Chronic Suppurative Otitis Media (CSOM)

Definition

Epidemiology

• Most common in children under 2 years old
• Higher prevalence in areas with limited health resources and low socioeconomic status
• Genetically predisposed populations: Native Americans, Inuit, Native Australians, Native New Zealanders
• Risk factors include: multiple episodes of AOM, AOM in the first few months of life, chronic secretory OM, Eustachian tube (ET) dysfunction, nasopharyngeal reflux, and cleft palate

Classification

• Retraction or perforation confined to the pars tensa (central perforation)
• Involves the mesotympanum
• Less prone to cholesteatoma

• Involves the pars flaccida (attic)
• Posterosuperior retraction pockets
• Cholesteatoma commonly present
• Higher risk of complications

Pathogenesis

1. Negative middle ear pressure - nitrogen-absorbing mastoid cells reduce middle ear volume, causing negative pressure and TM retraction
2. Persistent middle ear effusion - initially serous, becomes purulent with bacterial infection
3. Mucosal changes - bacterial toxins and inflammatory mediators cause edema, basement membrane rupture, and granulation tissue formation. Submucosal glands develop, converting mucosa to a secretory type
4. Granulation tissue and polyp formation - angiogenic and epithelial growth factors drive fibroblast recruitment and neovascularization
5. TM weakening - enzymes in the effusion break down the TM collagen skeleton, leading to retraction pockets and perforations
6. Cholesteatoma - deep retraction pockets and perforations allow keratinizing squamous epithelium to migrate medially

• Escape phagocytosis and humoral immunity via an impenetrable matrix
• Show dramatically increased antibiotic resistance (efflux pumps, altered gene expression, low metabolic rate)
• Are frequently polymicrobial, making treatment difficult
• Can be adherent to respiratory epithelium, within mucus, or intracellular
• KJ Lee's Essential Otolaryngology, p. 445-446; Shambaugh Surgery of the Ear, p. 527

Microbiology

• KJ Lee's Essential Otolaryngology, p. 446; Cummings Otolaryngology, p. 3072

Clinical Features

• Chronic or recurrent otorrhea - often malodorous/mucopurulent (cardinal symptom)
• Hearing loss - typically conductive (low-frequency), can be mixed; losses >30 dB suggest ossicular erosion
• Aural fullness
• Otalgia and headache - uncommon; if present, raise suspicion for intracranial complications or malignancy
• Vertigo - raises suspicion for labyrinthine fistula or labyrinthitis
• Facial nerve paresis/paralysis (complicated CSOM)

• Tympanic membrane perforation (central vs. marginal/attic)
• Otorrhea often obscures the TM - aural toilet essential before examination
• Retraction pockets, atelectasis
• Granulation tissue and aural polyps (aural polyp = cholesteatoma until proven otherwise)
• Cholesteatoma (pearly white debris, keratin flakes, squamous epithelium)
• Scutal erosion and ossicular erosion (in atticoantral disease)
• Shambaugh Surgery of the Ear, p. 527-528; KJ Lee's Essential Otolaryngology, p. 446

Diagnosis

Treatment

Goals

• Dry ear (no otorrhea)
• Safe ear (no keratin debris collection, reduced suppurative complication risk)
• Preservation or restoration of hearing

Medical Treatment

• Essential before any topical medication - removes debris and discharge, allows drug penetration

• Fluoroquinolones (ciprofloxacin, ofloxacin) - first-line topical; effective against Pseudomonas and gram-negatives; safe for perforated ears (non-ototoxic)
• Polymixin B or neomycin (+/- steroid) - second-line; note: neomycin is potentially ototoxic in the presence of a perforation
• Acetic acid/alcohol drops - antiseptic, useful for mild disease

Surgical Treatment

• Cholesteatoma (combined with refractory CSOM = near-absolute indication)
• Failure of multiple courses of medical treatment
• Symptoms suspicious of complications (vertigo, facial weakness, headache)
• Significant conductive hearing loss with ossicular erosion
• Atelectatic ears with significant CHL

1. Eradication of disease
2. Prevention of disease recurrence
3. Preservation or restoration of hearing

• Shambaugh Surgery of the Ear, p. 528-529; KJ Lee's Essential Otolaryngology, p. 447

Complications

Intratemporal Complications

Intracranial Complications

CSOM and Cholesteatoma

• Acquired cholesteatoma arises from retraction pockets (pars flaccida most susceptible) or via migration through perforations
• Cholesteatoma is destructive - produces enzymes (collagenases, cytokines) that erode bone
• Erodes ossicles, semicircular canals (fistula), tegmen, facial canal, and can penetrate intracranially
• An aural polyp should be considered cholesteatoma until proven otherwise
• Key diagnostic hallmark on examination: pearly white, cheesy keratin debris, often with foul smell

