Chronic suppurative otitis media disease of ear .pptx

chronic suppurative otitis media made simple and easy

1. Chronic suppurative otitis media Presentor - Dr.falaq faiyaz Moderator-Dr Jaya Gupta PG-JR-2 AP

2. Definition Diagnosis of chronic otitis media implies a permanent abnormality of pars tensa / flaccida Most commonly caused by earlier acute otitis media,negative middle ear pressure or otitis media with effusion.

3. Pathology Inactive mucosal COM- permanent perforation of pars tensa , but ME & mastoid mucosa are not inflammed Perforation may be surrounded by pars tensa may extend upto to fibrous annulus. Lamina propria around perforation is thickened due to proliferation of fibrous tissue .

4. Contd … Mucocutaneous junc. Is usually located at margin of perforation but not necessarily + Squamous epithelium can migrate med. Into ME.(higher incidences in perforation extending up to annulus) Squamous epithelium appears velvety under microscope and should be excised during T.plasty

5. Active mucosal (perforation with otorrhoea ) Chronic inflammation within mucosa of ME & mastoid,with varying degrees of oedema , submucosal fibrosis,hypervascularity & infiltration of lymphocytes,plasma cells & histiocytes . Areas of mucosa may ulcerate with proliferation of blood vessels,fibroblasts & inflammatory cells,leading to granulation formation.

6. Contd … Mucosal changes progress & coalesce to form ‘aural polyp’ that protrude through perforation. AM COM is asso . With resorption of ossicular chain( resorptive ostietis ) Ossicles thus affected show hyperemia with proliferation of capillaries & histiocytes Long process of incus,stapes crurae,body of incus & manubrium

7. Mechanism of bone erosion Diff. triggers such as infection , inflammation pressure & keratin lead to elaboration of molecular factors eg - IL-1,IL-6 , TNF,NO,prostaglandin These molecular factors initiate activation of osteoclast ( osteoclatogenic factors) Both mucosal & cholesteatomatous subtypes have focal areas of cholesterol granuloma

8. Contd … Precise pathogenesis of cholesterol granuloma is unclear ,they may be break down products of haemorrhage or derived from ME effusion. Inactive squamous epithelial COM- negative static ME pressure results in retraction of TM,’retraction pocket’ TM invagination into ME TM may be fixed when adherent to structures or free when depending upon state of invagination

9. Contd.. Epidermization - advanced type of retraction refers to replacement of ME mucosa by keratinizing squamous epithelium without retention of keratin debris. Epidermization remains quiscent & does not progress to cholesteatoma /active suppuration

10. Active squamous epithelial COM ( cholesteatoma ) Hallmark of cholesteatoma is its retention of keratinous debris,histologically it is squamous epithelium lining or matrix of cholesteatoma . Matrix is surrounded by inflamed ,vascular, subepithelial connective tissue . Cholesteatoma can be filled with keratin may be associated with active bacterial infection.

11. Cholesteatoma are potentially dangerous due to their potential to incite resorption of bone leading to intra-temporal /intracranial complications.

12. HEALED COM Healed perforation- loss of lamina propria of TM due to atrophy/failure to reform leads to dimeric membrane that consist of mucosa & epidermis ,prone to retraction (- ME pressure) Tympanosclerosis – hyaline deposits of acellular material visible as white plaques in TM.

13. Contd.. Tympanosclerosis is end result of healing process where collagen in fibrous tissue hyalinizes,loses its structure fuses to form homogenous mass with variable calcification It can occur in TM,ME mucosa , epitympanum , ossicular ligament & muscle tendons. Pathogenesis – local immunological hypersensitivity ,increased oxygen conc. In ME with exposure to radical oxygen & local inflammatory.

14. Contd … Tears patch involving TM usually of little consequence unless its large plaque extending from annulus to manubrium (fixing) Fibrocystic & fibro-osseous sclerosis- few cases of healing lead to end-stage pathology (fibrocystic sclerosis),that obliterates large portions of ME cleft.

15. Contd.. Obliterates large portion of ME cleft, cystic spaces become lined by mucosal epithelium that has proliferative connective tissue. Often associated with new bone deposition in mastoid antrum and surrounding mastoid cell tracts (fibro-osseous sclerosis) f/b sclerotic mastoid. Neo- osteogenesis can involve spaces around ossicles , epitympanum , contraindication of t.plasty .

