Acute inflammation of the middle ear. Mastoiditis. Chronic inflammation of the middle ear (mesotympanitis. epitympanitis)

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Ear Infections: Acute Otitis Media, Mastoiditis, and Chronic Otitis Media


I. Acute Otitis Media (AOM)

Definition & Epidemiology

AOM is a bacterial/viral infection of the middle ear characterized by the presence of a middle ear effusion with signs and symptoms of acute infection. It is the most common bacterial disease of childhood (80% of children aged 1–6 years experience at least one episode) and the leading driver of pediatric antibiotic prescriptions in the United States. Peak incidence is between 6–15 months of age.
Risk factors: daycare attendance, male sex, parental smoking, pacifier/bottle use, family history of recurrent OM, cleft palate, Down syndrome. Breastfeeding is protective.
Rosen's Emergency Medicine, p. 908

Pathophysiology

The fundamental mechanism is Eustachian tube dysfunction:
  1. Viral URI causes Eustachian tube inflammation → mechanical or functional obstruction
  2. Negative middle ear pressure develops → fluid accumulates
  3. Nasopharyngeal bacteria enter the middle ear cavity → inflammation, pus, increased pressure
AOM is commonly a co-infection: viruses are isolated from middle ear aspirates in ~70% of cases.
Common bacterial pathogens:
  • Streptococcus pneumoniae (most virulent; commonest cause)
  • Haemophilus influenzae (non-typeable; increasing in frequency post-pneumococcal vaccination)
  • Moraxella catarrhalis
  • Rarer: S. pyogenes, S. aureus, Mycobacterium tuberculosis, gram-negatives
  • In neonates: additionally Group B Streptococcus and gram-negatives
Rosen's Emergency Medicine, p. 908–909

Clinical Features

  • Otalgia (most important symptom — unilateral or bilateral)
  • Fever, irritability, pulling at ears (non-specific in children)
  • Otoscopy: erythematous, bulging tympanic membrane (TM) with decreased mobility (by pneumatic otoscopy) — the hallmark finding
  • Bullous myringitis (bullae on TM) may be seen; treatment is the same as standard AOM
  • Middle ear effusion present
  • Conductive hearing loss
Examination of the TM is essential — no constellation of symptoms alone reliably predicts AOM.

Management

"Watch and wait" (observation): Appropriate for selected children ≥2 years with mild symptoms for 2–3 days before prescribing antibiotics. Not validated in adults (antibiotics recommended for all adults).
Antibiotic therapy:
ScenarioFirst-line
Standard AOM, no PCN allergyAmoxicillin 80–90 mg/kg/day ÷ BID
AOM within 30 days / concurrent conjunctivitis / β-lactamase coverage neededAmoxicillin-clavulanate 90 mg/kg/day
Non-severe PCN allergyCefdinir, cefuroxime, cefpodoxime, or ceftriaxone IM
Severe PCN allergyAzithromycin or clindamycin (less coverage)
Treatment failure at 3 daysAmoxicillin-clavulanate or IM ceftriaxone × 3 days
Duration: 10 days for children <2 years, TM perforation, or chronic/recurrent disease; shorter courses acceptable in mild cases in older children.
Analgesia: NSAIDs (ibuprofen) or acetaminophen — antibiotics do NOT provide pain relief in the first 24 hours.
AOM with perforation: Treat identically to AOM without perforation; small perforations typically heal spontaneously.
AOM with tympanostomy tubes: Ototopical fluoroquinolone drops (e.g., ofloxacin, ciprofloxacin/dexamethasone) — not aminoglycosides (ototoxic with non-intact TM).
Rosen's Emergency Medicine, p. 909–910

Complications of AOM

  • Persistent otitis media with effusion (OME) — leading cause of childhood hearing loss
  • Acute mastoiditis (most common suppurative complication)
  • TM perforation, ossicular erosion, tympanosclerosis
  • Petrous apicitis (Gradenigo's syndrome)
  • Facial nerve palsy
  • Labyrinthitis
  • Intracranial extension (meningitis, brain abscess, lateral sinus thrombosis)
Cummings Otolaryngology, p. 2681–2682

