The document provides details on performing a clinical evaluation of the ear. It outlines aspects to cover in the patient history, including chief complaints, history of presenting illness, ear pain, impaired hearing, tinnitus, vertigo and other associated symptoms. Details on character, severity, duration, progression and relieving/aggravating factors are described for each symptom. The evaluation also involves taking past medical, family and treatment histories relevant to the ear condition.

1. CLINICAL EVALUATION
OF EAR
Presenter :DR.R.THAVAMANI MS PG

2. History taking
 Name
 Age
 Sex
 Occupation
 Residence
 CHIEFF COMPLAINTS
Elicit from patient
In children –informant is mother
Complaints noted in chronological order

3. History of presenting illness
 EAR DISCHARGE
 Side : right /left /bilateral
 Duration : short , intermittent ,Long
 Short duration discharge :Asom and frunculosis
 Intermittent :csom tubi tymbanic type
 Long :Attico antral type ,granulomatous condition and malignancy
 ONSET :
 Sudden onset after URI Common in ASOM
 Insidious onset :TT csom and granulomatous condition and malignancy

4. Severity and character of discharge
 Severity of discharge
 Profuse Discharge common in TubO tymbanic type of csom
 Due to secondary infection
 Scanty Discharge present in attico antral type due to osteitis
 Characteristics of discharge:
 Watery discharge :Csf otorrhea ,eczematous condition due to otitis
externa
 And viral myringitis
 Mucoid discharge : otitis media
 Prulent discharge : Frunculosis , mastoiditis ,Csom (attico antral
disease) ,malignant otitis externa
 Muco purulent Discharge :Csom tubo tymbanic type, secondary
infection in attico antral type

5. Progress of discharge
 Intermittent discharge seen in Tubo tymbanic type of csom
 Continous discharge : Attico antral type, granulomatous
condition , malignancy
 Blood stained discharge :Asom (stage of
suppuration),Csom attico antral type, myringitis Bullosa,
malignant otitis externa,granulation Tissues,trauma
instrumentation,slag burn injury , malignancy of Eac and
middle ear
 Bloody discharge :Trauma , rupture of jugular bulb ,
malignancy of Eac and middle ear ,glomus tumor

6. Cont..
 Pulsatile discharge: Asom with hole perforation, coexisting vascular tumor
with otitis media, Ica aneurysm ,glomus jugularae,glomus tympanicum
 Discharge with retro orbital pain : petrositis,patchy meningitis,Localized brain
abscess in pterous area
 Foul smelling discharge : AAD, Granulomatous Conditions myiasis,chronic
foreign body, Malignancy with secondary infection
 Brownish discharge: Due to wax
 Greenish discharge :pseudomonas infection
 How long each attack Last ?
 Short duration Indicative for good immunity ,Well controlled with
medication and organism sensitive to antibiotics –Suggestive of TTD
 Long duration : Indicates poor immunity drug resistance in TTD ,and
AAD
 Granulomatous condition

7. Impaired hearing
 Side –Right /left/bilateral
 Duration
 Onset- Since birth , acquired (sudden ,gradual, insidious)
 In congenital hearing loss –enquire about ante natal, perinatal ,postnatal
causes like Torch infection
 Acquired causes of hearing loss:

8. Cont..
 Causes in the middle ear
 I) Traumatic: haemotympanum, ossicular dislocation
 ASOM, CSOM,OME,ANOM
 Barotrauma otitis media
 Adhesive otitis media
 Tympanosclerosis
 Aural polyp
 Syphilitic otitis media
 I I ) Otosclerosis
 12) Growth in the middle ear. Glomusju sq cell carcinoma.
 Causes in the eustachian tube
 Tubal catarrh or obstruction
 ET dysfunction
 Barotrauma
 Enlarged adenoids
 Growth in the nasopharynx

9. Metabolic and systemic causes
 Wegener’s granulomatosis
 Relapsing polychondritis
 Fibrous dysplasia
 Eosinophilic granuloma
 Sarcoidosis

10. Causes of sudden sensorineural hearing
loss
 i) Cochlear causes:
 Inflamnlatory: bacterial, viral and chlamy-dial
 Traumatic: electricity, postoperative and head injury
 Vascular: as in hypertension and TAO
 Hematological: as in anemia, polycythemia, sickle cell anemia,
leukemia
 Connective tissue disorders:
 as SLE,
 PAN, Cogan’s disease
 Endolymphatic hydrops
 Metabolic causes: diabetes mellitus, hyperlipidemia, hypothyroidism
 Ototoxic drugs
 ii) Retrocochlear: Meningitis, VHK syndrome, CP angle tumors