CSOM and Cochlear Implantation

• Two-stage approach: stage 1 = mastoidectomy + ET obliteration + cavity obliteration; stage 2 = CI insertion 2-6 months later when ear is dry
• If the ear is dry at time of implantation, single-stage approach may be appropriate
• Biofilm formation on CI electrodes (including Candida biofilms) is a recognized complication
• Antimicrobial prophylaxis is given before implantation
• Cummings Otolaryngology, p. 3072

Key Points Summary

• CSOM = persistent/recurrent purulent otorrhea through a TM perforation (>6-12 weeks)
• Tubotympanic (safe, pars tensa) vs. Atticoantral (unsafe, pars flaccida, cholesteatoma-prone)
• Main organisms: Pseudomonas aeruginosa, S. aureus, anaerobes
• Biofilms underlie antibiotic resistance and persistence
• Aural polyp = cholesteatoma until proven otherwise
• Treatment: aural toilet + topical fluoroquinolones → surgery if refractory or cholesteatoma present
• Otalgia, headache, vertigo, or facial palsy in CSOM = red flags for complications
• Surgery priorities: eradicate disease > prevent recurrence > restore hearing

• KJ Lee's Essential Otolaryngology, pp. 445-447
• Shambaugh Surgery of the Ear, pp. 527-529
• Cummings Otolaryngology Head and Neck Surgery, p. 3072
• Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol. 2

Secretory Otitis Media (Otitis Media with Effusion / "Glue Ear")

Definition & Terminology

Epidemiology

• Most common cause of hearing loss in children
• Point prevalence on screening: up to 20% in children
• Peak incidence: around 1 year of age; by age 3, nearly all children have experienced at least one episode
• Bimodal incidence: 40% of 2-year-olds (starting nursery) and 20% of 5-year-olds (starting school)
• Higher incidence in autumn/winter months (suggesting infective aetiology)
• 90% of children will have had at least one OME episode by age 4

Risk Factors

Pathogenesis

1. Eustachian Tube Dysfunction

• The ET protects the middle ear from otopathogens, drains secretions, and equalizes pressure
• In infants and children, the ET is shorter, more horizontal, and more compliant than in adults - a key anatomical vulnerability
• ET dysfunction causes inadequate gas exchange, leading to increasingly negative middle ear pressure
• Negative pressure causes transudation of fluid that fails to clear
• ET dysfunction causes: inflammatory obstruction (allergies, URTI, GERD, biofilms), muscular abnormalities (cleft palate, palatal myopathies), anatomic obstruction (adenoids, nasopharyngeal masses)

2. Biofilm-Driven Chronic Inflammation (increasingly recognized)

• Traditional cultures of OME fluid are often negative - bacteria are not free-floating but sequestered as biofilms on the mucosal surface
• Hall-Stoodley (2006): Confocal laser-scanning microscopy found bacterial biofilms in 92% of middle ear mucosal biopsies from children with chronic OME (vs. 0% of controls)
• Coates (2008): Transmission electron microscopy demonstrated intracellular bacterial infection of middle ear mucosal epithelial cells in OME patients
• Biofilm bacteria secrete endotoxins and exotoxins that trigger a cytokine cascade: TNF-α, IL-1β, IL-6, IL-8 (pro-inflammatory) + IL-2, IL-4, IL-5, IL-10, IFN-γ (immunoregulatory)
• TNF-α and IL-1β are the two most important primary cytokines
• This chronic inflammatory state - rather than ET dysfunction alone - now appears to be the primary driver of OME

3. Sequence of Fluid Formation

1. Initial serous transudate (thin, clear) from negative middle ear pressure
2. Progresses to mucoid/viscous effusion ("glue") as goblet cells proliferate and mucin is secreted
3. Chronic mucosal changes: submucosal gland formation, goblet cell hyperplasia, mucus hypersecretion
4. Glycoproteins increase fluid viscosity and slow clearance from the middle ear cleft

Microbiology

• Non-typeable Haemophilus influenzae (NTHi) - most common biofilm pathogen
• Streptococcus pneumoniae
• Moraxella catarrhalis
• Viruses (RSV, rhinovirus, adenovirus) - act as co-pathogens, impairing mucociliary clearance

Clinical Features

Symptoms

• Hearing loss - typically conductive, often fluctuating (most prominent feature)
• Aural fullness / sensation of fluid in ear
• Delayed speech and language development (children)
• Behavioural problems and learning difficulties at school
• Reading difficulties
• Usually no pain (unlike AOM) - the ear is not acutely infected

Signs (Otoscopy)

• Dull, lustreless tympanic membrane (loss of normal light reflex)
• Retracted TM - handle of malleus more horizontal, short process more prominent
• Immobile TM on pneumatic otoscopy (pathognomonic)
• Radial blood vessels visible over the TM
• Amber/yellow discolouration - fluid level or bubbles visible through TM
• Air-fluid level or bubbles (serous effusion)
• Blue-grey TM (haemotympanum or very mucoid "glue")
• TM NOT bulging (unlike AOM)

Investigations

Important: Unilateral OME in an adult must raise suspicion for a nasopharyngeal mass obstructing the ET until proven otherwise.

