Acute Otitis Media
Acute infection of the mucous membrane lining the middle ear cleft (Eustachian tube, middle ear cavity, aditus...). It is extremely common in young children but can occur at any age. There is nearly always a preceding history of URTI.
Source of Infection
1. Through the ET following URTI e.g. rhinosinusitis adenoiditis, tonsillitis or nasal polyposis.
2. Through the EAM if there is a preexisting TM perforation or if the TM has been ruptured by trauma.
3. Blood borne infection.
Age
AOM is common in infants and young children because:
1. Anatomical factors: The wide horizontally placed ET which opens at a lower level in infants nasopharynx may allow easy access of infection into the middle ear.
2. The child has poorly developed immunity to URTI.
3. Adenoid hypertrophy.
4. Teething with its congestion of the gums and general upset.
5. The predominant horizontal position of the infants during breast or bottle feeding allows stagnation of regurgitated milk or of vomitus in the pharynx which may infect the ET.
Bacteriology
There is an initial viral infection which paves the way for pyogenic infection. The commonest bacteria isolated are Streptococcus pneumoniae, H. influerzzae and Branhamellacatarrhalis, a beta lactamase producing organism.
Pathology
The process usually started by URTI leading to infection of the ET (salpingitis). The air within the middle ear is absorbed and replaced by
exudates which may later become purulent. This suppuration if not treated leads to rupture of the TM and relief of pain.
Clinical Picture
The onset is fairly sudden and commonly there is a preceding URTI:
1. Pain (earache) is the most prominent symptom and usually it's described as sharp lancinate in character.
2. Conductive hearing loss due to fluid accumulation on the middle ear which hinders the movement of the TM and ossicles.
3. Mucopurulent discharge indicates rupture of the TM and usually associated with pain relief.
4. Constitutional symptoms as pyrexia, malaise, vomiting and diarrhea.
Examination
I. Otoscopy: Redness and injection of the TM and in severe cases there is outwards bulging of the TM with loss of surface anatomy. A mucopurulent discharge filling the EAM can be seen if perforation of the TM has occurred.
2. Tuning fork tests: Conductive hearing loss; Rime test is –ve and Weber test is lateralized to the affected ear.
3. P.T.A: conductive hearing loss.
Treatement
I. Medical
1. Treatment of URTI.
2. Bed rest, heat application, analgesics e.g. aspirin and paracetamol.
3. Nasal decongestants drops: ephedrine or nasophrine.
4. Antibiotics: Amoxicillin for I-10 days. In severe cases, drugs should be given I.M. for 48 hours and then the drug can be given orally later. In patient sensitive to penicillin, erythromycin and cefixime are suitable alternatives. Second line treatment may be necessary in complicated cases or if there is no response to treatment or where B-lactamase producing H. influenza or Branhamellacatarrhalis are suspected by amoxicillin-clavulanic acid combination or IM ceftriaxone.
5. AOM with discharge: Dry mopping by wisps of cotton wool and prevent water from entering the ear. A swab should be taken for culture and sensitivity. Antibiotic-steroid drops may be used in those patients in whom the discharge remains.
II. Surgical
Myringotomy is indicated if there is severe pain not responding to treatment. A swab will be taken for bacteriological study and continuing chemotherapy will depend upon the result. The object of myringotomy is not only pain relief but to facilitate healing with a good firm surgical scar instead of risking a large perforation closed with a thin fragile membrane. The incision of myringotomy is made semilunar on the posteroinferior portion of the TM.
Sequelae of ASOM
1. Healing: The perforation may be closed with a scar that is invisible.
2. Open perforation either dry or moist with deafness: Anterior small perforations are less deafening than larger central ones.
3. Tympanosclerosis: White-chalk like patches on the surface of the TM produced by calcium deposition. Small discrete plaques are asymptomatic whereas larger ones seriously hamper the mobility of the TM.
4. Adhesive otitis media: Formation of adhesions which bind the TM to the medial wall of the middle ear. They may also adhere to the ossicles causing conductive hearing loss.
Myringotomy
Tympanic membrane perforation
Chronic Otitis Media
1. Non-suppurative otitis media: Otitis media with effusion.
2. Suppurative otitis media.
3. Tuberculous otitis media.
Otitis Media with Effusion (Glue Ear, Secretory Otitis Media)
The presence of non-purulent fluid in the middle ear, occurring in the absence of acute inflammation.. It may vary from thin serous fluid to thick viscid material. Conductive hearing loss is the principle feature.