II. Mastoiditis

Definition & Pathogenesis

Mastoiditis is inflammation of the mastoid air cells and the most common suppurative complication of AOM, though its incidence has fallen dramatically with antibiotic use. It may occur with or without a known preceding AOM episode.
Anatomic basis: The middle ear communicates with the mastoid air cells via the aditus ad antrum — a narrow passage. If this becomes obstructed:
  • Pus accumulates in a closed space
  • Infection spreads via venous channels → periosteal inflammation
  • Destruction of bony trabeculae → coalescent mastoiditis (acute mastoid osteitis)
  • Subperiosteal abscess may form, pushing the auricle anteroinferiorly
Pathogens:
  • Streptococcus pneumoniae (leading cause)
  • Group A Streptococcus
  • P. aeruginosa, S. aureus, Fusobacterium necrophorum (particularly after prior antibiotic use)
Rosen's Emergency Medicine, p. 910–912

Clinical Features

  • Fever, headache, otalgia, hearing loss
  • Postauricular erythema, edema, and tenderness (classic)
  • Protrusion (displacement) of the auricle anteroinferiorly — highly characteristic
  • Abnormal TM (erythema, bulging) — may be normal in ~10% of cases
  • Symptoms of AOM lasting >2 weeks should raise suspicion

Differential Diagnosis

  • Severe AOM / otitis externa
  • Skull fracture
  • Posterior auricular lymphadenitis
  • Deep space neck infection (Box 58.4)

Investigations

  • Clinical diagnosis is possible with classic findings
  • CT scan of temporal bones: indicated when neurologic symptoms suggest intracranial spread, or failure to improve with conservative therapy. Shows opacification of mastoid air cells, bony destruction (coalescence), subperiosteal abscess
CT Scan of Mastoiditis — axial image showing opacification of the left mastoid air cells (arrow) with loss of normal trabecular pattern
CT scan demonstrating acute mastoiditis. — Rosen's Emergency Medicine, Fig. 58.1

Management

Hospitalization required for IV antibiotics.
ScenarioAntibiotic
No recent AOM or antibioticsVancomycin 15 mg/kg IV
Recent AOM (within 6 months) or prior antibioticsVancomycin + anti-pseudomonal agent (e.g., cefepime 50 mg/kg IV in children; 2 g IV in adults)
Surgical options (determined with ENT):
  • Myringotomy ± tympanostomy tube placement (to drain middle ear)
  • Mastoidectomy for coalescent mastoiditis, subperiosteal abscess, or failure of medical therapy
Early ENT referral is mandatory.
Complications of untreated mastoiditis: subperiosteal abscess, Bezold's abscess (spread along sternocleidomastoid), petrous apicitis, sigmoid sinus thrombosis, meningitis, subdural empyema, brain abscess.
Rosen's Emergency Medicine, p. 912–913

III. Chronic Otitis Media (COM)

Chronic otitis media encompasses prolonged inflammatory disease of the middle ear and mastoid, classified into two main forms based on the location of TM involvement:

A. Mesotympanitis (Tubotympanic Disease / "Safe" COM)

Definition: Chronic inflammation involving the central (pars tensa) portion of the TM with a central perforation. This form does not involve the attic and is considered "safe" because it carries a much lower risk of serious complications.
Features:
  • Central TM perforation (pars tensa), with intact annulus
  • Persistent or recurrent mucoid/mucopurulent otorrhea through the perforation
  • Conductive hearing loss proportional to perforation size and ossicular involvement
  • Mucosa of the middle ear is inflamed (granulation tissue in 97% of operated cases — Cummings, Table 140.3)
  • No cholesteatoma (distinguishes it from epitympanitis)
Bacterial pathogens in chronic otorrhea:
  • P. aeruginosa (most common in chronic disease)
  • S. aureus
  • Gram-negative rods
  • Anaerobes in long-standing cases
Pathology (temporal bone findings with perforated TM):
  • Granulation tissue: 97.4%
  • Ossicular changes: 90.5%
  • Tympanosclerosis: 19.8%
  • Cholesterol granuloma: 12.1%
  • Cholesteatoma: 4.3%
Treatment:
  • Conservative (dry ear): Aural toilet, topical quinolone drops (e.g., ofloxacin — avoids ototoxicity risk of aminoglycosides)
  • Systemic antibiotics for acute exacerbations guided by culture
  • Surgery (tympanoplasty / myringoplasty): TM repair once ear is dry; ossiculoplasty if ossicular chain is disrupted. Goal: eliminate infection, restore hearing, prevent recurrence
Cummings Otolaryngology, p. 2683–2685

