PATHOPHYSIOLOGY,

CLINICAL FEATURES AND

PRINCIPLES OF MANAGEMENT
OF INFECTIVE DISORDERS OF
MIDDLE EAR (AOM AND COM)
DR. TANAYA PANJA
OTITIS MEDIA DEFINITION: INFLAMMATION OF MUCOPERIOSTEAL LINING OF MIDDLE EAR CLEFT

MIDDLE EAR CLEFT-

ACUTE OTITIS MEDIA: < 3 MONTHS

CHRONIC OTITIS MEDIA: >3 MONTHS

TYPES: MUCOSAL/ SQUAMOUS
MUCOSAL: CENTRAL PERFORATION
SQUAMOUS: MARGINAL & ATTIC PERFORATION/ CHOLESTEATOMA/ BONE EROSION

WHY TUBOTYMPANIC/ ATTICOANTRAL?

(TYPE OF EPITHELIUM)

WHY NOT ‘SUPPURATIVE’? – TUBERCULAR OTITIS MEDIA/ MASKED MASTOIDITIS

WHY NOT SAFE/ UNSAFE?

SECRETORY OTITIS MEDIA: PRESENCE OF EFFUSION IN MIDDLE EAR WITHOUT ANY S/S OF INFLAMMATION.
ACUTE OTITIS MEDIA:

MOSTLY IN CHILDREN,
SADE ET AL 1986- 22% INCIDENCE IN FIRST YEAR, 15% IN 2ND YEAR, 10% IN THIRD AND FOURTH YEAR AND 2%
IN EIGTH YEAR.

PPT FACTORS:
AGE- < 7 YEARS, (URI MORE FREQUENT, ET TUBE SHORTER AND MORE HORIZENTAL, ABUNDANT
NASOPHARYNGEAL LYMPHOID TISSUE, IMMATURE IMMUNE SYSTEM)
SEASONAL CHANGE-
BREASTFEEDING- LOWER INCIDENCE (COMPOSITION- ANTIBACTERIAL AND ANTIVIRAL PROPERTY, FACIAL
MUSCLE DEVELOPMENT)
RECURRENT URTI-
NASAL ALLERGY-
ADENOID HYPERTROPHY- ET TUBE BLOCKAGE, RECURRENT INFECTION
UNDERLYING CONDITION- CLEFT LIP AND PALATE, PATULOUS ET TUBE, IMMUNOSUPPRESSED CONDITION

MICROBIOLOGY:
BACTERIA- STREPTOCCUS PNEUMONIAE, HAEMOPHILUS INFLUENZAE, MORAXELLA CATARAHLIS
ACUTE OTITIS MEDIA:

CLINICAL STAGES:
1. TUBAL OCCLUSION STAGE-
NASOPHARYNGEAL END OF ET TUBE OEDEMATOUS, EARACHE, LOSS OF CONE OF LIGHT, FORESHORTENED
HOM
2. PRE-SUPPURATIVE STAGE-
ASCENDING INFECTION VIA THE LUMEN OR SUBEPITHELIAL LYMPHATICS OF ET TUBE, FEVER WITH
THROBBING EARACHE, CART WHEEL APPEARANCE FOLLOWED BY FULL CONGESTION
STAGE OF HYPERAEMIA-
STAGE EXUDATION: FROM DIALATED CAPILLARIES OF MIDDLE EAR CLEFT (FIBRIN, PMN) AND METAPLASTIC
GOBLET CELLS
3. SUPPURATIVE STAGE-
FORMATION OF PUS IN MIDDLE EAR, FEVER & EARACHE, MAY BE A PUS POINT
4. RESOLUTION STAGE-
WITH OR WITHOUT PERFORATION AS A SEQUALAE
5. COMPLICATION STAGE-
COALESCENCE OF MASTOID AIR CELLS: HYPERAEMIC DECALCIFICATION AND OSTEOCLASTIC ACTIVITY,
PERSISTENT EAR DISCHARGE
FACIAL PALSY
MASKED MASTOIDITIS
PROGRESSION TO SOM
LABYRINTHITIS
ACUTE OTITIS MEDIA:

TREATMENT:
ANTIBACTERIAL SUPPORT- START EMPERICALLY, REVIEW AFTER 48-72 HOURS, CHANGE AND AGAIN REVIEW AFTER
10 DAYS
ANALGESIC AND ANTIPYRETIC-
NASAL DECONGESTANT DROPS-
ORAL NASAL DECONGESTANT-
MYRINGOTOMY- SURGICAL EVACUATION OF PUS

INDICATIONS OF MYRINGOTOMY:
SEVERE OTALGIA, TOXIC CHILD
IMPENDING PERFORATION
PRESENCE OF COMPLICATION
POOR RESSPONSE, PERSISTENT INFLAMMATION BEYOND 12 WEEKS