16. Pathology of complications of COM Routes of spread- natural communication , direct erosion of bone,abnormal performed pathways & vascular channels. Natural communication- b/w ME & labyrinth ie oval window & round window Abnormal preformed pathways- either congenital/acquired including archnoid granulations,meningo-encephalocoeles & temporal bone #

17. contd Arachnoid granulations are small herniations of archnoid tissue through congenital defect ,may occur along middle/post cranial fossa vascular channel- progressive thrombophlebitis of small venules result in spread of infection through intact bone.

18. Labyrinthine fistula Most common complication occurs in abt 4-13 % of cases.lat SCC most commonly affected. Labyrinthine fistulae can be caused not only by cholesteatoma but also active mucosal COM without cholesteatoma & even by local inf. In CWD mastoidectomy Histologically cholesteatoma /granulation tissue becomes apposed to endosteum of inner ear /directly to membranous labyrinth in large fistula.

19. If natural barrier ie menbranous labyrinth & endosteum is overcome by infection/surgery Fistula shows spontaneous bony closure after removal of offending cholesteatoma or infection (new bone arise from endosteal / periosteal layer of otic capsule)

20. Labyrinthitis Inflammation is usually serous/toxic or suppurative ,serous labyrinthitis is sterile inflammatory response of labyrinth to bacterial toxins. Characterised by acidophilic staining of endolymph and endolymphatic hydrops,in severe cases degeneration of organ of corti is seen Suppurative caused by bacterial invasion of inner ear characterised by collections polymorphonuclear leukocytes in perilymphatic space

21. Contd.. Suppurative labyrinthitis progresses to endolymphatic hydrops & necrosis of menbranous labyrinth Characterised by SNHL but HC,spiral ganglion,stria vascularis appear normal hence hl is metabolic in nature Inflammatory cytokines disrupt integrity of spiral ligament critical for ion & fluid homeostasis in cohclea

22. HL in serous is reversible but permanent in suppurative . Facial nerve paralysis- occurs due to bone erosion of facial canal by cholesteatoma /granulation tissue Histologically - infiltration of nerve by inflammatory cells,oedema & fragmentation of myelin sheaths & degeneration of axons

23. Petrositis- gradenigo recognized triad of otorrhoea,severe periorbital pain & abducennt nerve palsy features petrositis . Acute petrositis - includes inflammation in mucous membraneof petrous apex cells may progress to abscess & osteitis Chronic petrositis - in addition to inflammation bone resorption occurs& new bone formation occurs

24. Chronic petrositis can persists for months to years potentially serious complication due to close proximity with meninges,trigeminal nerve & carotid artery. Otogenic intracranial complication- bacterial meningitis,extra-dural or subdural abscess , cerebellar or temporal lobe brain abscess &sigmoid sinus thrombophlebitis .

25. Aetiology & epidemiology Prevelance of COM-overall prevalence of active ,inactive COM – is 4.1% with 3.1 % b/l and 1.0% unilateral ds . Higher prevalence in low socio-economic status. Rates of surgery is 13 per 1lakh for inactive COM,7 for active COM & 4 for active squamosal type.

26. Aetiology contd … Eustachian tube dysfunction – more common in pts with COM than in normal pts.it may be initiating factor for COM. Gastro- oesophageal reflux- there may be a relationship b/w GORD & COM. Cranio -facial abnormality- incidence of COM in cleft palate pt ,in a follow up of 10 yrs is 20%.with 2% having cholesteatoma,as tensor veli palatine muscle is hypoplastic in cleft palate children predisposing to ETD

27. Contd … Auto-immune- COM was present in 29% of pts with ankylosing spondylitis Immune deficiency – no evidence but pts with AIDS have higher rate of COM present as aural polyp by pneumocystis carinii inf.

28. Factors influencing activity of COM Upper respiratory tract infection – it produces transient ETD in healthy individuals & as respiratory mucosa of ET is cont. with ME it may be infected resulting activity of mucosa primarily or secondary bacterial superinfection Aetiology of MUCOSAL COM- generally believed cause for COM is recurrent ASOM,before immunization COM resulting from measles was common .

