Csom, cholesteatoma

ENT UG SEMINAR.
csom
cholesteatoma

1. CHRONIC SUPPURATIVE OTITIS MEDIA ( CSOM) NUR FARRA NAJWA BINTI ABDUL AZIM 082015100035

2. LEARNING OBJECTIVE By the end of seminar student should be able to Know what is CSOM Type of CSOM Etiology Pathology Feature Investigation Treatment

3. INTRODUCTION Long-standing infection of a part or whole of the middle ear cleft characterized By ear discharge A permanent perforation.

4. TYPES OF CSOM 1. Tubotympanic . Also called the safe or benign type; it Involves anteroinferior part of middle ear cleft, i.E. Eustachian tube and mesotympanum Associated with a central perforation. There is no risk of serious complications. 2. Atticoantral . Also called unsafe or dangerous type; it Involves posterosuperior part of the cleft (I.E. Attic, antrum and mastoid) Associated with an attic or a marginal perforation. The disease is often associated with a bone eroding process such as cholesteatoma , granulations or osteitis . Risk of complications is high in this variety.

5. TUBOTYMPANIC

6. AETIOLOGY The disease starts in childhood It is the sequela of acute otitis . The perforation central and becomes permanent and permits repeated infection from the external ear. Ascending infections via the eustachian tube. I nfection from tonsils, adenoids and infected sinuses may be responsible for persistent or recurring otorrhoea . Persistent mucoid otorrhoea is sometimes the result of allergy to ingestants such as milk, eggs, fish, etc.

7. PATHOLOGY 1 . Perforation of pars tensa . 2. Middle ear mucosa. It is oedematous and velvety when disease is active. 3. Polyp. It is usually pale in contrast to pink, fleshy polyp seen in atticoantral disease 4. Ossicular chain. It is usually intact and mobile but may show some degree of necrosis, particularly of the long process of incus . 5. Tympanosclerosis . It is seen as white chalky deposit on the promontory, ossicles , joints, tendons and oval and round windows and interfere with the mobility of these structures and cause conductive deafness. 6. Fibrosis and adhesions.

8. BACTERIOLOGY Pus culture in both types of aerobic and anaerobic CSOM Common aerobic organisms Pseudomonas aeruginosa , Proteus, Escherichia coli Staphylococcus aureus, A naerobes include Bacteroides fragilis and anaerobic Streptococci.

9. CLINICAL FEATURES Ear discharge. It is nonoffensive , mucoid or mucopurulent , constant or intermittent. 2. Hearing loss . It is conductive type; rarely exceeds 50 dB . (round window shielding effect) 3. Perforation. Always central 4. Middle ear mucosa. It is seen when the perforation is large.

10. INVESTIGATIONS 1. Examination under microscope 2. Audiogram. 3. Culture and sensitivity of ear discharge. 4. Mastoid X-rays/CT scan temporal bone.

11. TREATMENT Aural toilet. Ear drops. Antibiotic ear drops containing neomycin, polymyxin , chloromycetin or gentamicin are used. They are combined with steroids which have local anti-inflammatory effect. Systemic antibiotics Precautions Treatment of contributory causes Surgical treatment Reconstructive surgery

12. ATTICOANTRAL TYPE

13. INTRODUCTION It involves postero -superior part of middle ear cleft Associated with cholesteatoma (bone eroding properties) unsafe or dangerous type.

14. AETIOLOGY Aetiology of atticoantral disease is same as of cholesteatoma and has been discussed earlier. It is seen in sclerotic mastoid.

15. PATHOLOGY 1. Cholesteatoma . 2. Osteitis and granulation tissue. 3. Ossicular necrosis ( cholesteatoma hearer) 4. Cholesterol granuloma .

16. BACTERIOLOGY Same as in tubo - tympanic type.

17. SYMPTOMS Ear discharge . Usually scanty, but always foul-smelling due to bone destruction 2. Hearing loss . Hearing is normal when ossicular chain is intact or when cholesteatoma , having destroyed the ossicles , bridges the gap caused by destroyed ossicles ( cholesteatoma hearer). 3 . Bleeding . From gra nulations or the polyp when cleaning the ear.

18. SIGN Perforation . It is either attic or postero -superior marginal type . 2. Retraction pocket. An invagination of tympanic membrane is seen in the attic or posterosuperior area of pars tensa . There are four stages of tympanic membrane retraction. 3. Cholesteatoma .

19. Stage I Tympanic membrane is retracted but does not contact the incus . Stage II Tympanic membrane is retracted deep and contacts the incus . Middle ear mucosa is not affected.

20. Stage III Also called middle ear atelectasis . Tympanic membrane comes to lie on the promontory and ossicles . Middle ear space is totally or partially obliterated but middle ear mucosa is intact. Stage IV Also called adhesive otitis media. Tympanic membrane is very thin and wraps the promontory and ossicles . There is no middle ear space Mucosal lining of the middle ear is absent and tympanic membrane gets adherent to the promontory.

21. INVESTIGATIONS 1. Examination under microscope 2. Tuning fork tests and audiogram. 3. X-ray mastoids/CT scan temporal bone. 4. Culture and sensitivity of ear discharge.

22. FEATURES INDICATING COMPLICATIONS IN CSOM 1. Pain 2. Vertigo 3. Persistent headache. 4. Facial weakness indicates erosion of facial canal. 5. A listless child refusing to take feeds and easily going to sleep ( extradural abscess). 6. Fever, nausea and vomiting (intracranial infection). 7. Irritability and neck rigidity (meningitis). 8. Diplopia ( Gradenigo syndrome) petrositis . 9. Ataxia ( labyrinthitis or cerebellar abscess). 10. Abscess round the ear ( mastoiditis ).

