-OM: - most common disease of children,

- leading cause of hearing loss in children, and the

- most frequent indication for antimicrobial/surgical Rx in children. -costs of therapy over $1 billion expended each year US

more than I million operative procedures per yr in US

-85% of children experience at least one episode of OM

-causes of OM are multiple

-predisposing factors are:

-young age, maleness, bottle feeding, crowded living, heredity,

allergy, socioeconomic status, smoking by mother,

parental history of otitis media, viral infections at home,

-associated conditions (cleft palate, immunodef. ciliary dyskinesia,Down syndrome, &CF).

NB: less common in black (due to differences in size & angulation of ET

NB: birth wt not significant & breast feeding protective only until stopped



-OM: generic term for inflam’n within middle ear cleft behind intact TM

-Middle ear effusion (MEE) : generic term for liquid in middle ear cleft

regardless of etiology.

-Acute otitis media (AOM) : symptoms & signs of acute infection

(middle ear effusion with fever; pain; red, bulging TM).

-Chronic otitis media with effusion (OME) or "glue ear":

( <=>chronic secretory otitis media, chronic serous otitis media),

(middle ear effusion without pain, redness, or bulging TM)

- Others: chronic suppurative otitis media with:

-permanent perforation of TM or


Clinical and functional anatomy

-middle ear cleft: continuous space from nasopharyngeal orifice of ET to

the furthermost mastoid air cells.

-three main segments are :


-middle ear (tympanum);

-air cells of the mastoid, petrosa, and related areas.

-mucosal lining of middle ear cleft varies from

-thick,ciliated, respir. epth elium of ET & anterior tympanum to

-thin, featureless cuboidal epithelium in mastoid cells.

-middle ears of pts with OM=> hyperplasia & Ý in goblet cells Sade ‘66 NB: thought to predispose to formation of effusion.

-Tympanic mucous blanket is swept twd NPx by action of ciliated epth =>secretions/particles are cleared from mid.ear into NPx via ET


-normally closed to protect middle ear from entry of unwanted material

-opens with swallowing & other maneuvers due to TVP m contraction

=>equilibration of pressure in middle ear to ambient pressure

-three classic functions:

aeration, clearance, and protection of the middle ear.




-historically linked with abnormalities of eustachian tube function.


-early studies suggested obstruction(underaeration) of ET was the prob

-new work=>suggests failure of protection (abN patent or compliant ET) => bacteria enter ME

=> AOM

NB: Tubal obstruction with failure of clearance may be 2’ry rather than primary processes


-a bacterial disorder (majority)

Streptococcus pneumoniae

Haemophilus influenzae

Branhamella catarrhalis

Streptococcus pyogenes

Staphylococcus aureus

Staphylococcus epidermidis

-viruses in 20% of early cases,

(in some cases as sole agent, but more often with bacteria).

-Pathogenic bacteria subsequently are found in nasopharynges of 97% of patients with AOM,

with correspondence to organisms in middle ear effusion in 69% (Howie and Ploussard, 1972).

-Ad’s of children with recurrent AOM contains pathogenic bacteria in clinically significant amnts

-Ad’s (pharyngeal tonsil) forms uppermost part of Waldeyer’s ring

-is covered by resp epith rich in goblet cells

-numerous surface folds

-abundant lymphocytes are found within, esp. on crests of folds.

-is fully developed at 7th month, & increases in size until year 5

-nasal mucociliary blanket carries material posteriorly across ads.

-regarded as a B-cell organ.

-There is a significant age correlation with middle-ear pathogens in the

nasopharynges of clinically disease-free children;

-57% of under-2-year-old group were culture positive VS

-40% of 2 to 15-year-old children.

-Thus=> adenoid in AOM is a bacterial reservoir in nasopharynx.

- route of entry of NP bugs into middle ear is via reflux from ET:

-during swallowing (seen radiographically Bluestone 1972).

-facl’td by nose blowing & closed-nose swallowing,(Toynbee mnv)

-aspiration into middle ear due to negative pressure (eg sniffing)

-patulous eustachian tubes

-young children have shorter, straighter, more compliant ET’s

- adenoid is elevated by soft palate during swallowing,

\ when big may obstruct post choanae & Þ Ý NP P Þ reflux.

-Ad’s size in children with OM did not differ from control either radiographically (Hibbert 82) or

by weight (Gerwat, 1975)

-no difference in recurrence of effusion in kids with large vs small ads

-it is unnecessary to postulate ET obstruction as a necessary precedent for AOM to occur

-never been shown that adenoid physically obstructs the ET; in fact, has been shown it doesn’t.

-Study: Honjo (1988) studied 52 OME kids & compared ET fnct’n in pts with a large adenoid (which appeared to obstruct ET on scope )


pts with a clearly open tube.

