Anomalies of the development of the outer ear. Trauma to the Auricle, causes, classification, first aid. Traumatic rupture of tympanic membrane (causes and treatment). Foreign bodies of the external auditory canal, tactics of treatment. Haematoma of the auricle, diagnosis and treatment methods. External otitis media, etiology, pathogenesis, classification and treatment. Eczematous otitis externa (clinic, diagnosis and treatment) Furuncle of the external auditory canal, diagnosis and treatment methods. Otomycosis, diagnosis and treatment methods. Perichondritis of the auricle, diagnosis and treatment. Disorders of eustachian tube (tubal blockage) Acute suppurative otitis media (etiology, diagnosis and treatment) Otitis media with effusion (Glue Ear), diagnosis and treatment tactics. Cholesteatoma (classification) Paracentesis- Myringotomy (technique, indication). Complications of acute otitis media Mastoiditis, etiology, pathogenesis, classification. Classification of chronic otitis media. Chronic purulent otitis media, diagnosis and treatment methods.

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Comprehensive ENT Review: Ear Pathology

Sources: K.J. Lee's Essential Otolaryngology; Cummings Otolaryngology Head and Neck Surgery

1. Anomalies of Development of the Outer Ear

Embryology

The auricle develops from six Hillocks of His (mesenchyme of 1st mandibular and 2nd hyoid branchial arches) beginning at 5 weeks' gestation:
  • Hillock 1 → tragus; Hillock 2 → helical crus; Hillock 3 → remainder of helix; Hillock 4 → antihelix; Hillock 5 → antitragus; Hillock 6 → lobule
  • The EAC outer cartilaginous third forms from the first branchial groove at 8 weeks; the bony inner two-thirds from the meatal plug
  • Incomplete resorption of the meatal plug at 21 weeks produces atresia or stenosis
  • Pinna reaches 80% adult size by age 5, full adult size by age 9

Common Congenital Anomalies

Preauricular tag
  • Most common ear anomaly; due to supernumerary hillock formation
  • May be associated with branchio-oto-renal (BOR) syndrome (hearing loss, branchial cleft cyst, renal anomalies)
  • Treatment: elective surgical removal
Preauricular pit
  • Due to failure of hillock fusion; most common at the helical root
  • A pit below the tragus suggests a first branchial cleft anomaly
  • Associated with BOR syndrome
  • Acutely infected pits: antibiotics ± I&D; recurrent: complete surgical excision
Microtia / Anotia
  • Weerda Classification:
    • Grade I: All components present, length >2 SD below normal; minor reconstruction
    • Grade II: Some components present (e.g., rudimentary helix); partial reconstruction needed
    • Grade III: Structures not recognizable ("peanut ear") or anotia; total reconstruction required
  • 60% are syndromic (e.g., Goldenhar/OAVS, Treacher Collins, BOR)
  • Associated with aural atresia in 90% and hearing loss
  • Management:
    • Non-surgical: hair masking, adhesive prosthesis
    • Surgical options:
      • Bone-anchored auricular prosthesis (BAAP) — good for burns/avulsion/failed repair; requires daily maintenance
      • Autogenous rib cartilage graft (Brent 3-stage or Nagata 2-stage method) — maintenance-free but risks pneumothorax, infection, poor cosmesis; performed ≥5–6 years of age
      • Synthetic implant (Medpore) — can be done as early as age 3

2. Trauma to the Auricle

Causes

Blunt trauma (assault, sports), penetrating trauma (bites, knives, firearms), ear piercing (especially transcartilaginous), burns, frostbite, and iatrogenic injury.

Classification

  1. Contusion / Haematoma — blunt injury with subperichondrial blood collection
  2. Laceration — partial-thickness or full-thickness skin/cartilage tear
  3. Avulsion — partial or complete loss of auricular tissue
  4. Thermal injury — burns or frostbite
  5. Bite wounds — risk of polymicrobial infection

First Aid

  • Contusions: protect from further injury; drain haematoma if present
  • Lacerations: copious irrigation with saline, debridement of devitalised tissue, primary closure in layers; bolster suture if perichondrium is elevated; antibiotics; tetanus and rabies prophylaxis if indicated
  • Avulsion:
    • <1.5 cm: reattachment of segment or primary closure
    • 1.5 cm: composite graft from contralateral ear or local flap
    • Complete avulsion: microvascular reimplantation preferred; alternatives include banking deepithelialized cartilage under temporalis fascia for later reconstruction

3. Auricular Haematoma

Pathophysiology

Blunt trauma shears the perichondrium from the underlying cartilage. Blood accumulates in this subperichondrial space, cutting off the nutritional supply to cartilage (which is avascular). If untreated, organisation of clot and fibrocartilage formation produces the characteristic "cauliflower ear" deformity.

