-infection complications of otitis media include:

acute perforation, OME with effusion, adhesive otitis media,

acute & chronic mastoiditis, petrositis, labyrinthitis,

facial paralysis and intracrania infection

-noninfectious sequelae:

chronic perforation, ossicular erosion, middle ear atelectasis,

labyrinthine erosion, and tympanosclerosis, cholesteatoma, SNHL


- 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 as compared to normal children. -Two suggestions to explain this:

(1)"hereditary theory"Þ kids with hypoaeration of mastoid are prone to OME (Diamant, ‘40)

(2)"environmental theory"Þ chronic OMEÞ mastoid hypopneumatization (Wittmaak,’18) - there is evidence that chronic inflammation Þ new bone


-Middle ear atelectasis results from long-standing ET dysfn.

-TM becomes retracted onto promontory & ossicies of mid ear, but is not adherent to medial

wall of middle ear, and mucosal lining of the middle ear is intact.

-Adhesive otitis media, (in contrast) exists when mid ear space is

totally obliterated & TM is adherent to the ossicles & promontory,

mucosal surfaces are not present.

-Retraction of TM may Þ erosion of long process of incus & stapes SS

-Mechn: ?? rptd bouts of AOM Þ weakening & thinning TM Þ atelectasis. Sade & Berco (1976) Þ destruction of collagen-containing fibrous layer TM in some ears with

recurrent infection.

NB: collagen destruction within TM may Þ 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 Flacida (or attic retraction pockets)....(after Tos 1988)....

Grade I: Pars Flacida not in contact with malleus head.

Grade II: Pars Flacida in contact with malleus head

Grade III: Limited outer attic wall erosion.

Grade IV: Severe outer attic wall erosion

NB: Wullstein's five tympanoplasty techniques....

Type 1: reconstruction of TM (ossicular chain intact and mobile).

Type 2: malleus handle absent, reconstructn of TM over malleus remnant & long process of incus

Type 3: malleus & incus absent, reconstruction of TM over an intact and mobile stapes

(myringostapediopexy) with stapes acting as a columella

Type 4: mobile stapes footplate exteriorized with reconstruction of TM as a RW baffle.

Type 5: stapes fixed, Þ 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 the pars

tensa or pars flaccida


-Aural cholesteatomas defn:

-epidermal inclusion cysts of the middle ear or mastoid.

-a misnomer, does not contain cholesterol;

-contain desquamated keratin

-first described by Cruveilhier (1829)

-may be congenital or acquired.

- Acquired consequence of OME or AOM or both.


-made on otoscopic examination or surgical exploration.

-imaging CT used to

Fagan lists 5 following:

-revision sx

-only hearing ear

-any compln exists... I/C, VII, labyrinthine

-cant see fundus of canal

-??avoid Sx

-complement the clinical examination.

-operative planning

-symptoms; some asymptomatic, others get infected & Þ bone dest’n.

-some present with slowly progressive CHL

-most have chronic otitis with purulent otorrhea (often malodorous b/c of frequent inftn with

anaerobic bacteria)

-occasionally misdiagnosed as having external otitis.

-signs & symptoms of sequelae of cholesteatoma:

-vertigo, hearing loss caused by a labyrinthine fistula,

-facial nerve paralysis, or intracranial infection.

-otoscopic appearance:

-typical attic retraction cholesteatoma: a defect of variable size adjacent to postsup TM.

-If center of defect contains keratin debrisÞ 1ry acq’d cholestma.

-If keratin debris has migrated thru perf into ME Þ 2ry acq’d cholestma.

-If cholesteatomas appears behind or within an intact TMÞ cong cholst

-Infected cholesteatoma can present as an "aural polyp"; this is actually granulation tissue at junction b/w an eroding cholesteatoma & bone.

\ presence of an aural polyp in a chronically infected ear

Þ cholesteatoma until proven otherwise.


-Congenital cholesteatomas, by defn, arise from areas of keratinizing epithelium within ME cleft.

Michaels (1986) small area in anterior tympanum in developing fetus often contains a small

area of keratinizing epithelium.

