciprofloxacin with dexamethasone drops for 7 days.
Microsuction at 4 weeks, 3 months and 6 months. Early granulation is treated with silver nitrate cautery and topical corticosteroid.
Strict water precautions until the graft is fully epithelialised, usually 6 to 8 weeks.
Audiometry at 3 months to document the conductive gain.
Restenosis occurs in roughly 10 to 20 percent and usually reflects inadequate meatoplasty, incomplete removal of fibrous tissue or persistent underlying dermatitis.

Operative complications to anticipate

Restenosis and graft failure.
Tympanic membrane lateralisation and anterior blunting with a residual conductive gap.
Sensorineural hearing loss from drill energy transmitted through the ossicular chain. Avoid contact between the burr and the ossicles and interrupt the chain conceptually by working away from the malleus handle.
Facial nerve injury during inferior and posterior drilling, and dehiscence of the temporomandibular joint capsule anteriorly.
Chondritis of the pinna after meatoplasty.

Canal cholesteatoma and keratosis obturans

Limited canal cholesteatoma is managed by microsuction of keratin and local debridement, with canalplasty and grafting when bone erosion is present.
Extensive erosion into the mastoid or towards the facial nerve requires mastoidectomy with obliteration or exteriorisation.
Keratosis obturans is treated by regular microsuction, softening with olive oil or hydrogen peroxide before removal, treatment of coexisting sinonasal or pulmonary suppuration, and canalplasty only when impaction recurs despite this.

Follow up and long term control

Review at 4 to 6 weeks after initiating treatment to confirm response and reconsider the diagnosis if the canal has not improved.
Establish an individualised maintenance regimen, usually intermittent topical corticosteroid twice weekly plus acidifying drops after water exposure, plus scheduled microsuction.
Biopsy without delay any tissue that persists, bleeds or recurs.
Refer to dermatology for patch testing and for management of extensive psoriasis or atopic disease, and to otolaryngology for stenosis, suspected canal cholesteatoma, or any diagnostic doubt.

Barotrauma of the Ear

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management