23. TREATMENT 1. Surgical Canal wall down procedures (b) Canal wall up procedures. 2. Reconstructive surgery. Hearing can be restored by myringoplasty or tympanoplasty . 3. Conservative treatment.

24. CHOLESTEATOMA

25. LEARNING OBJECTIVE What is cholesteatoma Origin Classification

26. INTRODUCTION Normally, middle ear cleft is lined by different types of epithelium in different regions It is the presence of keratinizing squamous epithelium in the middle ear or mastoid. “Skin in the wrong place.” Essentially, cholesteatoma consists of two parts: ( i ) the matrix , which is made up of keratinizing squamous epithelium resting on a thin stroma of fibrous tissues and (ii) a central white mass , consisting of keratin debris produced by t he matrix . Also been named epidermosis or keratoma .

27. ORIGIN 1 . Presence of congenital cell rests. 2. Invagination of tympanic membrane from the attic or posterosuperior part of pars tensa in the form of retraction pockets ( Wittmaack’s theory ). 3 . Basal cell hyperplasia ( Ruedi’s theory). 4. Epithelial invasion ( Habermann’s theory). 5 . Metaplasia ( Sade’s theory).

28. CLASSIFICATION OF CHOLESTEATOMA The cholesteatoma is classified into : 1. Congenital 2. Acquired, primary 3. Acquired, secondary

29. 1. CONGENITAL CHOLESTEATOMA. It arises from the embryonic epidermal cell rests 3 important sites: Middle ear Petrous apex And the cerebellopontine angle Presents as a white mass behind an intact tympanic membrane and causes conductive hearing loss. It may sometimes be discovered on routine examination of children or at the time of myringotomy . It may also spontaneously rupture Present with a discharging ear indistinguishable from a case of chronic suppurative otitis media.

30. 2. PRIMARY ACQUIRED CHOLESTEATOMA No history of previous otitis media or a pre-existing perforation. Theories on its genesis are: (A) invagination of pars flaccida . (B) basal cell hyperplasia. (C) squamous metaplasia .

31. 3. SECONDARY ACQUIRED CHOLESTEATOMA Already a pre-existing perforation in pars tensa . This is often associated with posterosuperior marginal perforation or sometimes large central perforation. Theories on its genesis (A) migration of squamous epithelium. (B ) Keratinizing squamous metaplasia

32. EXPANSION OF CHOLESTEATOMA AND DESTRUCTION OF BONE It invades the surrounding structures, first the path of least resistance, and then by enzymatic bone destruction. An attic cholesteatoma may extend Backwards into the aditus , antrum and mastoid; Downwards into the mesotympanum ; Medially , it may surround the incus and/or head of malleus . Cause destruction of ear ossicles , Erosion of bony labyrinth, Canal of facial nerve, Sinus plate or tegmen tympani Attributed to various enzymes such as Collagenase , Acid phosphatase and proteolytic enzymes, Liberated by osteoclasts and mononuclear inflammatory cells, Seen in association with cholesteatoma .

33. COMPLICATION OF MIDDLE MIDDLE EAR DISEASES

34. FACTORS INFLUENCING DEVELOPMENT OF COMPLICATIONS 1. Age. 2. Poor socioeconomic group. overcrowding, poor health education poor personal hygiene, limited access to healthcare play an important part. 3. Virulence of organisms.

35. Cont. 4. Immune-compromised host. 5. Preformed pathways. Infection can easily travel beyond the middle ear cleft if preformed pathways exist, 6. Cholesteatoma .

36. PATHWAYS OF SPREAD OF INFECTION 1. Direct bone erosion 2. Venous thrombophlebitis . 3. Preformed pathways (a) Congenital dehiscences , e.g. in bony facial canal, floor of middle ear over the jugular bulb. (b) Patent sutures, e.g. petrosquamous suture. (c) Previous skull fractures. The fracture sites heal only by fibrous scar which permits infection. (d) Surgical defects, e.g. stapedectomy , fenestration and mastoidectomy with exposure of dura . (e) Oval and round windows. (f) Infection from labyrinth can travel along internal acoustic meatus , aqueducts of the vestibule and that of the cochlea to the meninges .

37. CLASSIFICATION A. INTRATEMPORAL (WITHIN THE CONFINES OF TEMPORAL BONE) B. INTRACRANIAL 1. Mastoiditis 2. Petrositis 3. Facial paralysis 4. Labyrinthitis 1. Extradural abscess 2. Subdural abscess 3. Meningitis 4. Brain abscess 5. Lateral sinus thrombophlebitis 6. Otitic hydrocephalus

38. SEQUELAE OF OTITIS MEDIA 1. Perforation of tympanic membrane 2. Ossicular erosion 3. Atelectasis and adhesive otitis media 4. Tympanosclerosis 5. Cholesteatoma formation 6. Conductive hearing loss due to ossicular erosion or fixation 7. Sensorineural hearing loss 8. Speech impairment 9. Learning disabilities

39. SUMMARY CSOM CHOLESTEATOMA COMPLICATION OF MIDDLE EAR INFECTION

40. REFERENCES Diseases of Ear, Nose, and Throat & Head and Neck Surgery, PL Dhingra , Shruti Dhingra , 6 th Edition http://www.radiologyassistant.nl/en/p49c62abe0880e/temporal-bone-pathology.html