-Acquired cholesteatoma

four basic theories of pathogenesis:

(1) invagination (retrcn pocket)

(2) basal cell byperplasia,

(3) migration (epithelial ingrowth thru perf)

(4) metaplasia of middle ear epithelium (Fig. 157-7).

Invagination theory ( Wittmaack, 1933)

-Retraction pockets of pars flaccida (less fibrous & less resistant), deepens b/c of neg ME press,

ET dysfn, OME & repeated inflammation.

-as retraction pocket deepens, desquamated keratin cannot be cleared Þ cholesteatoma

-so called primary acquired cholesteatoma

-otoscopically: see a defect in postsup quad of TM (marg perf) & erosion of adjacent canal wall.

Epithelial invasion theory (Habermann, 1889)

-keratinizing squ epith from surface of TM migrates into ME from a perf.

-Weiss (1958) showed epithelial cells migrating along surface by proces called contact guidance.

-when they encounter another epithelial surface Þ stop migrating, ie contact inhibition.

-?? in some TM perforations, inflammation damages inner mucosa allowing outer keratinizing

epithelium to migrate inward.

-Cholesteatoma after temp bone # may arise from this mechanism.

Basal cell hyperplasia theory Lange (1925)

-proposed that epith cells (prickle cells) of pars flaccida could invade basal lamina, then LProp

Þ by proliferating columns of epithelial cells.

-Ruedi (1959) supported this hypothesis with clinical & exp. evidence.

-Basal lamina disruptions have been documented in human & animal cholesteatomas.

-Huang (1988) and Masaki (1989) provided experimental support of this theory by demonstrating

that epithelial ingrowth from TM can be induced by instillation of propylene glycol into the

middle ear of chinchillas. These basal lamina breaks allow invasion of epith cones into

subepithelial CT & formation of microcholesteatomas.

-According to this theory, microcholesteatomas may enlarge and then perforate secondarily.

Squamous metaplasia theory Wendt (1873)

-squam/cuboidal epith of mid ear cleft can Þ metaplasia to keratz epith.

Clinically it appears that each of these pathogenic mechanisms accounts for a proportion of acquired cholesteatomas.

-Cholesteatomas are prone to recurrent infection,

-characteristically erode bone of ossicles & otic capsule.

-bacteriology of infected cholesteatomas :


Pseudomonasb aeruginosa (most common)

Pseudomonas fluorescens

Streptococcus spp.

Proteus spp.

Escherichia coli

Klebsiella- spp

Enterobacter- spp

Serratia spp.

Staphylococcus epidermidis

Staphylococcus aureus


Bacteroides (most common )


Peptostreptococcus spp

Propionibacterium acnes

Fusobacterium spp.

Bifidobacterium spp.

Clostridium spp.

Eubacterium spp.


-In some cases cholesteatom can be debrided of entrapped keratin by direct removal or irrigation. -Irrigatn with 1:1 distilled white vinegar & 70% isopropyl alcohol may keep some cholest’s stable

if their EAM opening is sufficiently large.



-Chronic otomastoiditis without cholesteatoma is marked by:

Þ presence of irreversible inflammatory changes within middle ear and mastoid.

-may occur in children with MEDITs.

-otorrhea may occur in 15% to 74% of children with MEDITs.

-common bacteria: Pseudomonas aeruginosa and Staphylococcus aureus. (esp in MEDITs)

-Aeration of ME, antrum, & mastoid depends on free movement of air from ET into mastoid.

-Proctor (1964): the middle ear is separated from antrum by ossicles & mucosal folds.

-only two constant openings:

(1) b/w tendon of tensor tympani muscle &stapes

(2) b/w short process of incus & stapedial tendon.

\ edema and inflammation with granulation tissue may block these.

-chronic obstruction of attic and antrum +/- infection Þ "irreversible" changes in mucosa & bone. -granulation tissue within the temporal bone can lead to bone erosion.


-Most infected perforations are treated conservatively with topical antibiotics.

- with or without hydrocortisone

-should cover, P. aeruginosa and S. aureus.