Diagnosis

Clinical: fluctuant, tender swelling of the auricle, most often involving the antihelix and concha, usually after trauma. The lobule is typically spared (it contains no cartilage).

Treatment

  1. Aspiration or incision and drainage — drain the haematoma completely
  2. Bolster / compression dressing — sandwich the pinna between two dental rolls (tie-over bolster) sewn through the ear for 7–14 days to obliterate the dead space and prevent reaccumulation
  3. Antibiotic prophylaxis to prevent secondary infection/chondritis (anti-staphylococcal coverage)
  4. Suspect non-accidental injury if identified in a non-ambulatory infant

4. Traumatic Rupture of the Tympanic Membrane

Causes

  • Direct trauma: cotton buds, foreign bodies, slap to the ear, welding sparks
  • Barotrauma: diving, aircraft descent, blast injury, forceful nose-blowing
  • Indirect: temporal bone fracture
  • Iatrogenic: instrumentation

Treatment

  • Most perforations heal spontaneously (~90%) within weeks with conservative management
  • Keep ear dry; avoid swimming; no cotton wool plugging
  • Topical antibiotics if signs of secondary infection
  • Vertigo or SNHL following perforation warrants audiological assessment and consideration of middle ear exploration (possible perilymph fistula / ossicular disruption)
  • Perforations failing to heal at 3 months → myringoplasty / tympanoplasty
  • If pressure differential exceeds 100 mmHg, TM may rupture; a differential of 90 mmHg can "lock" the Eustachian tube (critical pressure difference)

5. Foreign Bodies of the External Auditory Canal

Types

  • Inanimate: beads, foam, paper, insects, cotton wool, hearing aid components
  • Live insects

Tactics

  • Do not attempt blind removal with forceps if the object is deep or if patient is uncooperative — risk of TM perforation
  • Insects: instill mineral oil or lidocaine first to immobilise the insect before removal
  • Smooth round objects (beads): use a right-angle hook or suction; avoid crocodile forceps (risk of pushing deeper)
  • Soft/vegetable matter: avoid irrigation (swells); use instrumentation
  • Syringing/irrigation is appropriate for cerumen impaction and non-organic objects not near the TM, with an intact TM
  • Uncooperative children or deeply lodged objects: general anaesthesia required
  • After removal: inspect TM for trauma; treat secondary otitis externa if present
  • Post-removal: topical antibiotic-steroid drops if canal is traumatised or infected

6. External Otitis Media (Otitis Externa)

Classification

  1. Acute Otitis Externa (AOE) — onset <48 hours; most common
  2. Chronic Otitis Externa (COE) — prolonged inflammation >3 months
  3. Malignant (Necrotising) Otitis Externa (MOE) — skull base osteomyelitis

Etiology

  • AOE: Most commonly Pseudomonas aeruginosa and Staphylococcus aureus; mixed flora
  • COE: Allergic/contact dermatitis (most commonly to neomycin), systemic dermatoses (psoriasis, seborrhoea, lichen planus), chronic infection
  • MOE: P. aeruginosa >90%; also S. aureus, fungi (Aspergillus in HIV)

Pathogenesis

Disruption of the natural protective mechanisms of the EAC:
  • Cerumen maintains an acidic pH (~6.1) that inhibits bacterial/fungal growth
  • Water exposure raises pH and leads to maceration of the epithelium
  • Local trauma (cotton buds, ear plugs) disrupts the skin barrier
  • Absence of cerumen (overwashing) removes the protective layer
  • Change from acidic to alkaline environment predisposes to infection
  • Narrow canals, exostoses, eczema, psoriasis, and immunosuppression are predisposing factors

Clinical Features (AOE)