29. Contd … Permanent perforation of pars Tensa from insertion of ventilation tube used to occur in abt 16.6% cases in comparison to 2.2% in grommet insertion . Aetiology of squamous type of COM- squamous metaplasia & misplaced epithelium

30. Contd … Squamous metaplasia –theories cholesteatoma cells arise and originate from metaplasia of middle ear mucosa cholesteatoma arises from skin of TM. All cells contain cytoskeleton made from filaments comprised of proteins found in epithelial cells & ME cholesteatoma has cytokeratin typically resembling skin of EAC.

31. Cholesteatoma sacs are found in close proximity to TM & are not encapsulated but connected to TM by a neck of invaginated squamous epithelium. TM appears to follow progressive changes from normal to retraction pockets & then to choleateatoma

32. Misplaced epithelium Cholestatoma may form from retraction pockets,from papillary ingrowth through TM,from ingrowth of squamous epithelium through perforation or from implantation of squamous epithelium in ME. Cholesteatoma are most likely to arise from retraction pocket in PF/ post. Sup part of pars tensa due to there blood supply > than rest TM they can more easily affect by inflammatory cell infiltration .leaving fibrous layer thinner in them than rest of TM.

33. Ingrowth of skin through TM perforation which is known as opening of retraction pocket,retraction may continue to grow & sac fills with desquamated cells leading to accumulation of keratin & cholesteatoma . Papillary ingrowth of squamous epithelium through its own basement membrane in pars flaccida result in cholesteatoma . In cholesteatoma there is hyperproliferation & migration of epithelium ,area of max. growth is found in neck of cholesteatoma sac.

34. Diagnosis & assessment Otoscopy withaid of microscope is gold standard for diagnosis of COM Otoscopy – site of pathology - anatomically TM is div. into 4 quadrants but perforation tend to be ant,post or inf.hence div into 3 is preffered . Proportion of pars tensa involved is preffered in % rather than small,mod & large

35. By definition all pars tensa perforation come under central / tubotympanic type of disease All attic ds come under attico-antral /marginal perforation Open-mastoid cavities- usually created surgically or by cholesteatoma , opne mastoid cavities are difficult to detect if EAC is narrow ,in an operated case post canal wall should be closely examined.

36. Active/inactive Active- inflamed with production of inflammaotry products ie - pus.inflamed mucosa & secretions. Active in squamosal ds - active with choleteatoma ,invariable asso . Mucosal ds with squamous epithelial debris. Otoscopic diagnostic categories- healed otitis media,IM COM,AM COM,IS COM & CHOLESTEATOMA

37. Active mucosal COM It may remain active , become inactive or progress to complications. Continuing activity may be result of infection with particularly virulent or persistent organism-pseudomonas. Inflammatory reaction in ME associated with granulation is factor responsible for ossicular damage. Nonspecific changes in bone asso . With inflammatory reaction include osteoclastic & oesteoblastic activity resulting in remodelling & resorption of bone

38. DIAGNOSTIC CATEGORIES HEALED otitis media-term given when pars tensa is intact but abnormal,can be associated with otitis media with effusion Mc abnormality tympanosclerotic plaques f/b thin replacement membrane ie healed without middle,fibrous tissue layer Inactive mucosal COM- permanent perforation with inactive middle ear mucosa.

39. Active mucosal COM- inflamed ME mucosa with granulations which may become polypoidal ,in both active , inactive COM with post. Third perforation intactness of ossicular chain must be assessed. Inactive squamosal - retractions can occur in both pars tensa & pars flaccida Pars tensa retractions are primarily + in post.TM ,degree of retraction is dependent on sade & berco classification .

40. Pars flaccida retraction is classified into 4 stages by Tos ,stage 1 PF is dimpled & more retracted but not adherent to malleus . Stage 2 – retraction adherent to neck of malleus & full extent of retraction is seen . Stage 3 – part of retraction is out of view & there may be partial erosion of bony attic wall Stage 4- definite erosion of attic with full extension being uncertain .