B. Epitympanitis (Atticoantral Disease / "Unsafe" COM)

Definition: Chronic inflammation involving the pars flaccida (attic) or pars tensa posterior-superior quadrant, characteristically associated with a marginal (attic/retraction pocket) perforation and cholesteatoma formation. This form is "unsafe" due to the risk of bone erosion and serious complications.
Cholesteatoma — central to epitympanitis:
A cholesteatoma is an epidermal inclusion cyst of the middle ear or mastoid, filled with keratinous debris. Classified as:
  • Congenital: develops behind an intact TM from embryonic epithelial rests
  • Acquired (primary): most common — a retraction pocket in the pars flaccida or posterosuperior pars tensa deepens due to Eustachian tube dysfunction, accumulates keratin, and forms a cyst
  • Acquired (secondary): keratinizing epithelium migrates through a pre-existing TM perforation
Mechanism of bone erosion:
  • Osteoclastic activity driven by inflammatory cytokines, pressure, keratin, bacterial toxins
  • The attic communicates with the antrum only through two narrow openings (between the tensor tympani tendon and stapes; and between the short process of incus and stapedial tendon) — blockage by edema/granulation tissue promotes chronic infection and bone erosion
Cummings Otolaryngology, p. 2685–2690
Clinical features of epitympanitis:
  • Attic (marginal/posterosuperior) perforation of TM
  • Scanty, foul-smelling otorrhea (keratin debris; typically less profuse than mesotympanitis)
  • Conductive hearing loss
  • Otoscopy: white pearly debris or crusting in the attic area (Shrapnell's membrane region)
  • Aural polyp may protrude through the perforation
  • Potential for serious complications due to bone erosion
Complications specific to epitympanitis/cholesteatoma:
  • Ossicular erosion → conductive hearing loss
  • Labyrinthine fistula → sensorineural hearing loss, vertigo
  • Facial nerve canal erosion → facial palsy
  • Tegmen erosion → meningitis, brain abscess
  • Sigmoid sinus erosion → lateral sinus thrombosis
  • Petrous apicitis (Gradenigo's syndrome: trigeminal pain, abducens palsy, otorrhea)
Treatment:
  • Surgery is mandatory — cholesteatoma cannot be eradicated medically
  • Canal wall up (CWU) tympanomastoidectomy: preserves the posterior canal wall; better hearing outcome; requires "second-look" surgery at 12 months to check for residual cholesteatoma
  • Canal wall down (CWD) mastoidectomy / modified radical mastoidectomy: removes the posterior canal wall, creating an open mastoid cavity; better visualization and lower recurrence, but creates a permanent "mastoid bowl" requiring lifelong care
Cummings Otolaryngology, p. 2690–2695

Summary Comparison

FeatureAOMMastoiditisMesotympanitisEpitympanitis
DurationAcuteAcute complicationChronicChronic
TM findingBulging, intactBulging/abnormalCentral perforationAttic/marginal perforation
CholesteatomaNoNoNoYes
OtorrheaNone/after ruptureNone/with AOMMucoid, profuseScanty, fetid
Bone destructionNoMastoid trabeculaeUncommonCharacteristic
Risk of complicationsLow-moderateModerateLow ("safe")High ("unsafe")
Primary treatmentAntibioticsIV antibiotics ± surgeryTopical Abx ± tympanoplastySurgery mandatory

Sources: Rosen's Emergency Medicine: Concepts and Clinical Practice; Cummings Otolaryngology: Head and Neck Surgery

Acute inflammation of the middle ear. Mastoiditis. Chronic inflammation of the middle ear (mesotympanitis. epitympanitis)

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Middle Ear Infections: Acute Otitis Media, Mastoiditis, and Chronic Otitis Media