  • Otalgia (moderate to severe), worse with manipulation of the pinna/tragus — key distinguishing feature from otitis media
  • Itching, aural fullness, hearing loss (conductive from canal oedema/debris), otorrhoea
  • Erythema and circumferential oedema of the EAC, otorrhoea, preauricular lymphadenopathy

Treatment

  • Aural toilet / debridement (essential first step — removes biofilm and organic debris)
  • Analgesia
  • Acidifying agents: acetic acid 2% drops (restores acid pH)
  • Topical antibiotic-steroid drops (e.g., ciprofloxacin + dexamethasone, or neomycin + polymyxin + hydrocortisone)
  • Pope wick (otowick): if significant canal oedema prevents drops from reaching the medial canal — expands to fill the canal and delivers medication
  • Dry ear precautions: no swimming; use petroleum jelly-coated cotton wool when showering
  • Systemic antibiotics only if periauricular spread, fever, or immunocompromised state
  • MOE: hospitalisation, IV ciprofloxacin (or other antipseudomonal antibiotic), prolonged course (6–8 weeks); nuclear medicine scan (Technetium-99m then Gallium-67) to assess extent and treatment response

7. Eczematous (Allergic/Contact) Otitis Externa

Clinic

A form of chronic otitis externa characterised by:
  • Intense pruritus (predominant symptom, more prominent than pain)
  • Erythema, weeping, scaling, and crusting of the EAC and auricular skin
  • Thickening and lichenification in chronic disease
  • Bilateral in >50%
  • Most common allergen: neomycin (in topical ear preparations), also hair sprays, shampoos, hearing aid moulds, rubber

Diagnosis

  • Clinical (history + examination)
  • Patch testing to identify the offending allergen
  • Differentiate from fungal OE (look for hyphae), psoriasis, seborrhoea

Treatment

  1. Identify and eliminate the offending agent (e.g., stop neomycin-containing drops)
  2. Debridement of the canal
  3. Topical corticosteroid solution (e.g., betamethasone) — reduces inflammation
  4. In chronic granular OE: repeated debridement ± cauterisation of granulations; topical antibiotic-antifungal-steroid combination (e.g., bacitracin/polymyxin + clotrimazole 1% + betamethasone 0.05%)
  5. Topical gentian violet — effective drying and antimicrobial agent

8. Furuncle of the External Auditory Canal

A furuncle is a localised staphylococcal abscess of a hair follicle, occurring only in the outer cartilaginous third of the EAC (the bony canal lacks hair follicles).

Diagnosis

  • Severe, well-localised otalgia, often throbbing; exacerbated by jaw movement and manipulation of the tragus
  • Tenderness of the tragus on palpation
  • Otoscopy: a localised red, swollen papule or pustule (usually on the anterior or posterior canal wall); may contain a visible hair follicle; surrounding tissue oedematous
  • Regional lymphadenopathy (preauricular or cervical)
  • Conductive hearing loss if the lumen is obstructed
  • Systemic features (fever, malaise) are uncommon unless immunocompromised

Treatment

  • Mild/localised: topical antiseptic/antibiotic wick (e.g., bismuth iodoform paraffin paste — BIPP); analgesia; oral anti-staphylococcal antibiotic (flucloxacillin/dicloxacillin; erythromycin if penicillin-allergic)
  • Fluctuant abscess: incision and drainage (I&D) under local anaesthesia; culture swab
  • Recurrent furuncles: consider diabetes, immunodeficiency; nasal S. aureus carriage (treat with mupirocin nasal ointment)
  • Warm compresses to promote pointing

9. Otomycosis

Diagnosis

  • Etiology: 10% of all AOE; Aspergillus most common (often appears as black or grey spores on white/grey hyphae — "wet newspaper" fungal ball), Candida and Penicillium also seen
  • Predisposing factors: warm humid environments (swimmers, surfers, divers, tropical climates), chronic moisture (hearing aid users), previous antibiotic ear drops (disrupt normal flora), immunocompromised, mastoid cavity patients
  • Symptoms: intense pruritus (more prominent than in bacterial OE), otalgia, hearing loss, aural fullness, otorrhoea
  • Signs: fungal hyphae or spore masses visible on otoscopy — "wet newspaper" appearance (Aspergillus); creamy white plaques (Candida)
  • Cultures: not routinely helpful; biopsy if immunocompromised or atypical presentation