Aetiology
1. Occlusion of the ET which may result from:
a. Adenoid hypertrophy.
b. Tubal infection (salpingitis) due to extension of infection from the URT but not progressing to ASOM.
c. Traumatic stricture or adhesion following adenoidectomy.
d. Postnasal mass: Antrochoanal polyp or nasopharyngeal carcinoma.
2. Unresolved acute otitis media either from failure of natural immunity or inadequate antibiotic therapy.
3. Nasal allergy.
4. Barotrauma: Descend in an aeroplane or diving.
5. Cleft palate.
Pathophysiology
There is an initial ET obstruction due to various causes resulting in air absorption from the middle ear and vacuum formation. Consequently, the TM drawn inwards to compensate followed by transudation of secretions from the mucous membrane which is sterile to fill the middle ear. This fluid accumulation leads to CHL and with time this thin fluid changes to thick glue one.
Clinical Picture
The condition is suspected in children suffering from repeated tonsillitis with adenoid hypertrophy and in adults when CHL follows influenza or common cold.
1. Insidiousconductive hearing loss: It is the commonest cause of hearing loss in childhood between 4-6 years of age. Changes in head position cause changes in degree of deafness when the fluid is thin (fluctuant HL).
2. Tinnitus: Crackling, bubbling noises and sensation of fluid in the ear.
3. Pain occurs only if acute infection supervenes.
4. Delayed and defective speech.
Examination
1. Otoscopy:
a. The TM is dull, retracted and often has a yellow-orange tint.
b. Dilated blood vessels running parallel to the handle of malleus (cart-wheel appearance).
c. Air bubbles or a fluid level may be seen when the fluid is serous.
2. Seigle pneumatic speculum: Lack of normal mobility.
3. Tuning fork tests: Rinne test –ve.
Weber is lateralized to the affected ear.
Investigations
I. PTA: CHL of at least 40 dB.
2. Tympanometry: Flat tympanogram (type B).
3. Radiology: sinus X-ray and views of the postnasal space to exclude adenoid hypertrophy and SOL.
Treatment
1. Treatment of predisposing factors: Adenoidectomy, treatment of nasal and sinus infection.
2. Medical
a. Local and systemic decongestants, antihistamines: Xylometazoline, actifid.
b. Mucolytics: solvodin.
c. Antibiotics: Long term low dose antibiotics may be beneficial in 50% of cases.
d. Middle ear aeration: Repeated autoinflation by Valsalvamanoeuvre. Children can be given chewing gum to encourage swallowing which opens the tube.
3. Surgical
Surgery should only be recommended for diseases persistent more than 3 months. The surgical treatment consists of myringotomy, aspiration of thick mucoid material and the insertion of a grommet. This grommet provides adequate ventilation of the middle ear and is essentially an artificial ET. After several months however, the grommet is slowly extruded.
Complications
1. Retraction pockets and Cholesteatoma.
2. Tympanosclerosis.
3. Adhesive otitis media.
Otitis media with effusion Grommet
Grommet in place
Chronic Suppurative Otitis Media
Persistent disease, insidious in onset manifested clinically as long standing painless aural discharge with deafness. It is grouped into two clinical types; a tubotympanic (safe??) and atticoantaral (unsafe??) disease.
Tubotympanic Disease
It tends to follow a benign clinical course and rarely gives rise to any serious complications. It is considered as tubotympanic because in many cases the persisting or recurring infection spreads via the ET to the tympanic cavity.
Aetiology
It is virtually always a complication of AOM where there is persisting perforation of the TM. It therefore usually starts in infancy and early childhood. Reinfection either from the nasopharynx (tonsillitis, adenoid hypertrophy and sinusitis) or through the perforation allows active infection to persist or to recur.
· Dysfunction of Eustachian tube
· Chronic inflammation in nose and pharynx
· Dysfunction of immune system
Bacteriology
There is a high incidence of G –ve infection as pseudomonas aeruginosa, proteus and E. coli. anaerobic microorganisms can be found as well.
Pathology
The main pathological condition is a central perforation of the TM resulting from AOM. Repeated infection may cause polyp formation which consists of oedematous middle ear mucosa prolapsing through a perforation.