Result Þ No difference in opening pressure or in positive pressure

equalization was noted between the two groups.

Þ No diff in ET ventilation function pre- & after adnoidectomy

Takahashi (1987) studied 10 adults with OME using thin catheter

Þ site of ET obstr’n is at distal part of cartilag tube (5-15 mm from end orifice),

rather than at the orifice proper.

-Improvement in ET, does occur after adenoidectomy (Bluestone 1972)


- ET dysfuntion nearly always found in OME

-ligation of ET in animals Þ MEE

-2 categories of OME:

(1) persistent MEE following an acute effusion

(2) secretary otitis media.


- failure of the middle ear clearance mechanism.

-Factors involved include:

-ciliary dysfunction, mucosal edema & hyperplasia,

viscosity of secretions, middle ear/NP pressure gradient.

-Barotrauma: occurs when mid ear P becomes rapidly < atm P

Þ a clear, watery transudate

-Seen sporadically due to viral infection

-Cleft palate (nearly a universal finding)

(Mech: defect is related to function of TVP m, which lacks its usual insertion into soft

palate,Þ unable to open ET properly on swallowing Þ functional obstruction )


-temporal bone in OM shows:

-vascular dilt’n & prolif’n, mononucl cells,

-epith thickening & metaplasia; gland formtn, edema & exudation


-adverse effects of OME on hearing & development

-otologic sequelae: permanent perforation, CSOM, tympanosclerosis, adhesive OM,

ossicular necrosis, retraction pockets cholesteatoma, & SNHL


Hx: -Older children Þ earache,

-InfantsÞ fussy, sleep poorly, and pull at affected ear, fever

-may be completely asymptomatic.


1. AOM

-redness and bulging TM

-as effusion develops, drum mobility decreases

-severe cases no landmarks may be visible

-if process continuesÞ necrosis of TM occurs Þ perforation.

NB: -massive necrosis of drumhead is now rare

-necrotizing streptococcal infct’n Þ permanent perforation.

-pneumatic otoscope: pressures of 1-2mm H20 Þ detectable motion

-clinical variants of AOM:

- Myringitis: inflammation of TM without MEE

- Bullous myringitis:

- adults and children

- most cases associated with same pathobacteria as AOM

some with Mycoplasma pneumoniae

-pain is outstanding feature, not relieved by opening bullae.

2. OME

-retracted, hypomobile/immobile TM

-dark, fluid-filled drum (obscurring vision of incus long process)


- moderate conductive hearing loss

-studies show variable range of hearing loss in OM, with AC thresholds averaging 27.5 dB

-hearing loss due to MEE is a principal indication for surgical treatment


1. Acute otitis media

a. Antimicrobial therapy

-important to consider using B lactamase-resistant agents as first line

-duration of therapy: 10-day course

b. Adjunct medical therapy

-nasal decongestant open the airway, may be used for short periods,but prolonged use may worsen rather than improve airway b/c of rebound.

c. Tympanocentesis

-Knowledge of specific organism is important for:

(1) premature newborns

(2) immunocompromised patients

(3) patients with progression of Sx & signs while on Rx

(4) cases with intracranial infection

(5) research subjects

-method: - 18-gauge spinal needle attached to a 1-ml tuberculin syringe.

- no anesthetic is necessary

- needle inserted into anteroinferior quadrant of TM

d. Myringotomy

- AOM myringotomy, has proven to be of limited value.

-promptly relieves severe pain

-adds little to remission of inf’n or clearance of MEE.Englehard1989

-report of van Buchem (1981) has been cited as showed:

Þ no difference in outcome with AOM whether A/B, myringotomy, both, or neither used.

(NB:large amt of methodologic flaws)

e. Follow-up

-impt: i. to assure infection is responding to AB’s

ii. to determine that the MEE has resolved

iii. important to exclude meningitis

-Therefore, a 3-day check is performed to determine response

a 2-week check is to determine if MEE has cleared

-Natural history of AOM Þ approx 1/2 ears will have cleared by 2/52

-little evidence to suggest prolonged/repeated therapy is useful

-if TM has ruptured, indicating a severe episode,

Þ continue AB’s until drainage has ceased & TM has sealed.

f. Recurrence & Prophylaxis

-Perrin (1974) & Varsano (1985)Þ sulfisoxazole chemoprevention of AOM -Casselbrant, 1990 Þ daily dose of amoxicillin, 20 mg/kg, for 3-6 mths

-Indication for prophylaxis is 3 or more episodes of AOM in 6/12 period.

-If develop recurrent AOM while on prophylaxis Þ Sx.