-cultures should be used to adjust antibiotics.

-irrigation of perft’d infected ear with dilute acidic solutn(eg,distilled vinegar & H2O, 1:1) is often effective in refractory cases.

-in powder form by insuflation (including boric acid, sulfa, chloramphenicol, & HC)

NB:aminoglycoside antibiotics and propylene glycol no conclusive evidence ototoxicity.

-Systemic antibiotics used in refractory cases when specific pathogens are found on culture.

-In repeatedly infected ears but clear between episodes, tympanoplasty should be considered. Ideally, ear with perfn should be free from infection for >3 mnths before tympanoplasty.

-in some cases, chronic infectn + otorrhea (without cholest) may persist.

-these cases (2 options):

-i. L/T IV Ab’s or

-ii. tympanomastoid surgery.

( goals include aeration of ME& mastoid, R/O irreversibe disease, closure of ME, & OCR.)

-Post-tympanostomy tube otorrhea:

- usually Rx’dt with top & system Ab’s

-If infection persists, Þ intravenous antibiotic therapy.

- in refractory cases (Gates 1988) may need R/O tube,


-abandonment of pressure necrosis theory since it is unlikely that cholest’s could exert pressure > capillary perfusion P (app 25 mm Hg).

-Current theory : multinucleatd osteoclasts release enzymes

Þ bone resorptn in cholest & COM

-enzymes include:

-acid phosphatase (Chole1984; Thomsen1975),

-collagenase (Abramson & Huang,1977; Moriyama 1987),

-acid proteases (Blair, 1986).

-Yuasa 1978 Þ acid pH of keratin debris in cholesteatomas

?Þ demineralization of hydroxyapatite of bone.

-Moriyama 1984: keratin itself may Þ inflammatory rxn (FB granuloma)

-Thomsen 1981 Þ bone resorption can occur in COM +/- cholest eatoma.

-Recent studies Þ pressure +/- inflamtn is sufficient to Þ bone resorption

-this press effect of cholest may Þ

-transient electrical potentials (Binderman 1984) and

-recruitment of monocytes into subepithelial space.

-monocytes Þ produce PgE2 (a stimulator of bone remodelling.)

-other osteoclast activating factors(eg IL-1, TNFa)

Complns of COM


-Paparella (1969) Þ SNHL in pts with COM.

(? 2ry to passage of toxic substances through RW membrane)

-Chole & Chin (1988) Þ loss of cochlear hair cell stereocilia in animals with experimental cholesteatomas with or without infection.

-Meyerhoff (1978) : 20% of temporal bones with COM had histologic evidence of labyrinthitis.



- Tympanosclerosis is a complication of otitis media in which acellular

hyalin & calcified deposits accumulate within TM & submucosa of ME. - clinically insignificant (most times) & Þ little or no hearing impairment.

-found in 20% of drumheads 6 to 8 years after MEDITs.


- hyalinization of subepithelial CT of TM & ME +/-calcifctn.

-Osteoneogenesis can also occur within these lesions.

\ can Þ ossicular fixtn(esp in attic associated with heads of M & I)

-when plaques occur in TM, they are limited to LP.

-Tympanosclerosis within middle ear (histologically <=> that in TM)

but Þ CHL due to ossicular fixation.


-a consequence of resolved otitis media or trauma.

-Wielinga (1988) Þ ET obstruction alone +/- infection Þ tympanosclerosis -?? autoimmune process occurring in TM.


-Sx removal, stapedectomy & total OCR Þ mixed results:

- Smyth (1982) Þ excellent hearing results in 80% of ears. -Gormley (1987) only 7% of pts ABG < 20 db.

NB !! -an earlier series (Smyth, 1972)

20% of 57 cases result in cochlear losses.

\ Tympanoplasty & OCR can be performed in tympanosclerosis,

but risks of cochlear damage are > in other middle ear diseases

b/c of extensive dissectn requ d & coexistence of labyrinth erosion


Part 1 Acute / Chronic / Masked mastoiditis

Part 2 Complications of mastoiditis

Part 3 Surgery of the mastoid


· The mastoid is one of five regions of pneumatization within the temporal bone.