11. Cont..
 Is the hearing better in noisy or silent environment?
 Hearing better in noisy environment (paracusis willisii) is characteristic ofotosclerosis.
Better hearing in silent environment is suggestive of sensory neural hearing loss.
 Autophony: is abnormal perception ofone’s own voice. Is often associated with secretory
otitis media and patulous eustachian tube. F) Diplacusis: difference in pitch in different
ears seen in Meniere’s disease.
 Recruitment of loudness: a relatively small increase in the intensity of the auditory stimulus
may cause frank discomfort to the listener.
 Is the hearing loss fluctuating?
 Fluctuating hearing loss seen in: (1) Meniere’s disease, (2) Lermoyez’s disease, (3)
labyrinthine fistula, (4) otitis media with effusion, (5) glomusjugulare, (7) metabolic
causes — hyperglycaemia, hypoglycemia, hyperlipidimia, hypothyroidism, (8) Cogan’s
disease, (9) eustachian tube dysfunction
 Acute exacerbation of chronic hearing loss
 CochleaIar HL: renal dysfunction, thyroid dysfunction, diabetes mellitus, vascular disorders,
immune diseases and cervical syndrome.
 Retrocochlear: Acoustic neuroma, vascular damage, brainstem tumors and multiple
sclerosis.
 Hearing loss is progressive or not? Hearing loss is progressive in Meniere’s disease,
otosclerosis.

12. Cont..
 H/o noise-induced trauma
 H/o fever in childhood (measles, mumps, herpes
predisposes to SN loss)
 I) H/o drug abuse (ototoxicity)
 Family history of deafness: otosclerosis, Meniere’s disease
run in family
 Related to pregnancy: Hearing loss in otosclerosis gets
aggravated during pregnancy

13. Ear Pain

14. Earpain
 I ll. Ear Pain
 a) Site: right/leftfilateral b) Duration
 Onset: sudden/insidious
 Sudden onset is seen in furunculosis, ASOM, traumatic.
 Gradual onset is seen in CSOM, malignant otitis externa, granulomatous conditions,
malignancies.
 Type: buming/pricking/throbbing/stabbing
 Severity: Disturbs sleep constantly +/- ? Severe pain is not uncommon in frost bite.
furunculosis and acute diffuse infiltrative type ofotitis externa. Severe pain often
heralds the eruption ofvesicles in herpes zoster. Pain is seen in myringitis bullosa
characterized by the presence ofblebs in the tympanic membrane and meatus
associated with serous discharge.
 The intensity of the pain does not decrease even when the bleb ruptures. Sudden
spontaneous resolution ofpain is seen in cases ofacute otitis media indicating
perforation of the tympanic membrane.
 Severe pain in a chronically discharging ear may reflect neoplastic change or dural
invasion.

15. Aggravating factor
 Lying on the affected side of ear Applying pressure over the tragus/pulling auricle Change
in weather
 Pain during chewing and eating is common in otitis externa.
 Pain during sneezing and coughing is common in eustachian tube dysfunction in children.
Pain due to eustachian tube dysfunction in children occurs at night when the child is
sleeping and is due to venous congestion in the eustachian tube area with reduced
frequency ofswallowing, and consequently failure of middle ear ventilation. Pain due to
ET block may be experienced during winter as exposure to cold results in spasm of the
tensor tympani muscle.
 Relieving factors: medication
 Associated with otorrhea
 Referred pain.
 Via trigeminal nerve — can be ofdental, oral cavity or TMJ pathology. Via
glossopharyngeal nerve can be due to base of tongue or oral pathology. Via vagus can be
due to lesions in larynx and viaC2,and C3 due to cervical pathology

16. Tinnitus
Tinnitus is defined as any sound perceived by the patient when no external
source of sound exists.
Side: unilateral or bilateral
Duration,Progress: progressive/continuousfintermittent/
 Character: hissing, buzzing, rushing or bell
 High pitched/low pitched
 Sleep disturbances +/-
 Ho drug abuse: salicylates, quinine, amino –
 Ho trauma:

17. Significance of tinnitus
 Middle ear tinnitus is constant orpulsatile and usually oflow pitch.E.g.: (I)
Traumatic TM injury, (2) otosclerosis — constant tinnitus (3) ASOM — tinnitus
is pulastile, (4) Barotrauma — pulsatile — tinnitus, (5) glomus—tinnitus is
synchronous with pulse and (6) patuIous eustachian tube— synchronous with
respiration.
 Cochleartinnitus is high pitch. E.g.: (1) toxic—aminoglycosides, diuretics,
salicylates (2) Acute noise, (3) Meneire’s disease, (4) labyinthine apoplexy.
 Cervical tinnitus: fluctuating sound, low pitched which is more in the
morning
 Mixed cochlear neural tinnitus: Presbyacusis, syphilis.
 Neural tinnitus: Unilateral, constant, high pitched and usually masking well
above the threshold — acoustic neuroma.
 Central tinnitus: Resistant to masking
 Subjective type of tinnitus is heard only by the patient as seen in
psychological and Meniere’s disease and ototoxicity, and objective tinnitus is

18. Vertigo
 Vertigo is defined as a sense of rotation in relationship to the environment, where either the patient or
the environment is moving. Unsteadiness is characterised by loss ofequilibrium often with a sensation
offalling.
 Duration
 Episodes: constant/periodic
 Frequency of attacks
 Precipitating causes as different head position. Sudden onset of rotatory dizziness associated with certain
head position is diagnostic of BPPV
 Relieving factors
 Association with hearing loss
 Association with otorrhea
 Accompanied by nausea and vomiting
 Association with coughing and sneezing. Vertigo associated with coughing or sneezing suggests the
presence ofa perilymph fistula.
 Association with exposure to loud sound. Tullio phenomenon is the vertigo caused by loud sounds and
may be due to endolymphatic hydrops or a third labyrinthine fistula.

19. Vertigo with deafness
 Vertigo with deafness due to
 (l) Meniere’s disease,
 (2) labyrinthitis,
 (3) acoustic neruroma,
 (4) labyrinthine trauma,
 (5) perilymph fistula,
 (6) ototoxicity,
 (7) cholesteatoma,
 (8) otosclerosis

20. Fullness of ear
 VI. Fullness of Ear
 Blocking sensation Of ear without hearing loss which disappears on lying down and
alters with change of position of head is due to patuIous ET.
 Blocking sensation of ear is common in eustachian tube dysfunction and early
stages of otitis media with effusion. Blocking sensation of ear which is aggravated
on lying down is due to venous congestion around the ET in ET dysfunction.
Fullness of ear is one of the symptoms of Meniere’s disease.
 Vll. Itching and Irritation of the Ear
 • Associated with allergy
 products from CSOM.
 Fungal infection
 Otitis externa Foreign bodies Impacted wax
 Allergic reaction due to ear drops

21. Cont..
 VI”. Hyperacusis
 Patient experiences undue sensitivity toloud sound as in stapedial nerve palsy in facial nerve paralysis.
 IX. History of Etiology — H/o
 Nasal obsuuction
 Nasal discharge
 Postnasal discharge (hawking sensation)
 hroat initation/pain
 Dysphagia/odynophagia
 Change ofvoice
 X) Symptoms Associated with Ear Diseases
 Nausea: common in motion sickness, labyrinthitis, Meniere’s disease and vestibular neuronitis
 Vomiting: acute labyrinthitis, Meniere’s disease and perilymph fistula
 Light headedness: Meniere’s disease
 Headache: meningitis, extradural abscess, subdural abscess and brain abscess
 Fever: ASOM in children, sinus thrombophlebitis and meningitis
 Cervical pain: Patient may present With giddiness

22. Past history
 Past History
 History of similar illness in the past? Details of The same
 In adults the past history should include details ofany previous inflammatory conditions and
otological operations. Any history ofprevious head injury is also relevant since trauma may
damage the middle ear structures and the vestibular apparatus.
 The following conditions can lead to ear prob-
 Hypertension — sudden-onset SN loss.
 Allergy and bronchial asthma — Eustachian tube dysfunction, secretory otitis media. Patients with
allergic rhinitis are prone for eustachian tube dysfunction which acts as a precursor for all sorts
of otitis media. Diabetes mellitus —malignant otitis media, SN loss of sudden onset.
 Exanthematous diseases such as mumps, chickenpox, measles can cause SN loss.
 Radiation can cause SN loss.
 Thyroid disease — antithyroid frugs can cause giddiness.
 H/o diabetes mellitus, hypertension, CAD, allergic rhinitis (dust and drugs), tuberculosis and
asthma. Wo of any general surgery?
 In a child of breast-feeding age group, enquire about the breast-feeding technique and belching
habits after breast-feeding. Faulty feeding technique and avoidance ofbelching may predispose to
ET dysfunction