I. Acute Otitis Media (AOM)

Definition & Epidemiology

AOM is a bacterial infection of the middle ear space characterized by vascular dilation, mucosal edema, exudation, bacterial proliferation, white blood cell infiltration, and pus formation. It arises de novo in a previously normal middle ear — this distinction from acute exacerbations of chronic disease is important because bacteriology, treatment, and complication patterns differ.
AOM is the most common bacterial infection of childhood: ~85% of children have at least one episode. Peak incidence is at 6–24 months of age. By age 6, approximately 60% of children will have had at least one episode. It is the primary driver of pediatric antibiotic prescriptions.
Predisposing factors: young age, male sex, bottle-feeding, daycare attendance, crowded living conditions, parental smoking, cleft palate, Down syndrome, cystic fibrosis, ciliary dyskinesia, immunodeficiency. Breastfeeding is protective.
Cummings Otolaryngology, p. 2702; Harrison's Principles of Internal Medicine 22E, p. 297

Pathophysiology

A viral upper respiratory infection causes Eustachian tube inflammation and obstruction → negative middle ear pressure → fluid accumulation → bacteria ascend from the nasopharynx → suppurative infection. Viruses are co-isolated from middle ear aspirates in ~70% of AOM cases. The Eustachian tube is shorter, more horizontal, and more prone to dysfunction in infants, explaining peak childhood incidence.
Causative bacteria (roughly by frequency):
OrganismNotes
Streptococcus pneumoniae~30–50%; most virulent; most common in mastoiditis
Haemophilus influenzae (non-typeable)~20–45%; increasing post-PCV13; β-lactamase in 33–50%
Moraxella catarrhalis~10%; >90% β-lactamase-producing
S. pyogenes, S. aureusLess common but important in neonates and complications
Gram-negatives, Group B StrepNeonatal AOM specifically
Despite routine pneumococcal conjugate vaccination, S. pneumoniae remains one of the most commonly isolated pathogens.
Cummings Otolaryngology, p. 2702–2703; Harrison's 22E, p. 297

Clinical Features

  • Otalgia — the cardinal symptom (unilateral or bilateral)
  • Fever, irritability, poor feeding, ear-pulling (nonspecific in infants)
  • Otoscopy (essential for diagnosis):
    • Bulging, erythematous, opacified tympanic membrane (TM)
    • Obscured bony landmarks
    • Absent or reduced TM mobility on pneumatic otoscopy — the most reliable sign
  • Conductive hearing loss
  • Severe AOM criteria: otalgia ≥48 hours, temperature >39°C (102.2°F), moderate-to-severe bulging of TM
AOM should not be diagnosed without evidence of middle ear effusion. Bullae on the TM (bullous myringitis) may occur; treatment is identical.
Harrison's 22E, p. 297–298

Management

Analgesia first: NSAIDs (ibuprofen) or acetaminophen for pain relief. Topical benzocaine or lidocaine may provide brief added relief. Antibiotics do NOT relieve pain in the first 24 hours.
Observation vs. antibiotics: Up to 80% of cases resolve without antibiotics. Watchful waiting (48–72 hrs) is appropriate for:
  • Children ≥6 months with mild, unilateral AOM
  • Children ≥2 years with nonsevere symptoms
Antibiotics are indicated immediately for:
  • Age <6 months (all cases)
  • Bilateral AOM in children 6–24 months
  • AOM with otorrhea (any age >6 months)
  • Severe otalgia, fever >39°C, or symptoms >48 hours (any age)
  • Adults: treat all with antibiotics
Antibiotic regimens:
SituationRegimen
First-line (no PCN allergy)Amoxicillin 80–90 mg/kg/day ÷ BID (max 3 g/day)
Prior amoxicillin in 30 days / concurrent conjunctivitis / β-lactamase coverageAmoxicillin-clavulanate 90/6.4 mg/kg/day ÷ TID
Non-severe PCN allergyCefdinir, cefuroxime, cefpodoxime, or ceftriaxone IM
Treatment failure at 3 daysAmoxicillin-clavulanate or IM ceftriaxone × 3 days
AOM with tympanostomy tubesOtotopical fluoroquinolone drops (e.g., ofloxacin) — aminoglycosides are ototoxic through non-intact TM
Duration: 10 days for children <2 years, TM perforation, or severe/recurrent disease; 5–7 days for milder cases in older children.
The number needed to treat to prevent one case of mastoiditis is approximately 5,000 — antibiotics provide modest benefit but are warranted in higher-risk patients.
Harrison's 22E, p. 297–298; K.J. Lee's Essential Otolaryngology, p. 216