· All regions contiguous, if one is involved, ALL variably involved (Schuknecht 1974).

The five regions are: (i) Middle ear region (iv)Petrous apex region

(ii) Mastoid region (v) Accessory region

(iii) Perilabyrinthine region

Mastoiditis an extension and part of the pathologic process of middle ear infection.


· Middle Ear Cleft: (i) Eustachian tube.

(ii) Middle ear (or tympanic cavity).

(iii) Aditus (which leads posteriorly to the antrum).

The Clinical importance of the mastoid is its relation to the:

· posterior and middle cranial sinuses. · Sigmoid and lateral sinuses.

· Facial nerve canals. · Semicircular canals.

· Petrous apex.

· the mastoid air cells are lined with modified respiratory epithelium, which is interconnected with the middle ear.

· At birth, the mastoid consists of a single cell (the antrum) connected to middle ear by a small channel (the aditus ad antrum).

· Mastoid pneumatization takes place soon after birth and is extensive by 2 years of age. May continue throughout life.


Acute Mastoiditis with periostitis

(I) Acute Mastoiditis

         Acute Coalescent Mastoiditis( Sx Mastoiditis )

(II) Chronic Mastoiditis

(III) Masked Mastoiditis ( or Latent, Atypical, Silent ).


· Acute Mastoiditis ( Bluestone and Klein, 1983):

* inflammation of : (i) mucosa & epithelium (ii) lamina propria.

· Acute Mastoiditis with periostitis :

* above with inflammation of periosteum.

· Acute Coalescent Mastoiditis :

* above with rarefying osteitis and bony destruction.

· Chronic Mastoiditis :

* invasion of bone by granulation tissue & features of chronic inflammation.

· Masked mastoiditis :

* a variant or subacute stage of acute mastoiditis (without osteitis)

a "cold" coalescence of air cells in an infection dampened down but

unextinguished by antibiotics.


(A) Incidence: - disease of childhood ( peaks at 6th year).

- "under-privileged", overcrowded areas.

(B) Pathophysiology

(i) Progressive inflammation & hyperaemic thickening of mucoperiostiumÞ periostitis.

(ii)Obstruct’n of aditus ad antrum ("bottleneck") B/W mastoid & middle ear.

(iii) Accumulation of serous then purulent exudates in the cells.

(iv) The accumulation of pus combines with the marked hyperaemia to cause:

(a) venous stasis

(b) local acidosis

(c) halisteresis (dissolution of calcium from adjacent bone wall)

(v) Demineralisation of cellular walls & bone necrosis due to pressure & ischaemia.

(vi) Osteoclastic reabsorption of bone.

(vii)Coalescence of adjacent walls and formation of abscess cavities.

Chronic mastoiditis with bone destruction:

-As discharge progresses from serous Þ mucinous Þ suppurative,

probability Ý that mucosa is being replaced by granulation tissue. -As suppuration Ý in quantity or duration, probability Ý that the granulation tissue is irreversibly infected.

-As purulent discharge becomes fetid, probability increases that anaerobic organisms exist, suggesting poor aeration and the possibility of osteitis and bone destruction.

- greater the duration of irreversible suppuration, greater probability for complication (Sheehy et al., 1977).


(i) Infection >10 days Þ inflammatory granulation tissue & hypertrophic osteitis develop.

(ii)Absorption and deposition cycles may be repeated Þ

a. sclerosis of cellular walls & reduction of the pneumatized cavity

b. columnar metaplasia, new gland formation & extensive mucus production.

(C) Bacteriology· (Same as otitis media)

· Streptococcus pneumoniae · Haemophilus influenzae

· Branhamella catarrhalis · Staphylococcus aureus

· Some anaerobes (Bacteroides).

(D) Clinical Features

(i) Pain · antrum (surface marked by MacEwan’s triangle)

· throbbing character

· radiation to neck/ lower jaw.

· as infection subsides, pain is first relieved.

(ii) Tenderness:

· AOM nearly always tender over the antrum ( MacEwens triangle ).