23.  Family history
 Family history ofautoimmune diseases may help pinpoint the autoimmune origin
ofsuddenorfluctuant and progressive sensorineural hearing loss. History of
consanguineous marriage—causes high incidence ofdeafmutism.
 PERSONAL HISTORY
 Smoking and alcoholism Appetite
 Diet
 Sleep
 Bladder and bowel habits
 Weight loss
 Marital status and siblings
 Noise-induced hearing loss is common in industry workers. Habits such as smoking
and alcoholism can cause hearing loss and giddiness.
 TREATMENT HISTORY
 Any treatment taken before? Duration of treatment? Any benefits from the
treatment

24. Cont..
 Obstetrics HISTORY
 It is relevant when deafness is suspected in early infancy.
 It is particularly important to elicit a history ofmaternal contact with infectious
diseases such as rubella, mumps, measles, or of administration ofototoxic drugs
to the mother during the first trimester.
 Postnataljaundice may also cause deafness due to the deposition of conjugate
bilirubin in brainstem nuclei and deafness may follow birth trauma or anoxic
episodes in the neonatal period.

25. LOCAL EXAMINATION OF 👂
 LOCAL EXAMINATION
 Physical examination of the ear.Examine the normal ear first.When you
examine the diseased ear, it may be painful sometimes and may hurt the
patient and he may lose confidence in you and he may not cooperate for
the rest of the examination. Secondly, it can prevent transferring infection
from the diseased ear to a normal ear.
 Pinna
 Inspection
 Look for the following- size, displacement and shape of the pinna.
 Size ofPinna
 Anotia, microtia, macrotia, polysia and presence of accessory tubercles
 Anotia is absence of pinna
 Macrotia is presence of large pinna Microtia is presence of small pinna.
 Microtia is presence of small pinna

26. Congenital anomalies of auricle

28. Swelling in pinna
Looking for following sign in pinna : Swelling ,scalling , vesicles ,Scar ,keloid,Ulcer, growth

29. Keloid

30. Cont..
On palpation:
look for local rise of temperature (suggestive ofinflammation), thickness oftissue (perichondritis),
fluctuation (seroma < abscess) and tenderness (furunculosis of external auditory canal).
 Pain during traction of the pinna and pressure on the tragus is common in otitis externa.
 Il. Preauricular Region
 Look for scar and swelling in the preauricular region.
 Scar: can due to (I ) trauma and (2) previous operation.
 Swelling can be due to (I) zygomatic abscess, (2) lymph nodes, (3) cellulitis due to preauricular
sinus infection. The presence of
 Fistula: Mastoid fistula can be due to surgery or granulomatous conditions. Skin around the
fistula will be adherent to the mastoid.
 Obliteration of the retroauricular groove is characteristic of furunculosis ofthe meatal wall. It
is associated with protrusion of the pinna and positive tragus sign.
 Edema extending to the occipital region is Grie singer’s sign, seen in sinus throm bophlebitis
due to thrombosis ofthe emissary veins.
 Erysipelas: Infection of superficial dermis and consists of well-demarcated, erythematous,
edematous warm plaque.

31. Palpation of mastoid
 Palpation of Mastoid
 Normally skin over the mastoid is mobile and the mastoid
bone is uneven on palpation.
 Increased rise oflocal temperature is seen in mastoiditis and
abscess. Skin over the mastoid may be adherent in case of
osteoperiostitis, fistula and malignant conditions.
 Ironed out mastoid (smooth mastoid surface) is seen in
coalescent mastoiditis. Tenderness is to be elicited in the
mastoid tip along the posterior border of mastoid and in the
antrum which corresponds to the cymba concha (corresponds
to Mc Even’s triangle—bony landmark for mastoid antrum).
Tenderness is seen in mastoiditis

32. External auditory canal
 Method of examination: The pinna is held between the thumb and
index finger, and is pulled backwards, upwards and outwards in an
adult (Fig. I .9).
 In children, the pinna is pulled downwards instead of upwards as the
drum is more horizontal, to straighten out the curved cartilaginous
part of the external canal so as to allow a more direct vision of the
canal and tympanic membrane (Fig. I. 12).
 In case ear speculum is to be used for examination of the EAC, the
pinna is retracted with the middle and ring finger and speculum is held
wih the thumb and index finger and introduced slowly wih a rotating
movement into the EAC (Fig. 1.10)