II. Mastoiditis

Definition & Pathogenesis

Mastoiditis is inflammation of the mastoid air cells and is the most common suppurative (extracranial) complication of AOM. Its incidence has fallen sharply with antibiotics but it remains the most feared acute complication. It can occur without preceding clinically apparent AOM, and in older children with acute mastoiditis, an underlying cholesteatoma should be suspected.
Anatomic key: The middle ear communicates with the mastoid via the aditus ad antrum — a narrow passage. Obstruction creates a closed-space infection:
  1. Incipient mastoiditis — fluid fills mastoid cells, no bony destruction yet
  2. Coalescent mastoiditis (acute mastoid osteitis) — progressive demineralization and destruction of bony septa between air cells → coalescence into a single cavity
  3. Subperiosteal abscess — infection spreads through the mastoid cortex to the subperiosteal space, displacing the auricle
Infection can also spread via venous channels from mastoid veins. In infants, open cribriform channels near the spine of Henle allow direct passage to the subperiosteal space before bony fusion.
Pathogens: S. pneumoniae (leading cause), S. pyogenes, H. influenzae, S. aureus (including MRSA), P. aeruginosa (especially after prior antibiotic use), Fusobacterium necrophorum.
Cummings Otolaryngology, p. 2703; Harrison's 22E, p. 298

Clinical Features

  • Fever, otalgia, hearing loss, headache
  • Postauricular erythema, tenderness, and swelling — most consistent finding
  • Protrusion of the auricle downward and laterally — due to abscess displacing the upper mastoid → highly characteristic
  • TM typically shows AOM changes (bulging, erythema); may be normal in ~10%
  • Superoposterior protrusion of the posterior bony canal wall on otoscopy
  • Symptoms of AOM persisting >2 weeks should raise suspicion
Postauricular abscess with coalescent mastoiditis in an infant — the left auricle is displaced laterally and inferiorly
Fig. 141.4 Postauricular abscess associated with coalescent mastoiditis. Auricle is displaced laterally and inferiorly. — Cummings Otolaryngology

Masked Mastoiditis

A distinct variant where chronic granulation and bone erosion occur without otorrhea and with a near-normal TM — typically in patients receiving repeated antibiotic courses that partially suppress (but do not eliminate) the mastoid infection. Presents with chronic postauricular pain and mastoid tenderness. CT shows a localized area of mastoid opacification. Treatment is surgical.

Investigations

  • Clinical diagnosis is sufficient with classic findings
  • CT temporal bones (HRCT): Indicated for neurologic symptoms, failure to improve, or uncertain diagnosis. Shows:
    • Opacification of mastoid air cells
    • Loss/destruction of bony septa (coalescence)
    • Subperiosteal abscess
    • Erosion of tegmen, sigmoid sinus plate, labyrinth
    • Sensitivity 97%, positive predictive value 94% for AOM complications
  • MRI with gadolinium: Preferred for intracranial complications (meningitis, brain abscess, sigmoid sinus thrombosis) — better soft tissue detail
Axial temporal bone CT — opacification of the middle ear (white arrow) and mastoid (black arrow)
Fig. 141.3 CT scan: opacification of middle ear (white arrow) and mastoid (black arrow). — Cummings Otolaryngology

Management

Hospitalization and IV antibiotics are required for all patients.
PatientAntibiotic
No recent AOM / no prior antibioticsVancomycin 15 mg/kg IV (covers resistant S. pneumoniae and MRSA)
Recurrent AOM or prior antibiotic useVancomycin + anti-pseudomonal agent (cefepime 50 mg/kg IV in children; 2 g IV in adults; or ceftazidime)
IV therapy for 7–10 days, then complete a 4-week oral antibiotic course. Culture from myringotomy/abscess drainage guides de-escalation.
Surgical management (ENT referral essential):
  • Myringotomy ± tympanostomy tube: First step — decompresses middle ear, provides culture material
  • Mastoidectomy: If no improvement within 48 hours of IV antibiotics, coalescent mastoiditis confirmed on CT, or complications present
  • Abscess drainage: Subperiosteal or Bezold's abscess requires direct surgical drainage

