Chronic Suppurative Otitis Media (CSOM)

Infection complications of otitis media

• acute perforation, OME with effusion, adhesive otitis media
• acute & chronic mastoiditis, petrositis, labyrinthitis
• facial paralysis and intracranial infection

Noninfectious sequelae

• chronic perforation, ossicular erosion, middle ear atelectasis
• labyrinthine erosion, and tympanosclerosis, cholesteatoma, SNHL

Effects on Mastoid Pneumatization

• Cavity size on CT: big or small, well or poorly aerated, sclerotic or not
• Children with chronic OME have more sclerotic mastoids with decreased pneumatization compared to normal children.
• Two suggestions:
• “Hereditary theory”: kids with hypoaeration of mastoid are prone to OME (Diamant, ’40)
• “Environmental theory”: chronic OME → mastoid hypopneumatization (Wittmaack, ’18)
• There is evidence that chronic inflammation → new bone

Middle Ear Atelectasis and Adhesive Otitis Media

• Middle ear atelectasis results from long-standing ET dysfunction.
• TM becomes retracted onto promontory & ossicles of middle ear, but is not adherent to medial wall; mucosal lining intact.
• Adhesive otitis media: middle ear space totally obliterated & TM adherent to ossicles & promontory; mucosal surfaces not present.
• Retraction of TM may → erosion of long process of incus & stapes suprastructure.
• Mechanism: repeated AOM → weakening & thinning TM → atelectasis. Sade & Berco (1976): destruction of collagen-containing fibrous layer in some ears with recurrent infection.
• NB: collagen destruction within TM may → tympanosclerosis.

Stages of TM Retraction

Pars Tensa (after Sade and Berco 1976)

• Stage I: retracted tympanic membrane
• Stage II: retraction with contact onto incus
• Stage III: middle ear atelectasis
• Stage IV: adhesive otitis media

Pars Flaccida (attic retraction pockets) (after Tos 1988)

• Grade I: Pars flaccida not in contact with malleus head
• Grade II: Pars flaccida in contact with malleus head
• Grade III: Limited outer attic wall erosion
• Grade IV: Severe outer attic wall erosion

Wullstein's five tympanoplasty techniques

• Type 1: reconstruction of TM (ossicular chain intact and mobile)
• Type 2: malleus handle absent; reconstruct TM over malleus remnant & long process of incus
• Type 3: malleus & incus absent; reconstruction of TM over intact, mobile stapes (myringostapediopexy)
• Type 4: mobile stapes footplate exteriorized with TM reconstructed as a RW baffle
• Type 5: stapes fixed → fenestration

• Middle ear atelectasis may be reversible with ventilating tubes.
• Atelectasis and adhesive otitis media usually coexist with OME.
• Cholesteatomas may arise from deep retraction pockets in pars tensa or pars flaccida.

Chronic Otitis Media with Cholesteatoma

Definition

• Aural cholesteatomas: epidermal inclusion cysts of the middle ear or mastoid
• Misnomer; do not contain cholesterol; contain desquamated keratin
• First described by Cruveilhier (1829)
• May be congenital or acquired (often consequence of OME/AOM)

Diagnosis

• Made on otoscopic examination or surgical exploration
• CT used to complement clinical exam and operative planning
• Fagan’s list (consider imaging): revision surgery; only hearing ear; complications (intracranial, VII, labyrinthine); cannot see fundus; considering avoiding surgery
• Symptoms: asymptomatic to infected with bone destruction; slowly progressive CHL common; chronic malodorous otorrhea (anaerobes)
• Signs of sequelae: vertigo, HL from labyrinthine fistula, facial nerve paralysis, intracranial infection
• Otoscopic appearance:
  • Attic retraction cholesteatoma: defect adjacent to posterosuperior TM
  • Keratin in center of marginal defect → primary acquired
  • Keratin migrated through perforation into ME → secondary acquired
  • Behind intact TM → congenital
  • Aural polyp in chronically infected ear → cholesteatoma until proven otherwise

Pathogenesis

Congenital: keratinizing epithelium rests within ME cleft (Michaels 1986).

Acquired: four basic theories

• Invagination (retraction pocket) – Wittmaack 1933
• Basal cell hyperplasia – Lange 1925; supported by Ruedi (1959), basal lamina disruptions; propylene glycol animal models (Huang 1988; Masaki 1989)
• Migration (epithelial ingrowth through perforation) – Habermann 1889; contact guidance/ inhibition (Weiss 1958)
• Squamous metaplasia – Wendt 1873

Clinically, multiple mechanisms likely contribute.

Bacteriology of infected cholesteatomas

Aerobes

• Pseudomonas aeruginosa (most common), P. fluorescens
• Streptococcus spp., Proteus spp., E. coli, Klebsiella spp., Enterobacter spp., Serratia spp.
• Staphylococcus epidermidis, Staphylococcus aureus

Anaerobes

• Bacteroides (most common), Peptococcus, Peptostreptococcus spp.
• Propionibacterium acnes, Fusobacterium spp., Bifidobacterium spp.
• Clostridium spp., Eubacterium spp.