33. Cont..
 Inspection
 Incision scar of previous per-meatal operation of Lempert’s type Il and Heerman’s in-
cisions. The incision is noted in the area be tween the tragus and the helix
 Size of the meatus: narrow/wide
 Narrow EAC can be due to congenital or acquired causes. Congenital stenosis can be
unilateral or bilateral, partial or complete, membranous or osseous.
 Causes for acquired narrow EAC: ( 1 ) post operative (faulty meatoplasty), (2)
following trauma, (3) due to blunting following lateral graft technique, (4) due to
keloid in EAC, (5) chronic otitis externa (6) burns, (7) post radiation and 8)
malignancy.
 Wide EAC canal is seen in post tympanomastoi-dectomy with meatoplasty and
otosclerosis.
 Contents of lumen: Look for the presence of wax, debris, discharge, FB, polyp and
otomycosis.
 Wax: can be soft/hard. Wax can be impacted.
 Mass with pearly white surface (keratin plug) filling the deep meatus is characteristic
of keratosis obturans. The canilaginous meatus is not involved but granulations may
occur at the junction of the eroded bony and cartilaginous part.

34. Discharge and otomycosis..
 Discharge: Note the characteristics of the discharge. Mucoid,
mucopurulent, purulent, bloody, bloodstained or brownish.
 Polyp: DD — aural polyp, osteoma, papilloma, bony overhang,
rhinosporidiosis, ceruminoma, malignancy.
 Otomycosis: canal is clogged with pultaceous debris which on removal
reveals magenta-colored epithelial surface stud ded with glistening white
deposits.
 Aspergillosis is characterized by white deposits or wet blotting paper
appearance/ wet newspaper appearance (Fig. 1.13). Candida usually
causes edema and maceration ofthe external auditory canal and the
lumen may be filled with a curdlike

35. Swelling of Eac
 d) Swelling ofthe EAC: Furuncle, edema, os-teoma, exostoses,
vesicular eruptions, granulations, papilloma, sebaceous adenoma,
ceruminoma and neoplasms
 Furuncle seen as tender swelling in thecartilaginous part ofthe meatus
with posi-tive tragus sign (Fig. L. 18). Associated
 enlargement of the lymph node anteriorto the tragus may be seen in
case thefuruncle is seen in the anterior wall.
 In infiltrative type ofacute diffuse otitis externa, EAC is edematous,
but indesquamative type it is raw, red and shiny
 Bony overhang: smooth overhang usually bilateral and the skin over
the swelling will be normal. Compact osteoma
 (exostosis) is bilateral, attached to the underlying bone, broad based,
multiple, of slow growth and common in swimmers Single cancellous
osteoma is unilateral, single, seen in tympanosqua mous suture line,
pedunculated, with rapid growth.

36. Cont..
 Vesicular eruption on the meatus seen in Herpes zoster infection. Bleb may be seen in the meatus in
myringitis bullosa. Bleb is usually seen in the tympanic membrane which ruptures to discharge a se-
 rous fluid.Vesicles with serous discharge are characteristic of eczema due to an infecting organism or
an allergenic material, usually antibiotic ear drops.
 Granulations: seen in granular myringitis, malignant otitis externa, tuberculosis, syphilis, sarcoidosis,
early polyp, FB ear, glomusjugulare and malignancy. Granulations in malignant otitis externa, is
particularly seen on the floor.
 Papilloma: Typical papilloferrous appearance. Associated similar lesions may be seen on the fingers.
 Sebaceous adenoma presents as a smooth, painless, skin-covered swelling in the outer part of the
meatus.
 Keratoacanthoma: Discrete, globular, umbilicated and when the debris is scraped away a definite crust
is exposed.
 Molluscum contangiosum: White umbilicated tumor from the centre of which a pultaceous white
substance can be expressed on squeezing.
 Fibroma is pedunculated, firm and painless growth. Ceruminoma presents as a firm, skin- covered mass
in the cartilaginous meatus, which may be sessile or polypoidal.
 Sagging of the posterosuperior meatal wall is noted in acute mastoiditis.Compare with the normal side.
 Neoplasm: growth characteristics have to be detailed

37. Examination of TM
 Tympanic Membrane
 Normally it is pearly white in color and semitransparent and obliquely set at
the medial end of the meatus.The handle ofmalleus, normally is yellow in
color, passes downwards and slightly backwards from the lateral (short)
process.
 The light reflex passes downwards and slightly forwards from the umbo, the
lowest point of the malleus. The cone oflight is a reflection of light
 from that small part of the membrane which lies at right angles to the beam
oflight. The long process of incus can sometimes be seen behind the handle of
malleus, parallel to it and midway between it and the posterior bony wall of
the canal
 The anterior and posterior malleolar folds mark the upper end of the fibrous
layer and separate it into pars tensa below and pars flaccida
 The tympanic membrane is divided into four quadrants by drawing an
imaginary line horizontally touching the tip of the umbo, and a second line
vertically along the long process ofthe handle ofmalleus.The quadrants are (
I ) anterior superior quadrant, (2) anterior inferior quadrant , (3) posterior
superiorquadrant and (4) posterior inferior quadrant