Complications (Box 141.1)

ExtracranialIntracranial
Coalescent mastoiditisMeningitis
Subperiosteal abscessBrain abscess
Bezold's abscess (tracks along sternocleidomastoid)Epidural abscess
Temporal/zygomaticroot abscessSubdural empyema
Petrous apicitis (Gradenigo's syndrome)Lateral sinus thrombosis
Labyrinthine fistulaOtitic hydrocephalus
Facial nerve paralysis
Acute suppurative labyrinthitis
Cummings Otolaryngology, p. 2703–2715; Harrison's 22E, p. 298–299

III. Chronic Otitis Media (COM)

Definition: COM reflects inflammation and infection of the middle ear and mastoid persisting longer than 3 weeks (the usual resolution time of AOM in a previously healthy ear). COM can occur with or without cholesteatoma, and a third form occurs in children with patent tympanostomy tubes.
When infection does not resolve, mucosal edema and exudation increase, mucous glands proliferate, and blockage of the aditus/epitympanum prevents drainage of the antrum and mastoid, leading to "irreversible" mucosal and bony changes.
COM is divided into two clinical forms based on TM involvement:

A. Mesotympanitis (Tubotympanic COM / "Safe" Disease)

Location: Central/pars tensa of the TM.
Defining feature: A central (safe) perforation of the TM — the annulus fibrosus remains intact. Because the perforation is away from the attic, it does not carry the same risk of cholesteatoma formation as attic disease.
Pathological findings (temporal bone histopathology with perforated TM):
FindingFrequency
Granulation tissue97.4%
Ossicular changes90.5%
Tympanosclerosis19.8%
Cholesterol granuloma12.1%
Cholesteatoma4.3%
Data: da Costa et al., Laryngoscope 102:1229, 1992 — cited in Cummings Otolaryngology
Clinical features:
  • Persistent or intermittent otorrhea — mucoid or mucopurulent, typically odourless or mildly malodorous, often profuse
  • Central TM perforation visible on otoscopy
  • Conductive hearing loss — proportional to perforation size and ossicular involvement
  • Recurrent episodes often triggered by upper respiratory infections (water entering through the perforation)
  • Middle ear mucosa appears thickened, edematous, with granulation tissue
Bacteriology in chronic otorrhea:
  • Pseudomonas aeruginosa (most common in chronic disease)
  • Staphylococcus aureus
  • Mixed gram-negatives, anaerobes
  • Biofilms are common and contribute to antibiotic resistance
Treatment:
  1. Aural toilet — meticulous cleaning (microsuction) to remove debris and secretions
  2. Topical therapy: Fluoroquinolone ear drops (ciprofloxacin/dexamethasone, ofloxacin) — avoid aminoglycosides due to ototoxicity risk through perforated TM; acetic acid/alcohol solutions have antiseptic utility
  3. Systemic antibiotics for acute exacerbations guided by culture/sensitivity
  4. Surgery (definitive): Tympanoplasty (myringoplasty) once the ear is dry — to close the perforation and restore the sound-conducting mechanism. Ossiculoplasty if the ossicular chain is disrupted. Goal: dry ear, hearing rehabilitation, prevention of recurrence.

B. Epitympanitis (Atticoantral COM / "Unsafe" Disease)

Location: Pars flaccida (Shrapnell's membrane) or posterosuperior pars tensa — the attic (epitympanum).
Defining feature: An attic (marginal) perforation or retraction pocket, invariably associated with cholesteatoma — which is the key feature distinguishing this form and making it "unsafe."