Management

• Some can be kept stable by careful debridement or irrigation
• Irrigation: 1:1 distilled white vinegar & 70% isopropyl alcohol in select cases

Chronic Otitis Media without Cholesteatoma

Pathogenesis

• Irreversible inflammatory changes within middle ear and mastoid; may occur with MEDITs
• Otorrhea common; P. aeruginosa and S. aureus frequent pathogens
• Aeration depends on airflow ET → mastoid; mucosal folds and ossicles create only two constant openings (Proctor 1964)
• Edema/granulation can block attic/antrum → irreversible changes in mucosa & bone; granulation can erode bone

Management

• Topical antibiotics (± hydrocortisone) covering P. aeruginosa and S. aureus; culture-directed therapy
• Dilute acidic irrigation (e.g., 1:1 distilled vinegar & water) for refractory cases
• Insufflation powders in select cases; systemic antibiotics if refractory with specific pathogens
• Tympanoplasty considered when ear is quiet for > 3 months
• Refractory chronic infection without cholesteatoma:
  • Long-term IV antibiotics or
  • Tympanomastoid surgery (goals: aeration, rule out irreversible disease, close ME, OCR)
• Post-tympanostomy tube otorrhea: topical + systemic antibiotics; IV if persistent; consider tube removal in refractory cases

Bone Erosion in Cholesteatoma & Chronic Otitis Media

• Pressure necrosis theory abandoned; current: osteoclast-mediated resorption
• Enzymes: acid phosphatase, collagenase, acid proteases
• Low pH of keratin debris may demineralize bone; keratin incites foreign-body granuloma
• Bone resorption can occur in COM with or without cholesteatoma
• Pressure and inflammation sufficient to resorb bone; potentials and monocyte recruitment; PgE2, IL-1, TNFα involved

Complications of COM

Sensorineural Hearing Loss

• SNHL associated with COM (Paparella 1969) possibly via RW toxins
• Hair cell stereocilia loss in experimental cholesteatomas ± infection (Chole & Chin 1988)
• Labyrinthitis in 20% of temporal bones with COM (Meyerhoff 1978)

Tympanosclerosis

Complication with acellular hyalin & calcified deposits in TM & ME submucosa; often clinically insignificant.

• Found in ~20% drumheads 6–8 years post MEDITs
• Histology: hyalinization ± calcification; osteoneogenesis can occur; may → ossicular fixation
• TM plaques limited to lamina propria; ME tympanosclerosis can cause CHL
• Pathogenesis: post-otitis or trauma; ET obstruction ± infection; possible autoimmune in TM
• Management: surgery outcomes vary; risks of cochlear damage higher than other ME diseases

Mastoiditis

Part 1 Acute / Chronic / Masked mastoiditis

Part 2 Complications of mastoiditis

Part 3 Surgery of the mastoid

Introduction

• Mastoid = one of five pneumatized temporal bone regions; all contiguous (Schuknecht 1974)
• Clinical relations: posterior/middle cranial fossae, sigmoid/lateral sinuses, facial nerve, semicircular canals, petrous apex
• At birth: antrum only; pneumatization extensive by ~2 years

Types

• Acute Mastoiditis with periostitis → Acute Coalescent Mastoiditis
• Chronic Mastoiditis
• Masked (latent/silent/atypical) Mastoiditis

Definitions

• Acute mastoiditis: mucosa/lamina propria inflammation
• With periostitis: includes periosteal inflammation
• Coalescent: rarefying osteitis and bony destruction
• Chronic: bone invasion by granulation tissue & chronic inflammation
• Masked: subacute/atypical form, “cold” coalescence under antibiotic-masked infection

Acute Mastoiditis

Incidence

• Childhood disease (peak around 6 years); higher in overcrowded areas

Pathophysiology

• Progressive mucoperiosteal inflammation → periostitis
• Aditus ad antrum obstruction (“bottleneck”)
• Serous → purulent accumulation; venous stasis, local acidosis, halisteresis
• Demineralization and necrosis by pressure/ischemia; osteoclastic resorption; coalescence
• Chronic cases: irreversible mucosal/bony changes, fetid discharge suggests anaerobes/poor aeration/osteitis

Bacteriology

• Streptococcus pneumoniae, Haemophilus influenzae, Branhamella catarrhalis, Staphylococcus aureus; some anaerobes

Clinical features

• Pain (Macewen’s triangle), tenderness (tip/retroauricular/zygoma significant), postauricular erythema/oedema
• Deafness; sagging posterosuperior meatal wall; abnormal TM; fever/toxicity
• Signs of complications

Investigations

• Clinical suspicion; FBC/ESR; cultures; imaging (plain films; CT confirms/defines extent)

Differential diagnosis

• Furunculosis of EAM, lymphadenitis, other regional conditions

Management

• Treat as potential surgical emergency
• Coalescent with subperiosteal abscess: complete cortical mastoidectomy + large myringotomy
• Coalescent without abscess: close monitoring if not operating; many prefer surgery
• Antibiotics: high-dose coverage per likely organisms and duration
• Myringotomy for drainage and culture
• Indications for mastoid drainage: persistent pain, systemic signs, copious pulsatile discharge, progressive HL, facial palsy, complications

Chronic Mastoiditis

• Poor pneumatization common; part of CSOM
• Types: Cholesteatoma; Granulation tissue with osteitis; Cholesterol granuloma
• Clinical: persistent/recurrent fetid otorrhea; variable HL; bleeding from granulations/polyps; marginal perforations
• Investigations: plain films (limited), CT/MRI for planning/revision
• Management:
  • Cholesteatoma: surgical excision; vinegar/alcohol irrigation may stabilize in select cases
  • Granulation with osteitis: conservative care; aggressive debridement if refractory

Masked Mastoiditis (latent/silent/atypical)

• Persistent infection “dampened” by antibiotics → progressive coalescence without classic signs
• Etiology: inadequate antibiotic course/dose → resistance/persistence
• Clinical: mild OM features, recent AOM treated with antibiotics, malaise, mild tenderness, persistent deafness
• Investigations: variable labs; imaging shows opacity ± bone destruction; nuclear medicine can help
• Management: admission, high-dose IV antibiotics, close observation; cortical mastoidectomy if no improvement