41. Active squamosal ( cholesteatoma ) Cholesteatoma are end stage of retractions ,they not self cleansing ,retain epithelial debris that elicit secondary ,inflammatory mucosal reaction . Extent of cholesteatoma cannot be determined otoscopically because retraction pocket

42. History Symptom Active MUCOSAL cholesteatoma HL 74% 83% Otorrhoea 69% 56% Otalgia 37% 39% Childhood ear disease 26% 43%

43. Audiology Pure tone audiometry - air & bone conduction with appropriate masking provide degree of hearing impairment,magnitude of air-bone gap Vestibular assessment- pt with peripheral type of vertigo undergoinf revision surgery,fistulae test if positive with nystagmus is suggestive of SCC fistulae created by cholesteatoma or previous mastoid surgery

44. Radiology CT scanning with 1.5mm sections in both coronal and axial planes of temporal bone is preferred CT scans as helpful in diagnosis of pts where TM is not visualized such as canal stenosis ,congenital abnormalities or complicated COM It is mostly helpful in surgical management of pts and not done routinely for every COM pt.

45. Natural history and management Inactive mucosal- why doesn’t perforation heal by it self ?- due to failure of blood supply to perforation edges due to endarteritis also there may be other factors related to repair mechanisms at cellular level. Management- myringoplasty,ossiculoplasty , tympanosclerosis & eustachan tube management,

46. Myringoplasty Tympanoplasty - refers to any operation involving reconstruction of TM & ossicular chain . Myringoplasty is tympanoplasty without ossicular reconstruction . Outcomes of tympanoplasty - 95%,failure rates of ant. Perforation is higher ?,but it is reduced by anchoring ant. Margin of graft beneath annulus. Success rate after revision tympano - 60%

47. Outcomes In pts with air-bone gap -35dB or above there will be either erosion/fixation of ossicular chain Ossiculoplasty - mc long process of incus erodes , Outcome- 68 % success rate if only incus is absent and 46 % if stapes suprastructure is also absent this result is b/w 3-12 months success rate falls in follow up of 5 yrs.

48. Tympanosclerosis & surgery Found in 25 % of ear surgeries ,mobility of ossicular chain is reduced by tears patch in attic or in oval window If ossicular chain is intact and only incus & head of malleus are fixed,them removal of both with connection b/w HOM or TM & stapes is done.-effective in short term refixation occurs by fibrous tissue or bone.

49. Eustachian tube & surgery An aerated middle ear is necessary for ME function. If C/L ear is atelectic ie suggesting poor ET function it is unlikely that ET will function in operated ear. In actively inflamed ears ,ET function may resume after middle ear mucosa reverts back

50. Management Aural toilet – effectively carried under microscope also extent of ds is examined Topical medications – antibiotic e/d such as neomycin with hydrocortisone has shown effective against otorhheoa Quinolones are do not appear to be ototoxic and are effective as aminoglycosides in reduction of discharge .

51. Surgery – cases that do not become inactive are heal post surgery & inactive ear require perforation repair. Aural polyps – found protruding from ME ,they can be attached to stapes suprestructure / facial nerve . Cauterization of polyp with silver nitrate is helpful but not done to avoid damage to facial nerve

52. Inactive squamosal management Defined as retraction of pars tensa / flaccida with potential to become active with retained debris may have association damage to ossicular chain & other ME structures. Hyperinflated TM may be found ie hyperectesis of TM may be seen (ballooning of TM) usually preceding before atelectesis . Presence of retraction changes TM histologically –loss of elasticity & rigidity

53. Contd … Nasal ds asso - it is common practice to treatment sinonasal ds & allergy before Surgical treatment- prevent complications such as discharge,progression of TM retraction & restoration of hearing hence div. into TM management & ventilation of ME Thin retracted TM lacking elastin & collagen component will retract more due to – ME pressure.

54. Excision myringoplasty – just excision of retraction with graft placement leads to recurrence especially where temporalis fscia graft is used. Snadwich graft – perichondrial-chondrial graft sandwiched b/w 2 temporalis fascia have shown prevention of recurrence ,sandwich graft are kept in position with tissue glue.

55. Active squamosal cholesteatoma History – poor ET function with reduced middle ear cleft volume is mostly commonly seen in ears with cholesteatoma . Hearing in squamous COM- hearing preservation may occur in pts where cholesteatoma is bridges gap b/w functioning part of ossicular chain & inner ear.