Þ tenderness over antrum is NOT an exclusive sign of mastoiditis.

· Mastoid tip, retroauricular groove or root of zygoma tenderness is significant.

(iii) Postauricular erythema & odema push pinna down & out.(esp subperiosteal abscess).

(iv) Deafness: · due to the "engorgement" (+/- TM thickening).

(v) Sagging of posterosuperior meatal wall (Imp sign)

NB: May be mistaken for odema of otitis externa

(vi) Tympanic membrane:

· abnormal ( ranging from fullness, thickening , perforation discharge).

(vii) Fever: - may be high in children & usually falls dramatically with A/B’s.

(NB: persistence or spikes with absence of other clinical features warrants Ix)

(viii) Toxicity and tachycardia: acute illness.

(ix) Symptoms and signs of the complications (later).


The diagnosis should be suspected clinically!

· FBC/ESR: - Neutrophilia & Elevated ESR.

(NB: May be normal in the "postantibiotic mastoid")

· Cultures from ear drainage: for MC&S

· Radiography

Plain X-rays: (i) haziness, distortion or destruction of the mastoid outline.

(ii) loss of sharpness of cellular wall shadows

(iii) increasing opacity due to effusion and thickened mucosa.

C.T: (i) confirm the diagnosis

(ii) determine to extent of the disease.

(F) Differential Diagnosis

· Furunculosis of EAM: - intense pain (worse on moving pinna) +/- D/C.

- usually little deafness - ~ (N) X-ray

· Lymphadenitis: - due to scalp lesions or suppurative lymphadenitis (eg. T.B.)

· Others: Mixed salivary tumours, Infected sebaceous cyst, fibrositis of SCM attachment.

(G) Management

· Dx of acute mastoiditis should be treated as a potential surgical emergency.

- Acute coalescent mastoiditis + subperiosteal abcess Þ complete transcortical mastoidectomy and a large myringotomy.

-Acute coalescent mastoiditis without a subperiosteal abscess, if mastoidectomy is not performed,

Þ careful, repeated clinical& radiographic evaluation is indicated, until it is absolutely certain that the ear and mastoid have returned to normal.

-My preference therefore is to treat every case of acute coalescent mastoiditis surgically.

-Chronic mastoiditis +/- bone destruction is treated exactly like chronic mastoiditis without bone

destruction  unless unusually extensive osteitis and osteomyelitis exist.

In that case, long-term parenteral antibiotics are used.

-this occurs with necrotizing, or "malignant," external otitis

-NB: that extensive necrotizing process can originate in ME vs ext ear.

· (a) Antibiotics:

*Aim to "cool-off" & extinguish infection ,(unless empyema/subperiosteal abscess)

· If uncomplicated, Strep. pneumoniae or H.Infl , Þ IV Ampicillin in high dosage.

· If infection > 2 weeks, cover S.aureas & other GNeg’s , initially with a penicillinase

resistant penicillin & aminoglysoside.

· (b) Surgical Rx

(i) Myringotomy: · drain & material for MC&S.

· Most uncomplicated mastoiditis resolves with myringotomy & A/B’s (Glascock)

(ii) Surgical drainage of mastoid

· Indications:

(a)Acute coalescent mastoiditis +/- empyema +/- subperiosteal abscess)

(b) Continued pain and tenderness > 2-3 days despite A/B & myringotomy

(c) Increasing constitutional signs (fever and PR)

(d) Copious pulsating discharge, rapidly filling meatus after mopping (e) Development of complication (eg. progressive deafness ,facial paralysis)

Two types of drainage

(i) Incision/drainage of acute infection(Schambaugh)& formal mastoidectomy later (ii) Others; a cortical mastoidectomy at first.


(A) Introduction: (i) Pneumatization nearly always absent or "faulty".

(ii) Is part of a process of chronic suppurative otitis media.

(B) Types: Three pathological types of disease (i) Cholesteatoma..

(ii) Granulation tissue with osteitis.

(iii) Cholesterol granuloma.

(i) Cholesteatoma

· "a misnomer", Keratoma is more appropriate.