38. Cont..
 Non-lustrous membrane seen in (l) after grafting, (2) resolved chronic
otitis media and (3) fungal infection.
 Red and congested membrane is seen in (1 ) acute otitis media (Stage
ofhyperemia), (2) glomusjugulare, (3) glomus tympanicum (4)
highjugularbulb and (5) myringitis, (6) excessive crying
 Bluish membrane is seen in (l) secretory otitis media, (2)
hemotympanum, (3)
 otosclerosis (Schwartz’s sign), (4) leukemia, (5) middle ear vascular
tumors, (6) refractory chronic serous otitis media, , (8) barotrauma,
(9) idiopathic hemotympanum, (10) clotting disorders, (11)
cholesterol granuloma and

39. Colour of TM
 Pink and translucent tympanic membrane seen in (1) acute eustachian tube dysfunction and
(2) otitis media with effusion.
 Yellow tympanic membrane seen in chronic otitis media with effusion.
 Blackish grey coated membrane which can be cleared off is seen with Aspergillum niger.
 White membrane which can be cleared off is seen with Candida albicans.
 Reddened with dark brown bullae: Hemorrhagic bullae.
 Chalky patch membrane seen in ) 1) tympanosclerosis, (2) adhesive otitis media, (3)
atelectatic drum, (4) thinned tympanic membrane, (5) congenital cholesteatoma, (6)
ventilation tube in position.
 Fluid levels or bubbles are usually seen in the serous form of the middle ear effusion. The
bubbles are not usually seen unless the patient has had positive pressure applied to a closed
nasopharynx. Generally, it implies a favorable prognos- tic sign, because it indicates a
normfunction eustachian tube function.
 Dark grey dull membrane is seen in eustachian tube dysfunction.

40. Position of TM
 C) Position of the tympanic membrane: bulged/retracted
 Bulged tympanic membrane in pars tensa
 1. Acute otitis media (stage ofexudation),Hemotympanum
 Otitismedia with effusion with goodET function,Neoplasm
 Characters of bulged tympanic membrane
 Distorted COL light
 Apparent increase in length of handle of malleus
 Retracted membrane in pars tensa
 Chronic tubal obsü-uction
 Serous otitis media
 Atelectasis
 Adhesive otitis media
 Apparent shortening of the handle of malleus
 Prominent ossicles
 Prominent malleolar folds
 Siegalization is done to note the movements the tympanic membrane.

41. Classification of retracted TM
 Classification of retracted tympanic membrane (Berco & Sade)
 Stage 1 : Retracted tympanic membrane not in contact with the incus
 Stage 2: Retracted tympanic membrane in contact with the long process of-
incus Stage 3: Retracted tympanic membrane in. Contact with the•
promontory but moves on siegalisation (atelectatic tM) Stage 4: Tympanic
membrane is adherent to the promontory (adhesive TM)
 Retracted tympanic membrane in pars flaccida is seen in ( I) chronic tubal
dysfunction and (2) attic retraction pocket.
 Classification of attic retraction pocket (Tos et al)
 Grade I: Pars flaccida not in contact with the body of incus
 Grade Il: Pars flaccida in contact with body ofincus
 Grade Ill: Limited outer attic wall erosion
 Grade IV: Severe outer attic wall erosion

42. Surface of the TM
 d) Surface ofthe membrane: Bullae, epithelial pearls, calcareous deposits,
perforation and retraction pockets.
 Perforations seen in ASOM, CSOM, ANOM and traumatic perforation
 Bullae
 Epithelial pearls: seen in post myringoplasty.
 Calcareous deposits are tympanosclerosis

43. Perforation of TM
 In case of perforation, look for type, location, size, shape, margin, edge
ofperforation.
 Type: central/marginal/attic
 Location: Perforation is sen in which quadrant in pars tensa or in pars flaccida
 Size ofperforation
 Shape: Oval, round or irregular as in traumatic lesions
 Margins: Magins may be regular in CSOM and irregular in traumatic
 Edge: May be thick in CSOM and thin in ASOM. Look for any ingrowth ofsq
epithelium from the edges of the perforation. Residual drum: Whether it is
congested or atrophic and presence oftympanosclerotic patch

