2. Acute Otitis Media Acute infection of the mucous membrane lining the middle ear cleft. AOM is one of the commonest illnesses of childhood but can occur at any age. AOM most commonly develops three to five days after the onset of coryzal symptoms.

3. Source of Infection Through the Eustachian tube following URTI e.g. rhinosinusitis adenoiditis, tonsillitis or nasal polyposis. Through TM perforation or if there is ventilation tube. Hematogenous infection.

4. Risk factors for recurrent AOM 1. Anatomical factors: AOM is common in infants and young children due to the wide horizontally placed Eustachian tube which opens at a lower level in infants nasopharynx which allow easy access of infection into the middle ear. Adenoiditis "rather than adenoid enlargement" is important factor.

6. 2. Environmental factors: Day-care attendance.Day-care attendance. Bottle feeding and feeding in prone positionBottle feeding and feeding in prone position (exclusive breast feeding for 6 months is protective). Passive smoking.Passive smoking. The use of pacifier.The use of pacifier. 3. Syndromic associations: Cleft palate, Down syndrome and iron- deficiency anemia.

7. Bacteriology There is an initial viral infection which pave the way for pyogenic infection. The commonest bacteria isolated are H. influenzaH. influenza Streptococcus pneumoniStreptococcus pneumoni Moraxella catarrhalis.Moraxella catarrhalis.

8. Pathology URTI Infection of Eustachian tube (salpingitis). The air within the middle ear is absorbed and replaced by mucopurulent exudates. Rupture of TM and relief of pain.

9. Clinical pictures The onset is fairly sudden and commonly there is a preceding URTI: Rapidly developing earache. An infant putting his finger in the ear is NOT earache. Conductive hearing loss. This may take 2-3 weeks to resolve completely. Mucopurulent otorhea indicates rupture of TM and is usually associated with pain relief. Constitutional symptom: fever, excessive crying, irritability and vomiting.

10. Examination Otoscopy: Redness and bulging of the TM with loss of surface anatomy. Mucopurulent discharge may be visible. Tuning fork tests: Conductive hearing loss; Rinne test is negative and Weber test is lateralized to the more severely affected ear.

14. Treatment Two-thirds of children recover within 24 hours with or without treatment "watchful waiting" may be reasonable in mild AOM: the child is reassessed after 24-48 Hr. High fever Bilateral AOM Presence of otorhea AOM in children less than 6 months All considered "severe AOM" and require prompt treatment.

15. I. Medical Analgesia and heat application: paracetamol or ibuprofen. Nasal decongestant drops: xylometazolin or nasophrine. Antibiotics: Amoxicillin- clavulanic acid for 7 d

16. In severe cases, drugs should be given I.M. for 2 days and then the drug can be given orally for another 5 days. Allergic to penicillin: cefdinir. Allergic to both penicillin and cephalosporin: levofloxacin or clindamycin. Complicated cases or no response to treatment: Second line treatment :ceftriaxone alone or in combination with clindamycine.

17. AOM with discharge: Dry mopping by wisps of cotton wool and prevent water from entering the ear. Topical antibiotics are not indicated. Repeat otoscopy in 3 weeks: if effusion is still present in the middle ear, this is diagnosed as secretory otitis media (OME).

18. II. Surgical Myringotomy is rarely indicated if there is severe pain not responding to treatment. It is also done when AOM is complicated by facial palsy. The object of myringotomy is not only pain relief but to facilitate healing with a firm surgical scar instead of risking a large perforation closed with a thin fragile membrane.

19. Sequelae of AOM Healing: The perforation may be closed with a scar that is invisible.Healing: The perforation may be closed with a scar that is invisible. Persistent perforation either dry or moist with deafness. CSOM is diagnosed when otorhea persists for more than 3 months..Persistent perforation either dry or moist with deafness. CSOM is diagnosed when otorhea persists for more than 3 months.. Tympanosclerosis: White chalky patches on the surface of TM produced by calcium deposit. Small discrete plaques are asymptomatic.Tympanosclerosis: White chalky patches on the surface of TM produced by calcium deposit. Small discrete plaques are asymptomatic.

20. Adhesive otitis media: Formation of adhesions which bind TM to the medial wall of the middle ear and ossicles causing conductive hearing loss. This is a complication of recurrent AOM.Adhesive otitis media: Formation of adhesions which bind TM to the medial wall of the middle ear and ossicles causing conductive hearing loss. This is a complication of recurrent AOM. Other complications include: acute mastoiditis, meningitis, facial nerve palsy and sigmoid sinus thrombosis.Other complications include: acute mastoiditis, meningitis, facial nerve palsy and sigmoid sinus thrombosis.

21. Chronic Otitis Non-suppurative otitis media: OME (Otitis media with effusion) (Otitis media with effusion) Chronic Suppurative otitis media CSOM

22. 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 (glue).

23. Aetiology 1.Eustachian tube dysfunction

24. Aetiology 1.Eustachian tube dysfunction which may result from: a.Adenoid hypertrophy. b.Tubal infection (salpingitis) due to extension of infection from the URT but not progressing to AOM. infection from the URT but not progressing to AOM. c.Traumatic stricture or adhesion following adenoidectomy. adenoidectomy. d.Postnasal mass: Antrochoanal polyp or nasopharyngeal carcinoma (unilateral OME in adult: nasopharyngeal carcinoma (unilateral OME in adult: nasopharynx should be examined with endoscope). nasopharynx should be examined with endoscope).

25. 2.Unresolved acute otitis media either from failure of natural immunity or inadequate antibiotic therapy. 3.allergic rhinitis and chronic sinusitis. 4.Gastro-esophageal reflux disease. 5.Cleft palate

26. Pathophysiology   Initial Eustachian tube dysfunction due to various causes   Air absorption from the middle ear and vacuum formation   TM drawn inwards to compensate

27. Pathophysiology   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.

28. Clinical Picture The condition is suspected in children suffering from deafness especially those with snoring due to adenoid hypertrophy, and also in adults when CHL follows influenza or common cold. 1. Insidious conductive hearing loss: It is the commonest cause of hearing loss in childhood between 4-6 years of age. Changes in head position causes changes in degree of deafness when the fluid is thin (fluctuant hearing loss).

29. 2.Tinnitus: crackling, bubbling noises and sensation of fluid in the ear. 3.Pain is absent except when acute infection supervenes.

30. Examination 1.Otoscopy: a.TM is dull, retracted and immobile, cone of light is lost or scattered. b.Dilated blood vessels running from the periphery to the center of TM (cart- wheel appearance). c.Air bubbles or a fluid level may be seen behind the TM.

31. 2.Tuning fork tests: Rinne test is negative. Weber is lateralized to the more severely affected ear.

32. Investigations PTA: CHL, usually 40 dB or more. Impedance audiometry: Flat (type B) tympanogram. Radiology: X-ray of postnasal space to exclude adenoid hypertrophy.

34. Treatment Medical Topical nasal steroid. Antibiotics: they are indicated when there is infection in the sinuses or the pharynx. Auto-inflation may be helpful.

35. Surgical Surgery should only be recommended for disease persistent for more than 3 months. Surgical treatment consists of myringotomy, and the insertion of ventilation tube (grommet). This grommet provides adequate ventilation of the middle ear. After several months however, the grommet is slowly extruded. Adenoidectomy.

36. Complications Retraction pockets and cholesteatoma. Tympanosclerosis. Adhesive otitis media.