Treatment

  1. Frequent aural toilet (mechanical removal of fungal debris) — most important step
  2. Dry ear precautions
  3. Acidifying/drying agents: gentian violet, boric acid in alcohol
  4. Topical antifungals (first-line pharmacologic):
    • Clotrimazole 1% solution or cream
    • Cresylate otic
    • Ketoconazole ointment
    • CSF powder (chloramphenicol + amphotericin B + sulfanilamide)
  5. Systemic antifungals (oral itraconazole or voriconazole) reserved for refractory disease or invasive fungal disease in immunocompromised patients

10. Perichondritis of the Auricle

Etiology

Perichondritis is infection of the auricular perichondrium; chondritis denotes extension into the cartilage itself.
  • Trauma (most common cause): blunt trauma → haematoma → secondary infection; penetrating trauma; ear piercing through cartilage; bites
  • Iatrogenic (post-otological surgery)
  • Extension of otitis externa or subperiosteal abscess
  • Superficial infections: Staphylococcus and Streptococcus
  • Deeper infections (perichondritis/chondritis): Pseudomonas aeruginosa is the most common causative organism
  • Erysipelas: beta-haemolytic Streptococcus (well-demarcated border)
  • Exclude: relapsing polychondritis (autoimmune; spares lobule), gouty tophus, cutaneous lymphoma

Diagnosis

  • Pain and erythema of the auricle
  • Induration and oedema (distinguish from simple cellulitis, which is non-indurated)
  • Fluctuation indicates abscess formation
  • Lobule is typically spared (no cartilage) — differentiates from erysipelas which can involve the lobule
  • "Cauliflower ear" deformity in chronic/untreated cases
  • Fever, elevated WBC in severe cases
  • Diagnosis made on clinical grounds; incision and drainage with culture when abscess is present

Treatment

  • Cellulitis (mild): oral anti-staphylococcal + anti-streptococcal antibiotic
  • Severe infection or immunocompromised: IV antibiotics with anti-staphylococcal, anti-streptococcal, and anti-pseudomonal coverage
  • Perichondritis/chondritis without abscess: oral fluoroquinolone (ciprofloxacin — anti-pseudomonal coverage) for 2–4 weeks
  • Abscess: incision and drainage + cartilage debridement as needed; bolster placement; 2–4 weeks of anti-pseudomonal antibiotics

11. Disorders of the Eustachian Tube (Tubal Blockage)

Anatomy

  • Length: 17–18 mm at birth, grows to ~35 mm in adulthood
  • Neonatal tube is horizontal; becomes angled at 45° in adulthood (pharyngeal orifice ~15 mm lower than tympanic orifice — explains why children are more prone to middle ear disease)
  • Two portions: anteromedial cartilaginous portion (24 mm) and posterolateral bony portion (11 mm); narrowest at the isthmus (bony-cartilaginous junction)
  • Opens by action of tensor veli palatini (CN V3) ± levator veli palatini (vagus CN X)
  • In children, only the tensor palati is functional — hence cleft palate → ET dysfunction

Physiology

  • Normal pressure differential to produce airflow: 200–300 mmHg
  • Easier to expel air from ME than admit it — explains tubal problems on aircraft descent
  • Negative pressure of -30 mmHg for 15 min → transudate in ME
  • Critical pressure difference: 90 mmHg — locks the ET, preventing tensor palati from opening it
  • Pressure >100 mmHg → tympanic membrane rupture
  • Valsalva generates ~20–40 mmHg

Obstructive Eustachian Tube (Tubal Blockage)

Causes:
  • Upper respiratory tract infections (mucosal oedema)
  • Allergic rhinitis / adenoid hypertrophy
  • Cleft palate
  • Nasopharyngeal tumour (unilateral OME in adult — must exclude!)
  • Barotrauma
Consequences: negative middle ear pressure → TM retraction → middle ear effusion → conductive hearing loss → risk of cholesteatoma
Treatment:
  • Valsalva manoeuvre (self-inflation)
  • Nasal decongestants / corticosteroid nasal spray (for mucosal oedema)
  • Treat underlying cause (adenoidectomy, allergy management)
  • Balloon Eustachian tuboplasty (endoscopic dilation) — emerging surgical treatment
  • Tympanostomy tubes for refractory OME

