Otitis media with effusion

Otitis media
Paediatrics

1. SCOTT BROWN LEARNING 2020 OTITIS MEDIA WITH EFFUSION HOD: Dr. Dhinakaran M.S Moderator: Dr. Arul sundaresh kumar M.S Presentor:Dr.E.Selvapriya MS PG Volume II Chapter : 13 Pages no: 115 - 131

2. DEFINITION: Accumulation of mucus with in the middle ear and mastoid air cell system. 3 months or longer- chronic also known as GLUE EAR, Serous otitis media Secretory otitis media Can occur with or without history of AOM. May present with delayed speech, language development, poor social behaviour and difficulties with balance.

3. PREVALANCE 8O% of children had single episode of OME before 3 years, 40% have 3 or 4 episodes. Among children who had AOM ,45% have persistent effusion after 1 month. B imodal at 2 and 5 year s first attends playgroup school when goes to primary school. Above 15 years- prevalance 0.6%.

4. HISTOLOGY: ET and anterior mesotympanum – ciliated pseudostratified columnar epithelium. This mucosa contains goblet cells and mucus secreting glands. Middle ear mucosa contains flat cuboidal epithelium. Inflammation of the epithelium and production of mucus or serous effusion results in OME. Flat cuboidal epithelium is replaced by thicker pseudostratified mucus secreting epithelium.

5. Ciliary lining is less efficient at moving the secretions in to the nasopharynx than normal. Goblets cells are frequently present and mucus secreting glands are formed. Submucosa is edematous , inflamed with dilated blood vessels, increased number of macrophages, plasma cells and lymphocytes.

6. CHARACTERISTICS Glycoprotein mucin IgA Lysozyme Interleukins Cytokines Adhesiveness and poor mucociliary transportability are characteristics of the effusions

7. MICROBIOLOGY Streptococcus pneumoniae Hemophilus influenza Moraxella catarrhalis 66% of cultures were negative by traditional culture techniques. In case of PCR techniques, 36% of middle ear mucosal biopsy shows intracellular streptococcus pneumoniae.

8. ROLE OF BIOFILMS Biofilms – communities of sessile bacteria, resistant to disruption, low metabolic rate. They are embedded in matrix of extracellular polymeric substances and adhere to a foreign body or mucosal surface. Biofilms demonstrated in 92% of middle ear mucosal specimens of patients undergoing ventilation tube surgery. High grade biofilm formation is also found on adenoid samples – aetiology of OME.

9. PREDISPOSING FACTORS URI Age Allergy GERD ET dysfunction Craniofacial abnormalities Genetic factors Racial and sex differences Seasonal variations

10. AGE: In infants, Eustachian Tube – nearly in horizontal orientation. Develops 45 degree angle after several years. This orientation is highly unfavourable for ventilation.

11. ALLERGY There is conflicting evidence on the importance of atopy and allergy in pathogenesis of OME. Among the children with history of OME, 89% had e/o allergic rhinitis, 36% had asthma and 24% eczema which implies allergy. Nasal smears and skin prick testing, with blood eosinophil count and total immunoglobulin IgE could be done. Children with OME with a family history of allergy most likely to have a positive finding of Rhinovirus in the middle ear cavity.

12. GERD During swallowing, fluid can travel from the nasopharynx via the eustachian tube in to the middle ear. Common in two thirds of infants at 4 months of age. Pepsin was identified in middle ear fluid in children with OME. Mucosal damage can be mediated by proteolytic activity of pepsin. Helicobacter pylori confirmed by PCR in middle ear effusions.

13. ET DYSFUNCTION ET has 3 main functions: • Equalisation of pressure • Clearance of secretions • Protection of middle ear In case of persistent ET dysfunction, Defective aeration of middle ear Negative pressure sets in Transudation from mucosa– effusion.

14. GENE REGULATION THEORY URI, AOM, infection of adenoid Release of inflammatory mediators Upregulation of mucin genes Effusion of increased mucus from the glands

15. CRANIOFACIAL ABNORMALITIES Cleft palate and even if repaired – d efective palatine muscles and resultant poor ET function . Downs syndrome Turner’s syndrome Bifid uvula do not appear to have a higher incidence of OME. Subtotal removal should be performed under direct vision to reduce the higher risk of velopharyngeal insufficiency.