Cholesteatoma

A cholesteatoma is an epidermal inclusion cyst of the middle ear or mastoid filled with desquamating keratin debris. Classified as:
  • Congenital: Develops behind an intact TM from embryonic epithelial rests; found in children
  • Primary acquired (most common): A retraction pocket in the pars flaccida deepens progressively due to chronic Eustachian tube dysfunction and negative middle ear pressure. Keratin accumulates, and the self-cleaning mechanism of the skin fails, creating an expanding cyst
  • Secondary acquired: Keratinizing squamous epithelium migrates through an existing TM perforation (typically in mesotympanitis), invades the middle ear/mastoid, and forms a cholesteatoma
Why cholesteatoma erodes bone: The attic communicates with the mastoid antrum through only two constant narrow openings (between the tensor tympani tendon and the stapes; and between the short process of the incus and the stapedial tendon). Edema/granulation tissue blocks these, causing persistent infection. Bone erosion is driven by:
  • Osteoclastic activation by inflammatory cytokines (IL-1, TNF-α), localized pressure, keratin, bacterial toxins
  • Fibroblasts in the subepithelium with invasive phenotype
Cummings Otolaryngology, p. 2685–2690
Clinical features of epitympanitis:
  • Attic/marginal or posterosuperior perforation on otoscopy — white pearly debris, crust, or granulation in the attic (Shrapnell's membrane area)
  • Scanty but foul-smelling (fetid) otorrhea — keratin debris; less voluminous than mesotympanitis
  • Conductive hearing loss (progressive with ossicular erosion)
  • Aural polyp may prolapse through the perforation
  • High risk of serious complications from bone destruction
Complications specific to epitympanitis/cholesteatoma:
  • Ossicular erosion → conductive hearing loss (incus long process most commonly eroded)
  • Labyrinthine fistula (most often horizontal SCC) → sensorineural hearing loss, vertigo; positive fistula test (Hennebert's sign)
  • Facial nerve canal erosion → peripheral facial palsy
  • Tegmen plate erosion → meningitis, brain abscess, CSF otorrhea
  • Sigmoid sinus erosion → lateral sinus thrombosis
  • Petrous apicitis → Gradenigo's syndrome (trigeminal pain, abducens palsy, otorrhea)
Investigations:
  • High-resolution CT temporal bones: Reveals the extent of cholesteatoma, ossicular chain erosion, tegmen/sigmoid sinus/labyrinthine erosion. Guides surgical planning.
  • MRI (non-EPI DWI): Diffusion-weighted MRI is now the gold standard for detecting residual/recurrent cholesteatoma post-surgery without the need for a "second-look" operation.
Treatment — Surgery is mandatory: Cholesteatoma cannot be eradicated by medical therapy alone.
TechniqueDescriptionAdvantage/Disadvantage
Canal wall-up (CWU) tympanomastoidectomyRemoves disease while preserving posterior canal wallBetter hearing; more physiological; requires second-look at 12 months to detect residual disease
Canal wall-down (CWD) / modified radical mastoidectomyRemoves posterior canal wall, creating open mastoid cavityLower recurrence risk; better visualization; permanent mastoid bowl requires lifelong aural toilet
Radical mastoidectomyExenteration of all middle ear contentsReserved for extensive disease/complications; abolishes hearing
Labyrinthine fistula at surgery: the cholesteatoma matrix is carefully peeled from the endosteum under high magnification; the fistula site is addressed last and covered with fascia/bone.

Summary Comparison

FeatureAcute Otitis MediaMastoiditisMesotympanitisEpitympanitis
NatureAcuteAcute complicationChronicChronic
TM findingBulging, intact, erythematousBulging / abnormalCentral perforation (pars tensa)Attic / marginal perforation (pars flaccida)
OtorrheaNone (unless TM ruptures)With AOM or absentMucoid, profuse, odourlessScanty, fetid (keratin)
CholesteatomaNoNoNo (rarely)Yes — defining feature
Bone destructionNoMastoid trabeculaeUncommonCharacteristic, progressive
Safety classification"Safe""Unsafe"
Hearing lossMild conductive (effusion)ConductiveConductiveConductive → sensorineural
Complication riskLow-moderateModerate-highLowHigh
Primary treatmentAntibiotics ± observationIV antibiotics + surgeryAural toilet + topical Abx ± tympanoplastySurgery mandatory

Sources: Cummings Otolaryngology: Head and Neck Surgery, 7th ed. — K.J. Lee's Essential Otolaryngology, 11th ed. — Harrison's Principles of Internal Medicine, 22nd ed.
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