12. Acute Suppurative Otitis Media (AOM)

Etiology and Microbiology

Most common bacterial infection of childhood. Pathogens:
  1. Streptococcus pneumoniae (35%)
  2. Haemophilus influenzae (non-typeable, 25%)
  3. Moraxella catarrhalis (10%)
  4. S. aureus, S. pyogenes
  5. Anaerobes (newborns); Gram-negative enteric organisms (infants)
  6. Viral (RSV, rhinovirus, influenza)
  • 20–30% produce beta-lactamase

Predisposing Factors

Male sex, craniofacial abnormality, immunodeficiency, bottle-propping, day care attendance, smoke exposure, sibling with recurrent AOM, age <6 months

Diagnosis

Based on any one of:
  1. Rapid onset of middle ear inflammation
  2. Moderate to severe bulging of the TM
  3. Mild TM bulging + recent ear pain (<48 hours) or intense erythema
  4. New-onset otorrhoea not due to otitis externa

Treatment

Non-pharmacological: breastfeeding, avoid smoke, influenza vaccine (up to 55% reduction), pneumococcal conjugate vaccine (29% reduction)
Observation without antibiotics is acceptable if:
  • Parents reliable AND
  • Age 6 months–2 years with unilateral, non-severe AOM, OR age >2 years with bilateral non-severe AOM
  • No craniofacial anomalies, immunodeficiency, or chronic disease
  • Give antibiotics if worsening or no improvement at 48–72 hours
Antibiotic therapy:
  • First-line: Amoxicillin (high-dose 90 mg/kg/day in areas of high resistance)
  • Failure: amoxicillin-clavulanate; penicillin-allergic: ceftriaxone IM or clindamycin
  • Duration: 10 days (<2 years or severe), 5–7 days (older children, mild)
Recurrent AOM (3 episodes in 6 months or 4 in 1 year with 1 in preceding 6 months): myringotomy and tympanostomy tubes

13. Otitis Media with Effusion (Glue Ear / OME)

Diagnosis

  • Middle ear fluid without signs of acute infection or inflammation
  • Conductive hearing loss
  • Otoscopy: TM retraction, amber fluid visible, air-fluid level, reduced mobility (best assessed with pneumatic otoscopy)
  • Flat (type B) tympanogram
  • Predisposed by AOM and poor ET function (cleft palate)

Natural History

  • 70% of children clear within 3 months; 90% when OME follows treated AOM
  • 90% of children have had OME by age 4; highest incidence age 1–2 years

Treatment

  • Watchful waiting with serial audiograms is first-line — observation for 3 months
  • No role for antibiotics, steroids, antihistamines, or decongestants
  • Re-evaluate every 3 months
Tympanostomy tube indications:
  1. Chronic bilateral OME ≥3 months with hearing loss
  2. Chronic unilateral or bilateral OME with vestibular/behavioural problems, ear discomfort, or poor school performance
  3. Children at risk (sensory, physical, cognitive, or behavioural deficits) with OME unlikely to resolve (flat tympanograms)
Adenoidectomy: indicated in children >4 years with recurrent OME or undergoing repeat tympanostomy tubes; reduces rate of recurrence

14. Cholesteatoma (Classification)

A cholesteatoma is keratinised squamous epithelium within the middle ear or mastoid space. It destroys bone through pressure and matrix metalloproteinase (collagenase) activity.

Classification

I. By Origin
  1. Congenital cholesteatoma
    • Well-circumscribed pearly white mass behind an intact tympanic membrane in the absence of prior ear disease or surgery
    • Most common in children; most frequently in anterosuperior quadrant
    • Thought to arise from embryological rests of squamous epithelium
  2. Primary acquired cholesteatoma
    • Develops from retraction pocket of the pars flaccida (Shrapnell's membrane — attic/epitympanic retraction)
    • Caused by chronic negative middle ear pressure due to ET dysfunction
    • Retraction pocket accumulates keratinous debris → expansion into middle ear/mastoid
  3. Secondary acquired cholesteatoma
    • Arises from marginal or central perforation of the pars tensa
    • Squamous epithelium migrates through perforation into the middle ear
    • Also can result from implantation of keratin following surgery or trauma
II. By Location
  • Atticoantral (pars flaccida / epitympanic) — more dangerous; erodes ossicles, facial canal
  • Tubotympanic (pars tensa margin) — retraction of pars tensa
  • Middle ear / mesotympanum
  • Mastoid extension