16. GENETIC FACTORS In children who had OME during the first 2 years of life, there was a greater concordance in monozygotic twins than dizygotic sets. RACIAL AND SEX DIFFERENCES No difference in prevalance rates between White and Black population Males have a slightly higher prepondarance (statistically not significant)

17. SEASONAL VARIATIONS Twice an amount of children – winter > summer Propable reason - increased frequency of URIs and ear infections. Due to close house hold contacts.

18. DURATION AND RECURRENCE OF EPISODES Median duration of effusions was 3 months. Infants were twice as likely to develop unilateral as opposed to bilateral OME. After one month, in infants with a unilateral effusion, 50% had resolved 20% had become bilateral 30% remained unilateral.

19. RISK FACTORS FOR PERSISTENCE In primary care, whether a child had frequent or upper respiratory symptoms at the time of assessment is an important determinant for persistence of OME. In secondary care, the degree of associated hearing impairment predicts persistence. The only modifiable risk factor is maternal smoking.

20. OTHERS Bottle feeding Having sibling with otitis media Attending day care Lower socioeconomic status Living in a home where people smoke Parental history of otitis media with effusion

21. HISTORY Ear pain Decreased hearing- 19.7% Recurrent URI Mouth breathing and snoring Poor speech and language development Signs of difficulties with balance Inattention and behaviour problems Difficulty taking part in group activities

22. Also important to confirm • Normal pregnancy • Delivery • Neonatal period • Neonatal hearing screening (OAE) Because children with co morbidities are most commonly affected by OME and is mostly persistent.

23. EXAMINATION Otoscopy Otomicroscopy Pneumatic otoscopy Tuning fork tests Free field voice testing

24. OTOSCOPY • Difficult to attempt due to uncoperative child or else view obscured by wax. (Sodium bicarbonate and olive oil drops to soften the wax) Findings: • Retraction of pars tensa • OME fluid and bubbles - For severe cases • Variations in colour of TM

25. OTOMICROSCOPY Intraoperative oto microscopy performed by specialist im the anesthetized child prior to myringotomy achieves greater diagnostic accuracy – 94.1%. PNEUMATIC OTOSCOPY: • Primary diagnostic method for OME • But requires greaterclinical skills to diagnose.

26. PNEUMATIC OTOSCOPY

27. TUNING FORK TESTS • Poorly predicts conductive hearing loss in children among 2 to 11 years. FREE FIELD VOICE TESTING • In children over the age of 3 years, the sensitivity of modification of the voice test is 96% and specificity is 98%. • This is useful if audiometry is unavailable.

28. INVESTIGATIONS TYMPANOMETRY: • Type B tympanogram is most of the times associated with OME. • Type A infrequently associated with OME . • Type C falls inbetween . • Otoscopy suggests OME with type B tympanogram- combined sensitivity – 98%. • When otoscopy suggests no OME with type A tympanogram – specificity – 98%.

29. AUDIOMETRY Audiometry is mandatory in all children with a suspected hearing impairment Irrespective of whether OME is diagnosed Routine audiometric testing of every child with OME at secondary care is recommended Presence of air bone gap of greater than 30 dB is necessary to predict OME. OME with CHL, ass with Cahart notch in bone conduction thresholds around 2 kHz.

30. X RAY X ray nasopharynx lateral view - to rule out adenoids.

31. COMPREHENSIVE ASSESSMENT Speech and language : • Hearing impairment from OME is likely to impede normal speech and language development. • Speech reception in noise ( SiN ) is a better tool than pure tone audiometry to predict benefit from surgical intervention. • Appears to be a small but significant long term effects in sound discrimination in children with a history of OME.

32. Cognition - The influence of OME as one of many interrelated variables affecting a child’s intellectual development is difficult to determine. Balance – 30% of children are clumsy and imbalanced. 61% of children have objectively defective motor proficiency. Behaviour can be assessed using Questionarrie reporting by parents or teachers. RUTTER SCORE – Antisocial , neurotic, hyperactive and inattentive behaviour scores .

33. MANAGEMENT Wait for spontaneous recovery Medical Surgical

34. MEDICAL Nasal topical steroids Systemic steroids – are effective in short term (2 weeks) when combined with antibiotics. Antibiotics: no statistically significant benefit in the short term. In the longer term appeared to be slight benefit from use of antibiotics. Nasal decongestants

35. Mucolytics – no significant benefit. HAVE NO SIGNIFICANT EFFECT IN RESOLUTION OF OME ACC TO RCT AND META ANALYSIS. Autoinflation : Because of low cost and absence of reported adverse effects , autoinflation – the most promising non surgical management to augment active monitoring.( Watchful waiting ) Homeopathy: No randomized controlled trials have been identified.

