CHRONIC SUPPURATIVE OTITIS MEDIA (CSOM)

OBJECTIVES Etiology What is CSOM Pathology Feature Investigation Type of CSOM Etiology Pathology Feature Investigation Treatment

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

TYPES OF CSOM Involves anteroinferior part of middle ear cleft, Tubotympanic. Also called the safe or benign type; 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. 1. • it • 2. • Atticoantral. Also called unsafe or dangerous Involves posterosuperior part of the cleft (I.E. Attic, antrum and mastoid) type; it • 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. •

Atticoantr al(unsafe) Tubotympani (safe) Atticoantr al(unsafe) Discharge Profuse, mucoid, odourless Central Uncommon Pale Absent Rare Scanty, purulent, smelling foul Perforation Granulations Polyp Cholesteatoma Complications Audiogram Attic or marginal Common Red and fleshy Present Mild to moderate Conductive deafness or mixed conductive deafness

TUBOTYMPANIC

ETIOLOGY The disease starts in childhood permanent and • 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. – Infection 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. • •

PATHOLOGY 1. Perforation of pars tensa. is active. 3. 2. Perforation of pars tensa. Middle ear mucosa. It is oedematous and velvety when disease Polyp. is active. 3. It is usually pale in contrast to pink, fleshy polyp seen in atticoantral disease Ossicular chain. It is usually intact and mobile but may show some degree necrosis, particularly of the long process of incus. Tympanosclerosis. 4. of 5. 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. Fibrosis and adhesions. 6.

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

Retraction Mucosal Squamosal diseases diseases Active Inactive Healed CHRONIC OTITIS MEDIA Mucosal Squamosal diseases diseases Active Inactive Healed Active Retract Retract pockets Retraction

CLINICAL FEATURES 1. Ear discharge. It is nonoffensive, mucoid or mucopurulent, intermittent. 2. Hearing loss. constant or It is conductive type; rarely exceeds (round window shielding effect) 3. Perforation. Always central 4. Middle ear mucosa. 50 dB. It is seen when the perforation is large.

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

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

ATTICOANTRAL TYPE

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

ETIOLOGY cholesteatoma and has been discussed earlier. Etiology of atticoantral disease is same as of cholesteatoma and has been discussed earlier. It is seen in sclerotic mastoid. • •

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

BACTERIOLOGY • Same as in tubo-tympanic type.

Hearing is normal when ossicular chain is intact or SYMPTOMS 1. Ear discharge. Usually scanty, but always foul-smelling destruction Hearing loss. due to bone 2. 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 granulations or the polyp when cleaning the ear.

SIGN 1. Perforation. marginal It is either attic or postero-superior type. 2. Retraction pocket. marginal An invagination of tympanic membrane is seen the attic or posterosuperior area of pars tensa. There are four stages of tympanic membrane retraction. 3. Cholesteatoma. in

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.

•Middle ear space is totally or partially obliterated but middle ear Stage III •Also called middle ear atelectasis. on the promontory and ossicles. •Middle ear space is totally or partially obliterated but middle ear mucosa is intact. •Tympanic membrane comes to lie Stage IV •Also called adhesive otitis media. 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. •Tympanic membrane is very thin

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

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

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

CHOLESTEATOMA

What is cholesteatoma Origin Classification •

INTRODUCTION epithelium in different regions 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 the matrix . • Also been named epidermosis or keratoma.

ORIGIN 3. Basal cell hyperplasia (Ruedi’s theory). 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. 4. 5. Basal cell hyperplasia (Ruedi’s theory). Epithelial invasion (Habermann’s theory). Metaplasia (Sade’s theory).

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

1. CONGENITAL CHOLESTEATOMA. • It arises from the embryonic epidermal 3 important sites: cell rests – 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. • •

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

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

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. •

COMPLICATION OF EAR MIDDLE MIDDLE DISEASES

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

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

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.

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

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