MYRINGOTOMY:
INCISION IN THE ANTERO-INFERIOR QUADRANT, CIRCUMFERENTIAL INCISION, WITH A MYRINGOTOME
ACUTE NECROTIZING OTITIS MEDIA:

ASSOCIATED WITH VIRAL EXANTHEMES LIKE MEASLES, SCARLET FEVER, INFLUENZA

CAUSED BY BETA HAEMOLYTIC STRPTOCOCCI
RAPID DESTRUCTION OF WHOLE TYMPANIC MEMBRANE WITH ITS ANNULUS, MUCOSA OF PROMONTARY,
MASTOID AIR CELLS, OSSICULAR CHAIN ETC
PROFUSE OTORRHOEA
VERY PRONE TO DEVELOP SECONDARY ACQUIRED CHOLESTEATOMA
TREATMENT- ANTIBIOTIC THERAPY, AS TRIAL, IF DOES NOT RRESPOND, CORTICAL MASTOIDECTOMY

RECURRENT ACUTE OTITIS MEDIA:

BETWEEN 6 MONTHS TO 6 YEARS OF AGE,ATTACKS 4/5 TIMES A YEAR, MOST LIKELY WITH UNDERLYING
PATHOLOGY I.E. VELOPHARYNGEAL INSUFFICIENCY, ADENOID HYPERTROPHY, ENLARGED TONSILS, NASAL ALLERGY,
IMPROPER FEEDING POSTURE
TREATMENT- ANTIBIOTICS, MYRINGOTOMY AND GROMMET INSERTION, TREATMENT OF UNDERLYING CAUSE.
CHRONIC OTITIS MEDIA:

ALWAYS CHARACTERISED BY A PERMANENT DEFECT IN THE TYMPANIC MEMBRANE

BASIC PATHOLOY: HISTOLOGICAL DEGENERATION OF LAMINA PROPIA

RELATION WITH MASTOID PNUMATIZATION:

INFECTION IN EARLY CHILDHOOD HAMPERS NORMAL PNEUMATIZATION
FAILURE OF PNEUMATIZATION AGAIN LEADS TO WIDESPREAD DISEASE PROGRESSION

DISEASE OF LOWER SOCIO-ECONOMIC STATUS

BACTERIOLOGY- MIXED FLORA, PSEUDOMONAS, PROTEUS, E COLI, STAPH. AUREUS, BACTEROIDS

TYPES:
MUCOSAL- ACTIVE, INACTIVE, HEALED
SUAMOUS- ACTIVE, INACTIVE
WHAT IS A PERMANENT PERFORATION?
VARIOUS TYPES OF PERFORATION- PARS TENSA (CENTRAL, MARGINAL), PARS FLACCIDA
CLINICAL PRESENTATION:
EAR DISCHARGE- MUCOSAL VS SQUAMOUS DISEASE
HEARING LOSS- AUTO Type III, SHIELDING EFFECT, CHOLESTEATOMA HEARER

APPROACH TO DIAGNOSIS:
EUM, MICROBIOLOGY, PTA, RADIOLOGY, PAC TESTS

MANAGEMENT: MUCOSAL VS SQUAMOUS

SEQUALE OF CHRONIC OTITIS MEDIA:

PERFORATION, OSSICULAR EROSION, ATELECTASIS, TYMPANOSCLEROSIS, CHOLESTATOMA FORMATION,
CONDUCTIVE HEARING LOSS, SENSORINEURAL HEARING LOSS

COMPLICATIONS OF CHRONIC OTITIS MEDIA:

BEYOND THE MUCOPERIOSTEAL LINING OF MIDDLE EAR CLEFT
UNCOMMON THESE DAYS DUE TO HIGHER ANTIBIOTIC USE
(DIRECT BONE EROSION, VENOUS THROMBOPHLEBITIS OF DURAL EMISSARY VEINS, PREFORMED PATHWAYS-
PATENT SUTURE, OVAL WINDOW, ROUND WINDOW, IAC, SURGICAL WINDOW LIKE STAPEDOTOMY, FRACTURES)
INTRATEMPORAL- MASTOIDITIS, FACIAL PALSY, LABYRINTHITIS, PETROSITIS
INTRACRANIAL- MENINGITIS, EXTRADURAL ABSCESS, SUBDURAL ABSCESS, BRAIN ABSCESS, LATERAL SINUS
THROMBOPHLEBITIS, OTITIC HYDROCEPHALUS
CHOLESTEATOMA:
DEFINITION- IT IS A THREE DIMENSIONAL SAC LIKE STRUCTURE, FORMED BY EPIDERMAL AND CONNECTIVE
TISSUE, WHICH SPREADS VIA BONE EROSION AND CONFORMS THE SHAPES OFVARIOUS MIDDLE EAR CLEFT
STRUCTURES AND HAVE A TENDENCY TO RECURR EVEN AFTER REMOVAL.
PARTS- CENTRAL KERATIN PEARL, MATRIX (KERATINISING SQUAMOUS EPITHELIUM ON FIBROUS STROMA,
PERIMATRIX