44. Cont..
 Perforation may be central (pars tensa), attic (pars flaccida) or marginal (at the periphery involving
the annulus).
 Central perforation is one that is confined to the pars tensa of the tympanic membrane and its entire
circumference is bounded by a rim of intact membrane with associated intact annulus. Marginal
perforation is one that involves the periphery of the membrane and the adjacent annulus.
 Central perforation may be small/medium/ large/subtotal/total. Small central perforation: central
perforation involving 25% of the tympanic membrane (one quadrant of the membrane). Moderate
central perforation: central perforation).
 Involving 50% of the tympanic membrane (two quadrants of the membrane). Large central
perforation: central perforation involving 50—75% of the tympanic membrane (involving three quad-
 Sub total central perforation: Central perforation involving more than 75%, but less than 100% of the
membrane. Total perforation: involves 100% of the tympanic membrane (four quadrants Of the
membrane).
 Single small central perforation seen in ASOM and after grommet extrusion
 Single large central perforation: seen in (l ) CSOM, (2) late stages of tuberculosis and (3) ANOM.
 Central perforation with jagged edges seen in recent trauma.
 Multiple perforation seen in (l) acute onset tuberculosis, (2) otitis media in measles and (3) Wegener

45. Retro tympanic mass
 White mass: congenital cholesteatoma (inferior) or facial nerve schwannoma
(superior)
 Red anteroinferior mass: Glomus tympanicum, paraganglioma
 Blue posteroinferior mass: Dehiscent jugular bulb
 Red mass crossing TM from posterior to anterior: Aberrant ICA
 Traumatic TM perforation can be classified as follows:
 I. Compression injuries: Usually due toa blow to the ear
 2. Instrumental injuries: Can be iatrogenic due to small procedures in the
external canal with occasional injuries to the tympanic membrane orduring
middle ear surgery
 Slag burn injuries: Seen in industries, caused by welding or caustic agents.
These are caused by hot metal from the machines or a welder’s torch
contacting the membrane and passing into the middie ear.
 Blast injuries: These are result of air compression of the tympanic membrane

46. Middle ear
 Structures seen through subtotal perforation are
 Promontory
 Stapes
 Incudostapedialjoint
 ET opening
 Round window niche
 Oval window
 Stapedius tendon

47. Middle ear mucosa
 Middle ear mucosa
 Pale/congested mucosa: Pale mucosaIs seen in allergic rhinitis and in the normal
phase of CSOM. Congested mucosa is seen in inflammatory phase ofCSOM.
 Discharge: Mucoid or mucopurulent discharge is seen in chronic otitis media of
tubotympanic type and bloody discharge with foul smell is seen in chronic otitis
 media of attico antral type and malignancy with secondary infection.
 GranulAation are mostly present in attico antral type of com in granuLomatous
conditions
 Polypoidal mucosa seen in (l) cystic fibrosis, (2) alcohol addiction (3) fungal
infection, (4) Drugs induced — aspirin, anti hypertensives and (5) allergy rhini
tis.
 Look for the presence of tympanosclerotic patches in the middle ear mucosa. Look
for the integrity of the ossicular chain: disruption of the incudostapedial joint,
necrosis ofthe long process of incus, medial retraction and shortening of the
handle of malleus.

48. Eustachian tube
 Vll. Eustachian tube
 Tympanic opening of the tube can be seen in the anterior part of the
middle ear in case of large perforation. Pharyngeal opening of the
tube can be seen by posterior rhinoscopy.

49. Auscultation
 Ausculatation of the Ear and TemporalRegion
 bruits from vascular region can be heard. In cases of patulous eustachian tube, a
stethoscope end inserted into the meatus will pick up the transmitted sounds from the
nasopharynx.
 Vlll. Examination of the Neck
 Exmination of the neck to r/o the presence of Bezold’s abscess where pus traces down
from the mastoid to the medial aspect of the sternomastoid. In case of lateral sinus
thrombosis, the IJV is palpable like a hard cord anterior to the stemomastoid.
 Examination of the Eyes
 Inspection of the eyes may reveal features such as hypertelorism, coloboma, blue scelra
associated with congenital hearing syndrome. Interstitial keratitis is suggestive of syphilis.
Check for corneal reflex, absence of which indicates retrocochlear pathology. Fundoscopy
revealing papiiloedema

50. Nystagmus
 Check for the presence of nystagmus. The term nystagmus is applied to a disturbance of
ocular movement characterized by involuntary, conjugate, often rhythmical oscillations of
the eyes. Nystagmus is most easily seen with the patient looking to the front and the
observer viewing slightly from the side.
 Visual fixation is obtained by placing a finger central to the eye and at least 4 cm from
the nose. The presence or absence of nystagmus is noted, and the finger moved laterally
in the same horizontal plane 30 degees to either side, asking the patient to follow the
finger.
 Congenital nystagmus is pendular in type.
 Vestibular nystagmus may be horizontal or rotatory and has two components, a slow phase
with a fast corrective component in The opposite direction