Presentation

  • Foul-smelling, painless otorrhoea through a perforated or retracted TM
  • Conductive hearing loss
  • Vertigo or facial nerve paralysis if untreated

Diagnosis

  • Fine-cut CT temporal bone (0.625 mm) without contrast — surgical planning
  • MRI: diffusion-weighted imaging (DWI) — sensitive/specific for recurrent/residual cholesteatoma post-surgery

Treatment

Surgical: goal is a safe, dry ear. Hearing preservation is secondary.
  • Small lesions: tympanomeatal flap (transcanal)
  • Larger lesions: tympanomastoidectomy (canal wall-up or canal wall-down)

15. Paracentesis / Myringotomy (Technique and Indications)

Indications

  • Therapeutic myringotomy: AOM with severe pain unrelieved by analgesics, AOM with suppurative complications, AOM in neonates or immunocompromised patients, diagnosis of causative organism
  • Myringotomy + tympanostomy tube insertion: recurrent AOM (3 in 6 months or 4 in 12 months), chronic OME with hearing loss or complications, OME with developmental risk, barotrauma
Contraindication: suspicion of high-riding jugular bulb or aberrant carotid artery in the TM area — do not perform myringotomy

Technique

  1. Examination and cleaning of the EAC under microscope
  2. Local anaesthesia (topical phenol or EMLA, or general anaesthesia in children)
  3. Using a myringotomy knife (paracentesis blade), make a radial incision in the anteroinferior quadrant of the pars tensa (avoids ossicles, facial nerve, round window, and chorda tympani)
  4. Aspirate fluid/pus from the middle ear
  5. For tube insertion: the tympanostomy tube (grommet) is inserted through the incision using alligator forceps; the tube flanges hold it in place

Types of Tubes

  • Short-term (grommet): extruded in 6–12 months (e.g., Shepard, Armstrong)
  • Long-term (T-tubes): remain 2–4 years; used in patients likely to need prolonged ventilation (cleft palate, Down syndrome)

16. Complications of Acute Otitis Media

Intratemporal (within the temporal bone)

  1. Conductive hearing loss (from ossicular involvement/perforation)
  2. TM perforation — spontaneous in ~5% of AOM cases; typically heals (90%)
  3. Mastoiditis — most common suppurative complication
  4. Facial nerve palsy — from spread along facial canal
  5. Labyrinthitis — serous or suppurative; may cause SNHL
  6. Petrositis (Gradenigo syndrome) — triad: retro-orbital pain (CN VI palsy), otorrhoea, deep facial pain
  7. Sensorineural hearing loss
  8. Bezold abscess — pus tracks through tip of mastoid into sternocleidomastoid muscle; presents as neck swelling/stiffness

Intracranial

  1. Meningitis (most common intracranial complication)
  2. Sigmoid sinus thrombosis — septic thrombophlebitis
  3. Otitic hydrocephalus — raised ICP with sinus thrombosis
  4. Epidural abscess
  5. Subdural abscess
  6. Brain abscess (temporal lobe or cerebellum)
Note: Up to 10% of patients with acute mastoiditis on parenteral antibiotics still develop intracranial complications.

17. Mastoiditis

Etiology

Extension of AOM into the mastoid air cells (they communicate directly with the middle ear via the aditus ad antrum). Most common organisms mirror those of AOM: S. pneumoniae, H. influenzae, S. aureus, P. aeruginosa (in chronic cases), group A Streptococcus.

Pathogenesis

  • Middle ear mucosa is continuous with mastoid air cell mucosa
  • AOM → mucosal inflammation of mastoid → purulent fluid fills air cells (mastoid opacification)
  • Persistent infection → breakdown of bony septa between air cells → coalescent mastoiditis
  • Pus can extend: through lateral cortex (subperiosteal abscess), into neck (Bezold abscess), intracranially