CLASSIFICATION-
CONGENITAL- DERLACKI AND CLEMIS CRITERIA
AQUIRED-
PRIMARY- WITTMACK’S INVAGINATION THEORY, RUEDI’S BASAL CELL HYPERPLASIA THEORY, SADE’S
METAPLASIA THEORY
SECONDARY- HABERMANN’S EPITHELIAL MIGRATION THEORY, SADE’S METAPLASIA THEORY

MECHANISM OF BONE EROSION-

HYPERAEMIC DECALCIFICATION, OSTEOCLAST ACTIVATION, ENZYMES- COLLAGENASE, ACID PHOSPHATASE,
MATRIX METALLOPROTEINASE, INTERLEUKINS.

TYPES-MESOTYMPANIC VS ATTIC CHOLESTEATOMA (ANTERIOR & POSTERIOR)

ROLE OF ET TUBE AND MASTOIDS, HOW CHOLESTEATOMA IS FORMED:

MIDDLE EAR IS A GAS FILLED (0.5 ML) STRUCTURE TO ALLOW LEAST RESISTANCE FOR THE OSSICLES, ALMOST
SIMILAR TO AIR PRESSURE OF EAC FOR OPTIMAL SOUND TRANSFER
1 -2 MICROLIT GAS PER MINUTE LOST FROM MIDDLE EAR VIA DIFFUSION INTO SURROUNDING CIRCULATION
BALANCED BY ET TUBE SPONTANEOUSLY OPENING (VIA SWALLOWING) ALMOST 1000 TIMES A DAY, ENTRY OF 1 -2
ML AIR INTO MIDDLE EAR EVERY DAY BY ET TUBE ACTION
MASTOID AIR RESERVE RANGE 1ML TO 30ML DEPENDING ON PNEUMATISATION, BUFFERS PRESSURE CHANGE
INSIDE MIDDLE EAR CLEFT, (MIDDLE EAR ONLY EXCEPT MASTOID AIR CELL SYSTEM HAS ONLY 0.5 ML AIR RESERVE)

BLOCK IN ET/ POOR PNEUMATISATION LEADS TO POOR VENTILATION AND ABSORPTION OF AIR FOLLOWED BY
TYMPANIC MEMBRANE RETRACTION
GRADES OF PARS TENSA AND STAGES OF PARS FLACCIDA RETRACTION

PARS TENSA POSTEROSUPERIOR PART AND ATTIC AREA MORE PRONE

ROLE OF TYMPANIC ISTHMII- SELECTIVE AND GLOBAL DYSVENTILATION

RETRACTION POCKET FIRST SELF CLEANSING, THEN DEVELOPES CHOLESTEATOMA PEARL

TUBERCULAR OTITIS MEDIA:
EITHER SECONDARY TO PTB OR HAEMATOGENOUS SPREAD FROM TB LN
SLOWLY PROGRESSIVE PAINLESS OTORRHOEA WITH PALE GRANULATIONS, MULTIPLE PERFORATIONS, SEVERE
HEARING LOSS AND FACIAL PALSY
ATD AND SURGICAL MANAGEMENT

SYPHILITIC OTITIS MEDIA:

FOETID EAR DISCHARGE AND SENSORINEURAL HEARING LOSS

SECRETORY OTITIS MEDIA:

ET TUBE DYSFUNCTION DUE TO ADENOID HYPERPLASIA, CHRONIC TONSILLITIS, CLEFT LIP/ PALATE; UNRESOLVED
OTITIS MEDIA; VIRAL INFECTION- ADENO & RHINO
INTACT TYMPANIC MEMBRANE WITH CONDUCTIVE HEARING LOSS; MAINLY IN SCHOOL GOING CHILDREN
C TYPE/ B TYPE CURVE IN TYMPANOMETRY
TREATMENT- MYRINGOTOMY AND GROMMET INSERTION, CORTICAL MASTOIDECTOMY

BIOFILM:
PROTECTIVE POLYSACCHARIDE COAT SECRETED BY BACTERIA ITSELF/ BACTERIAL COLONY WHEN BACTERIA ATTACHES
TO A ORGANIC/ INORGANIC SURFACE
PROTECTS FROM PHAGOCYTOSIS AND ANTIBODY IN BLOOD, BUT PROVIDES NUTRITION
PERSISTS ON TYMPANOSTOMY TUBE, TONSIL/ ADENOID
PREVENTED BY ANTIBIOTIC COATED TYMPANOSTOMY TUBE