· sac of keratinising squamous epithelium surrounded by granulation tissue

producing lysosomes => erode mastoid bone, eardrum, and ossicles.

· Pathogenesis (several theories)

(a) Congenital cholesteatoma: · from cell rests of keratinising epithelium

occurs in posterior fossa, temporal bone, and middle ear. (Michaels 1986)

(b) Invagination theory: (most widely accepted) (Wittmack,1933)

· Starts as retraction pocket post-sup segments & attic region (TM thin).

· As pocket develops, a sac with narrow neck forms =>dead squames trapped

(c) Epithelial invasion theory (Habermann 1889).Keratinising squamous epithelium

from TM surface invades or migrates into middle ear from a perforation.

(d) Basal cell hyperplasia theory.

(e) Metaplasia theory: (Resp epith to squamous)

· Microbiology · subject to recurrent infection

· Aerobes: Pseudomonas aeruginosa · Anaerobes: Bacteroides

Streptococcus species Peptococcus species.

(ii) Granulation tissue with osteitis

Definition: · Low grade osteitis. · May be local or diffuse.

Incidence: · 3 X’s Sx for this in the US (1978) Vs Cholesteatoma (Ruben 1982).

Pathogenesis: · irreversible inflammatory change in mucosa & bone (? mech).

· Super-imposed infections ( Pseudomonas and Staph. aureus )

(iii) Cholesterol granuloma

· Seen on own or in combination with cholesteatoma or granulations.

· Associated with marked bone destruction.

· Histologically: cholesterol crystals surrounded by FB giant cells & granulation tissue.

(C) Clinical Features

· Some assyptomatic

· Ottorhea: persistent / recurrent, usually purulent and foul smelling.

· Deafness: varies from trivial to severe because of involvement of ossicular chain.

· Bleeding from granulations or polyps.

· T.M. perforation: -usually marginal, ( polyps / granulations may protrude).

· Symptoms and signs of complications

NB: Diagnosis of cholesteatoma is made on otoscopic examination or surgical exploration.

(D) Investigations

· Plain x-rays: sclerotic mastoid (? role)

· C.T. and MRI: * suggests cholesteatoma * complements clinical examination.

* Useful for operative planning (esp. R/V surgery).

(E) Management

(i) Cholesteatoma

· can only be eradicated by surgical excision.

NB: Irrigation with 1:1 distilled white vinegar & 70% isopropyl alcohol may keep some stable.

(ii) Granulation tissue with osteitis

· Conservative Rx: *as for Chronic otitis media, (A/B’s; topical vinegar etc)

· Surgical Rx: aggressive local debridement in refractory cases.

(not always achieved in a single stage.)


( or latent/ silent/ atypical).


· an infection of the mastoid bone so modified by antibiotic therapy as to allow

steady progressive coalescence to continue without the warning signs and

symptoms previously recognised as indicative of this dangerous process.



· failed adequate A/B treatment, (esp. too short course Vs inadequate dose)

· results in development of resistant bacterial strains and persistent infection.


· Otitis media symptoms and signs, (very variable, but usually mild).

· Hx of recent acute otitis media Rx’d with A/B’s Þ ALARMS!

· Others: general malaise, anorexia, headache, mild mastoid tenderness,

conductive deafness (usually < 20dB), TM is usually thickened, or D/C.

· Others: no pain/ no D/C /no swelling / no fever / only mild tenderness but patient

does not feel well.

(NB: persistence of deafness is an important sign.)


: WCC:} may be (N) or ­ ’d

ESR: } may be (N) or ­ ’d

X-ray: opacity and haziness +/- bone destruction.

Nuclear Med: white cell (technetium) labelled scan will show infection in many cases.


(1) Admission and high dose IV A/B’s.

(2) Observe closely: Temp/ P.R./ general condition.

(3) If no early signs of improvement, or if any doubt Þ cortical mastoidectomy.


Cummings, C. Otolaryngology.  chapter 155

Gates Current Therapeutics

Scott Brown, , Otolaryngology

Schucknect, Pathology of the Ear