-Adenoidectomy should be an effective preventive:

-San Antonio trial (Gates 1987), number of episodes of AOM in

2 adenoidectomy gps did not differ from 2 nonadenoidectomy gps

g. Complications

see mastoiditis compln notes

2. Otitis media with effusion

a. Antimicrobial therapy

-MEE is known to contain viable, pathogenic bacteria (Liu et al., 1975).

\ Antimicrobial therapy is logical

-kids with asymptomatic OME discovered by screeningÞ recomm’d.

-followed by > 1-month observation period.

-If improved Þ second course or additional observation

-If no change at I month Þ Sx

b. Antihistamines and decongestants

-no routine use of decongestants in OME ( study by Cantekin 1983)

-steroid Rx of OME is experimental but worthy of continued study.

c. Middle ear inflation

- ET cathetrz’n (Politzer's maneuver) or autoinflation (Toynbee's mnvr)

Þ not generally used.

- Transiently good, but long-term net effect bad

Reason: it worsens the (-’ve) middle ear P pressure b/c the excess air injected into middle ear

passes out the ET, & the O2 remaining is absorbed through middle ear mucosa

-Important to remember gas in middle ear differs substantially from air, being hypercapnic and hypoxic, with gas tension values similar to arterial blood (Segal et al., 1983).

-Ex-vacuo theory : O2 in mid ear is continually absorbed, until replaced

by the ingress of nasopharyngeal air with swallowing.

Surgical therapy

-Surgical therapy does not cure patients with OME, but substantially reduces morbidity when

medical therapy has failed.

-OME & hearing loss persisting > 90-120 days with adequate A/B Rx Þ Sx is recommended.

-The time criterion is tempered by season.

-In Autumn Sx > Spring b/c of higher chance of URTI

-Types of procedures:

-Myringotomy +/- tubes, adenoidectomy +/- tonsillectomy

NB: tonsillectomy has no additional effect on MEE over adenoidectomy alone in cases of

OME (Maw, 1983)

-Myringotomy and suction alone:

- results not effective (Gates 1985; Mandel 1989).

-Tympanostomy tubes.

- introduced by Armstrong in 1954

Þ improved hearing & less AOM

- complications of tubes Þ purulent d/c, recurrent effusion, permanent perf’n,

(short-term tubes app 1%)( up to 5% longer term, bigger diam tubes)

-Long Tshaped tubes introduced by Goode (1973).

-Short have retention times of < year VS T-shaped tubes for years

-Experimental evidence Þ mucosal hyperplasia of tympanum revert to

more normal condition with aeration (Sade, 1966).

Technical considerations.

-Antibiotic drops often used after TT insertion. These have not been

associated with SNHL in humans (but have in experimental animals),

b/c of diff’s in anatomy of RW niche & membrane (Morizono, 1990).

Adenoidectomy. recent studies have confirmed its effectiveness

(Gates 1987; Maw, 1983; Paradise 1990).

Rationale for adenoidectomy.

-1st chief rationale is enlargement Þ nasal obstructn & mouth breathing.

-removal should lessen ET reflux

-removal for OM on size alone, has little scientific basis b/c ad & T enlargement results from

clonal expansion of immunocompetent cells (Fujiyoshi et al., 1989).\ large ad’s may be more

immunocompetent than small ad’s b/c chronic infection is associated with cellular depletion (Bernstein, 1990).

-3 separate studies (Gates 1987; Maw, 1985; Paradise 1990)

Þ effect of adenoidectomy on OM is independent of size.

-2nd classic rationale is improvement in ET function.

-In children with hypercompliant ET’s, adenoidectomy may Ý reflux.

-3rd and most current rationale is removal of chronically infected ad’s

to eliminate a nasopharyngea source of infection (Gates 1988).


-principal studies cited as showing a lack of effect of adenoidectomy are

Þ (Roydhouse 1980), FiellauNikolajsen 1983), Widemar 1985).

-studies demonstrating a significant effect from adenoidectomy are

Þ Maw (1983), Gates 1987), and Paradise 1990).

Technical considerations

-goal of adenoidectomy is complete removal of midline adenoid pad Þ smooth reepithelialization

of the nasopharynx.

-must avoid direct injury to torus tubarius ( Rosenmuller's fossa) that might Þ stenosis.

-most common complication of adenoidectomy is postop bleeding.

- 0.4% require operative treatment for bleeding (esp 1st 6hrs postop)

-Transient VPI may occur after R/O large ads but resolves in most

(most cases of postop VPI are due to undetected submuc cleft pal )

-occult submuc cleft is more obvious on post than ant surface of palate -it is clear that no major systemic immunologic deficiencies result from Ts & As (Siegel, 1984).


Cummings, C. Otolaryngology.  chapter 156

Gates Current Therapeutics

Scott Brown, , Otolaryngology

Schucknect, Pathology of the Ear