Natural History

• Self-limiting in most cases - about 50% of children with bilateral OME resolve within 12 weeks
• Appropriate initial management: "watchful waiting" for 3 months (unless bilateral hearing loss is significantly affecting development)
• Spontaneous resolution rates are high in the first year; persistent OME (>3 months) is less likely to resolve without intervention
• Risk of long-term sequelae with persistent bilateral OME: reduced IQ, speech/language delay, behavioural problems

Complications & Long-Term Consequences

Treatment

1. Watchful Waiting ("Watch and Wait")

• First-line for most children
• Appropriate for bilateral OME of <3 months duration
• 50% resolve within 12 weeks
• Re-assess at 3-month intervals
• While watching: hearing aid, preferential classroom seating, teacher awareness

2. Non-Surgical / Medical Treatment

3. Surgical Treatment

• Most common elective surgical procedure in children (UK/worldwide)
• Indications:
  • Persistent bilateral OME for ≥3 months with significant hearing loss (≥25-30 dB)
  • Impact on speech, language, development, or behaviour
  • Recurrent OME with hearing impairment
  • Chronic OME in at-risk populations (Down syndrome, cleft palate, craniofacial abnormalities)

• Short-term (grommet): e.g., Shah, Shepard - lasts 6-12 months; extruded spontaneously
• Long-term (T-tube / Goode): retained for several years; used for recurrent OME or when short-term tubes are insufficient; requires surgical removal

• Immediate resolution of effusion and hearing improvement in virtually all cases
• TM perforation closure rates: 60-90% after tympanoplasty (if persistent perforation after tube extrusion)
• TM closure rates are NOT increased by concomitant mastoidectomy

• Persistent TM perforation after extrusion (~2%)
• Tympanosclerosis
• Tube otorrhoea (treat with topical fluoroquinolone drops)
• Tube blockage or early extrusion

4. Adenoidectomy

• Indicated in children ≥4 years with OME, especially when adenoid hypertrophy is present
• Reduces OME recurrence by decreasing the nasopharyngeal reservoir of otopathogens
• Often combined with grommet insertion

Prevention

OME in Special Populations

Down Syndrome

• Very high risk of OME due to hypotonia of palatal muscles, small nasopharynx, and ET anomalies
• Examination often difficult (narrow EACs, uncooperative patient); ABR under GA sometimes needed
• Ventilation tube insertion is commonly required but controversial due to increased complications

Cleft Palate

• Near-universal OME due to abnormal levator veli palatini and tensor veli palatini muscle function → ET dysfunction
• Bilateral grommets at time of palate repair is standard practice in many centres

Adults with OME

• Less common than in children
• Always exclude nasopharyngeal carcinoma (NPC) - particularly in unilateral OME, especially in adults of Chinese/Southeast Asian descent
• Also consider: post-radiotherapy ET dysfunction, Eustachian tube dysfunction, barotrauma

Key Points Summary

• OME = non-purulent middle ear effusion with intact TM and no acute infection = secretory otitis media = glue ear
• Most common cause of conductive hearing loss in children; peak at 1 year of age
• Driven by ET dysfunction + biofilm-mediated chronic inflammation; bacteria not culturable by standard methods
• Cardinal feature: fluctuating CHL + immobile TM on pneumatic otoscopy + Type B tympanogram
• Natural history: 50% resolve within 12 weeks - observe before intervening
• Surgery: myringotomy + grommet insertion restores hearing immediately; most common elective paediatric surgery
• Unilateral OME in an adult = exclude nasopharyngeal carcinoma
• Long-term untreated OME causes speech/language delay, learning difficulties, TM retraction, cholesteatoma

• Shambaugh Surgery of the Ear, pp. 451-452
• Cummings Otolaryngology Head and Neck Surgery, pp. 3755, 3767-3772
• KJ Lee's Essential Otolaryngology
• Bailey and Love's Short Practice of Surgery, p. 778
• Scott-Brown's Otorhinolaryngology Head & Neck Surgery Vol. 2