36. SURGICAL MANAGEMENT INCLUSION CRITERIA •Children aged 3,5,7 years • Bilateral OME • Persistent over 12 weeks • Hearing impairment of 20 dB HL/poorer MYRINGOTOMY AND ASPIRATION • Without insertion of ventilation tube is ineffective .

37. VENTILATION TUBES Introduced in 1954 by ARMSTRONG TEFLON, Silicone, Titanium, Gold and silver oxide coated tubes. Ionized, processed silicone- resistant to biofilm formation – reduces the incidence of plugging of the tube and otorrhea. Short and long term tubes Usually self extrudes within 6 months.

38. TYPES A-Shephard’s Grommet B-Armstrong’s Grommet C-Donaldson’s Grommet D-Shah’s Grommet E- T Tube – LONG TERM Absorbable ventilation tubes made from poly bisphosphazene .

39. SITE OF INSERTION Anteroinferior quadrant –reduces the incidence of perforation. radial or circumferential incision – stay slonger . Posterosuperior insertion is not Recommended because of damaging of ossicular chain.

40. Associated aspiration of middle ear fluid before insertion of tube is not significant. Aspiration produces some complications: Tympanosclerosis Trauma Bleeding Noise induced hearing loss Biofilm infection

41. HEARING OUTCOMES Ventilaton tubes alone improves the hearing level by 9 dB at 6 months 6 dB at 12 months 4 dB at 24 months (decrease in improvement of hearing due to non functioning of VT over a period of time) Younger children at day care and those with binaural hearing thresholds poorer than 25 dB HL and persistent over at least 12 weeks will benefit most.

42. ADENOIDECTOMY Not a definitive treatment Considers as a Chronic source of infection Chronic inflammatory changes in mucosa of ET and middle ear secondary to biofilm infection of adenoid rather than physical obstruction of Eustachian tube is the likely cause and removing this is how adenoidectomy is beneficial in the management of OME

43. PROCEDURES Blind curettage - risk of bleeding, poor access to the choanal adenoid and risk of trauma to the eustachian tube. Suction diathermy (minimal loss) Coblation and microdebrider – direct vision techniques. KTP laser- nasopharyngeal stenosis

44. HEARING OUTCOME S Metaanalysis – effect of hearing at 6 months was 8 dB . Adenoidectomy at the time of insertion of ventilation tubes doubled the benefit and extended hearing and reduces the need for re insertion of VT.

45. COMPLICATIONS OF VENTILATION TUBES Operative: • Displacement of the ventilation tube into the middle ear – 0.5%. • Posterosuperior myringotomy is avoided due to damage of ossicular chain and incudostapedial joint. • A high dehiscent jugular bulb may be pierced byh inferiorly placed myringotomy.

46. Early postoperative: Blockage of lumen of tubes – Early infection around 9%. Topical antibiotic steroid drops at the time of surgery reduces the incidence up to 1 %. Otorrhea in association with ventilation tube in situ may due to upper respiratory tract infection or due to chronic biofilm infection. Post operative otorrhea is the most common complication with incidence of 10 to 50 %.

47. Granulation tissue secondary to infection occurs in approximately 1 % Ofloxacin is the preferable topical antibiotic than ciprofloxacin.

48. Late postoperative Hearing loss – myringotomy or insertion of ventilation tubes not resulted in a significant difference in long term hearing level Tympanic membrane perforation: • Initial pars tensa perforation usually heals. • Perforation may reoccur at the same site following another episode of AOM – normally heals spontaneously.

49. Pars tensa retraction: Thinning and retraction of the tympanic membrane are complications of persistent OME. In children with bilateral OME, pars tensa retraction up to incus or promontory occurs in 8% of the better ear and 10% of the poor hearing ears. Pars tensa atrophy: Ventilation tubes are not inserted to prevent the occurrence of atrophy and retraction.

50. Myringosclerosis The most common structural complication after ventilation tube insertion – long term tubes. Hyaline degeneration of the collagen tissue in the fibrous layer of the pars tensa is visible otoscopically as white patches or plaques. Do not occur in the absence of history of otitis media. Frequency of myringosclerosis increases with frequency of OME. No hearing impairment resulted from the presence of myringosclerosis .

51. Myringosclerosis

52. Swimming and water contamination: Ear protection does not or only slightly reduces otorrhea in children following insertion of ventilation tubes.

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