Classification

  1. Acute Mastoiditis (non-coalescent)
    • Signs of AOM on otoscopy + local inflammation over mastoid (pain, erythema, tenderness, auricular protrusion)
    • Fullness and oedema of the posterior-superior EAC skin
    • Mastoid opacification on CT (can be present in uncomplicated AOM)
    • Systemic toxicity (fever, leucocytosis)
    • More common in children ≤4 years; only 30% have a history of recurrent AOM
  2. Coalescent (Acute Surgical) Mastoiditis
    • Bony erosion of mastoid septa on CT
    • Recurrent/persistent purulent otorrhoea for ≥2 weeks
    • Subperiosteal abscess common
    • Requires urgent surgical intervention (mastoidectomy ± cortical mastoidectomy)
    • Concomitant intracranial complication not uncommon
  3. Chronic Mastoiditis
    • Complication of chronic suppurative otitis media
    • Often with cholesteatoma

Additional Variants

  • Masked mastoiditis: inadequate antibiotic treatment partially treats AOM but allows coalescent disease to develop silently
  • Bezold abscess: rupture through mastoid tip into SCM
  • Subperiosteal abscess: rupture through lateral cortex → pinna displaced anteriorly and inferiorly

18. Classification of Chronic Otitis Media

Chronic otitis media (COM) is defined as persistent or recurrent middle ear infection lasting >3 months.

Primary Classification

TypeTM StatusCholesteatomaAlso Known As
Tubotympanic (safe)Central perforation (pars tensa)AbsentChronic mucosal OM
Atticoantral (unsafe/dangerous)Marginal/attic perforation or retractionPresentCholesteatoma OM

Further Classification

By disease activity:
  • Active (with otorrhoea)
  • Inactive/quiescent (dry ear)
By anatomical site:
  • Tubotympanic: pathology involves pars tensa; retraction confined to pars tensa
  • Atticoantral: involves pars flaccida and epitympanum; frequently associated with cholesteatoma; "unsafe" because more likely to cause complications
Chronic OM with Effusion (COME): persistent middle ear effusion without perforation; may coexist

19. Chronic Purulent Otitis Media (CSOM)

Etiology / Pathogenesis

  • Biofilms play a central role: organised bacterial communities within an extracellular matrix that resist antibiotics and immune clearance; P. aeruginosa is the most common pathogen; also S. aureus, non-typeable H. influenzae, M. catarrhalis, anaerobes
  • ET dysfunction → negative ME pressure → TM retraction → perforation (compensatory mechanism for aeration)
  • Tympanostomy tube or perforation allows contamination of ME from the EAC
  • Occurs most commonly in areas with limited health resources; highest incidence in children <2 years

Diagnosis

  • TM perforation (central in tubotympanic type; marginal/attic in atticoantral)
  • Hearing loss (typically low-frequency conductive or mixed)
  • Chronic or recurrent, often malodorous otorrhoea
  • ME mucosal inflammation, granulation tissue, aural polyps (always suspect cholesteatoma until proven otherwise)
  • TM retraction pockets ± cholesteatoma
  • Complicated CSOM: facial nerve paresis, vertigo (labyrinthine fistula), intracranial infection
Investigations:
  • Otomicroscopy with pneumatic insufflation
  • Audiometry
  • High-resolution CT temporal bone: surgical planning, complicated CSOM, suspected cholesteatoma, revision surgery
  • MRI with contrast: suspected intracranial complications; DWI for recurrent/residual cholesteatoma
  • Biopsy: granulation tissue unresponsive to topical therapy (exclude malignancy)

Treatment

Primary goal: safe, dry ear (no otorrhoea, no keratin accumulation)
Medical (topical):
  • Aural toilet (debridement) — removes biofilm; essential before any topical therapy
  • Topical antibiotics: fluoroquinolones (ciprofloxacin) or polymyxin B ± neomycin ± hydrocortisone; 4–6 week course
  • Combination ointment for chronic/refractory cases: equal parts bacitracin/polymyxin + clotrimazole 1% + betamethasone 0.05%
Surgical:
  • Tympanoplasty (60–90% success): repair of TM perforation; best outcomes with healthy ET function; poor outcome if contralateral ear has OME or negative pressure
  • Tympanomastoidectomy: for cholesteatoma, otorrhoea refractory to medical treatment
    • Canal wall-up (CWU): two-stage procedure; better hearing; higher recidivism
    • Canal wall-down (CWD): modified radical or radical mastoidectomy; single stage; open cavity requires regular cleaning
    • Bondy procedure: for limited epitympanic disease
    • Canal wall-down with mastoid obliteration: reduces cavity problems

— K.J. Lee's Essential Otolaryngology | Cummings Otolaryngology Head and Neck Surgery
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