56. Management Aims of surgery- eradication of ds,an epithealized self cleaning ear & hearing improvement. Surgical techniques used – canal wall down (open mastoid cavity ) or canal wall up (intact canal wall) Canal wall down- done in post. To ant. Approach ,mastoid is opened behind EAC , choleateatoma identified followed forward through aditus to attic with removal of post. Canal wall

57. This leads to wider cavity hence requires squamous debris cleaning & wax removal (in clinic), meatoplasty is usually required. CWD procedures have lower rate of recurrence (5-15 %) of cholesteatoma Intact canal wall – combined approach with tympanoplasty ,no large mastoid cavity is created,recurrence rate is higher (20-50%) ,second look operations are often required.

58. Contd. MC incus is found eroded in cholesteatoma cases and surgery is often accompanied with ossiculoplasty but is using eroded incus actually safe ?

59. Complications of Active COM Classified as intratemporal ( cochlea,labyrinth & facial nerve)/ extracranial &intracranial Extracranial -post auricular abscess , facial palsy,petrous apicitis & bezold abscess Intracranial- meningitis,brain abscess,extradural abscess,subdural abscess,lat . Venous sinus thrombosis & otitic hydrocephalus

60. Risk of complications Study of complications –out of 268 complications of COM – 32% extreacranial & 56% was intracranial complications . Traditionally squamous type of ds is regarded to cause complications but there have been evidence that both type can lead to complications Relative incidence of complications – post aural abscess- 75%,facial palsy-6%,bezold abscess- 2%,meningitis-12%,brain abscess- 51%, Subdural abscess- 20%,extradural- 10%,lat. Sinus thrombosis- 20%.

61. Extracranial complications SNHL- toxins in COM can damage cochlea ,chances increase with increasing age also it may be associated with use of ototoxic drug in active COM. Labyrinthine complication- acute bacterial labyrinthitis / cochleolabyrinthitis results in dead ear.may present as chronic low grade imbalance , nystagmus +/- ,sudden acute vertigo may be present in labyrinthine fistula

62. Facial nerve complication Usually asso . With dehiscence of fallopian canal,present in around 10 % of ears,can occur in active mucosal but more common in squamosal More common with granulations ,granulation may form on nerve sheath itself Facial palsy with active COM should be managed almost always surgically ,intravenous anti- biotics,squamous com- cholesteatoma must be removed carefully from fallopian canal . Active mucosal cortical mastoidectomy & exploration of middle ear with careful removal of granulation tissue must be done.

63. Intracranial complications Routes of infection – proximity of dura & sigmoid sinus are responsible for more chances of intracranial complications. Normal anatomical weakness include- oval & round window ,Internal acoustic meatus,coachlear aqueduct. Mechanism of infection – infalmmatory changes leading to osteitic bone & thromboplebitis of emissary vein .

64. Meningitis- acute illnes with severe headache,neck stiffness later stage presents with drowsiness & coma ,confirmed with lumbar puncture & culture of CSF. Intracranial abscess – low grade headache,mild pyrexia,drowsiness & lethargy ,vomiting .MC site- temporal lobe & cerebellum Mortality rate – 6-14 % ,diagnosis is confirmed with CT scanning.

65. Lateral venous sinus thrombosis Infection spreads to venous sinus directly from mastoid or via venous channels draining middle ear & mastoid . Prior to infected thrombus formation there may be abscess near vein , intially mural thrombus is formed which gradually propagates.f /b septic embolisation , metastatis abscess formation & occlusion of sinus Papilloedema is present due to raised ICT,initially CT scanning is done but MRI gives information regarding venous flow of sinus.ligature of internal jugular vein may ocassionally necessary

66. Otitic hydrocephalus Benign intracranial hypertension , aetiology is obscure but results from lat. Sinus thrombosis & obstruction of intracranial venous channels Papilloedema with no other CT scanning finding helps diagnose. Management- reduction of ICP,diuretics,hyperosmolar dehydrating agents,ventriculoperitoneal shunt.

67. Referances Scott-Brown’s Otorhinolaryngology ,head & neck surgery – volume-3

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