Clinical Picture
1. Non- offensive mucoid or mucopurulent discharge which may be intermittent or persistent.
2. CHL: Its degree varies with the size and position of the perforation.
Examination
1. Otoscopy: Central TM perforation in the pars tensa.
2. Tuning fork tests: CHL.
Investigations
1. PTA: CHL.
2. X-ray and CT scan shows sclerosis with clouding of the mastoid air cells.
3. Swab of the aural discharge for C/S.
Treatment
1. Elimination of URTI: Treatment of sinusitis, adenoidectomy and tonsillectomy.
2. Medical
a. Aural toilet: Suction clearance and mopping with cotton-wool wicks at home. The patient should be warned not to get water into the ear when washing or swimming.
b. Local antibiotic/steroid drops e.g. ciprofloxacin, neomycin or gentamycin. These drops are instilled after mopping the ear and the head should be on the side so that the affected ear is uppermost. After that the tragus is pressed inwards to assist the drops to pass into the middle ear.
c. Systemic antibiotics. Has little role in treatment. It’s indicated if the ear fails to city or in acute exacerbation of chronically infected ear.
d. Precautions: Patients are instructed to keep water out of the ear during bathing and swimming.
3. Surgical treatment is indicated if the ear fails to dry.
a. Removal of polypi and granulation tissue.
b. Myringoplasty +/- ossiculoplasty: Repair of the TM perforation +/-ossicles is indicated when there is recurring discharge or there is disabling deafness.
Atticoantral Disease
In this type of infection the bone of the attic, mastoid antrum and air cells are involved as well as the mucosa of the middle ear cleft. It is therefore referred to as atticoantral disease. As erosion of bone may extend to adjacent vital structures there is always a danger of serious complications; both intra and extracranail. This type of infection is usually associated with cholesteatoma.
Cholesteatoma
Cholesteatoma is a sacof keratinizing squamous epithelium containing keratinous debris and surrounded by granulation tissue. Otherwards, it is a skin in a wrong place.
The surface layers of epithelium keep producing keratin and this result in the appearance of a thin-walled sac containing cheesy material.
The granulation tissue on the outside of the sac produces lysozymes and this gradually erodes the ossicles, ear drum and mastoid bone.
The suffix "oma" may suggest that it is a tumor, this is not the case, though if untreated it will continue to expand and destroy surrounding structures.
Theories of origin of cholesteatoma
I. Congenital: This is unrelated to Ch.S.O.M as it arises from embryonic epithelial tissue and occurs in the temporal bone and in the middle ear.
II. Aquired
1. Invagination theory: Cholesteatoma starts as a retraction pocket of the TM due to ET obstruction. The TM tends to be retracted in the attic region where the pars flaccida is thin. If the retraction pocket is more marked, a cholesteatoma sac may be formed inside the middle ear.
2. Emigration theory: Cholesteatoma arise from extension of squamous epithelium into the middle ear through a marginal TM perforation.
3. Metaplasia theory: Squamous metaplasia of the middle ear mucosa in response to chronic infection.
Bacteriology
Same as in tubotympanic disease.
Clinical Picture
The onset of symptoms is insidious so that the patient may be unaware of the starting point.
1. Persistent or recurrent purulent aural discharge. The discharge however, is purulent rather than mucopurulent and is frequently scanty and foul smelling.
2. CHL; Usually marked hearing loss because of involvement of the ossicular chain.
3. Bleeding from the ear if granulation tissue is present.
4. Headache, vertigo and facial paralysis all indicate complications.
Examination
1. Otoscopy: Attic (unsafe perforation) situated in the pars flaccida. Cholesteatoma may be seen as a grayish substance projecting from attic perforations. Granulation tissue may be seen as well occupying such perforation.
2. Tuning fork tests: CHL.
3. Fistula sign: Cholesteatoma can cause erosion of the lateral semicircular canal leading to fistula. If such fistula is present, any change of pressure in the middle ear as by Seigle aural speculum will probably produce vertigo and nystagmus. If the test is positive, it is an indication of urgent surgery because of the risk of labyrinthitis.
Investigations
1. PTA: CHL.
2. X-ray and CT scan of cholesteatoma appear as an area of translucency with a clearly outlined bony margin.
3. Swab of the aural discharge for C/S.
Cholesteatoma
Treatment
1. Conservative: It's used when no complications are suspected and if the cholesteatoma is small and accessible. It includes removal of the cholesteatoma and granulation tissue by fine crocodile forceps and suction clearance under magnification.