51. Cont..
 nystagmus is defined in terms ofthe direction of the fast phase. The intensity of the
nystagmus is described in terms of the direction of gaze. Observe the rate,
amplitude and rhythm of nystagmus in each direction and whether or not the
nystagmus is sustained. Direction-changing nystagmus is suggestive ofcentral
pathology.
 Alexander’s law for peripheral nystagmus
 1st degree: Nystagmus when patient looks in the direction of fast component of
nystagmus.
 2nd degree: Nystagmus when patient looks in the direction offast component
ofnystagmus and when patient looks straight ahead.
 3rd degree: Nystagmus when patient looks in the direction of fast component of
nystagmus and the direction ofslow component of nystagmus.

52. Examination of facial nerve
 . Facial Nerve palsy may co exist with any ear disase, hence it is essential to test for facial nerve every
ear cases.
 TEsting the Facial nerve:
 Ask the patient to frown his forehead.
 Look as the normal side.
 Look for spontaneous rolling up of the eyeball termed as Bell’s phenomenon. Try to open the eyes as
the patient tries to keep it closed. If the orbicularis oculi is acting normally, it should be almost
imposSible to open them against the patient’s effort.
 Ask the patient to whistle. He is unable to blow his cheek on the side of facial nerve palsy.
 Ask him to smile or show his upper teeth. The mouth is drawn to the healthy side.
 Xl. Examination of other Cranial Nerves
 Sixth nerve palsy is associated wih (1) petrositis, (2) patchy brain abscess over the temporal region.
Palsy of the lower cranial nerves suggests advanced malignant otitis externa or glomus jugulare.Facial
palsy can be secondary to otitis media

53. Examination of other systems
 Examination of the Nose andThroat
 To rule out sinusitis, pharyngitis and tonsilitis which contribute to the
earpathology.
 Respiratory system: Trachea , air entry on both sides and presence of normal
adventitious sounds
 Cvs: Sl and S2/murmurs
 Per abdomen :organomegaly

54. Functional Examination of the Ear
 Rinne’s test
 Weber’s test
 Absolute bone conduction test
 Rinne’s Test
 Test: The threshold Comparison Method Strike the tuning fork against any bony surface and place it against the mastoid
process of the patient (bone conduction) and when the patient stops feeling the vibration place it 2.5 cm away from the
external auditory canal holding it vertically (air conduction)
 Interpretation
 Rinne’s positive: seen in normal person or SN loss. Here, air conduction is better than bone conduction.
 Rinne’s equal: Air conduction is same as bone conduction. Seen in mild conductive hearing loss. Rinne’s negative: Air
conduction is less than bone conduction. Seen in conductive deafness.
 False negative: seen in severe unilateral sensorineural deafness. Bone conduction is better because of the contribution of
the other ear.
 The test has to be carried out with all the frequencies: 256 1—1z, 512 Hzand 1024 Hz.
 If 256 Hz is negative, it indicates 20 to 40 decibel loss
 The 512 Hz is negative, it indicates 40-60 decibel
 If 1024 Hz is negative, it indicates severe hearing loss.
 Rinne’s test has high specificity but low sensitivity. The cross point at which the Rinne’s test is likely to become negative

55. Weber test
 Weber’s Test
 Aim:To detect the better hearing cochlea
 Technique:Place the tuning fork in mid place of the face (Fig. 1.33) and ask
the patient in which ear he appreciates the sound better (unilateral or
equivocal).
 Inference
 1. Normal: vibration can be appreciated in the vertex, then it is normal
hearing on both sides 2. Conductive deafness: If the vibration is lateralized to
the diseased ear, it is interpreted
 as conductive hearing loss in the diseased side.
 3. Sensorineural deafness: If the vibration is lateralized to the better ear, it is
interpreted as sensorineural hearing loss in the other ear.

56. Absolute bone conduction test
 Technique
 Press the tragus against the external auditory canal and place the vibrating tuning fork against the
mastoid of the patient. When the patient stops appreciating the vibration, transfer the tuning fork
to the mastoid region of the doctor and appreciate the vibration.
 Interpretation



 Gelle’s test
 Procedure: The air pressure in the EAC is altered by using Siegle’s speculum. In a normal person, or
in patients with SN hearing loss, increasing the pressure in the EAC results in decreased sensation of
the loudness from a bone conduction stimulus. If there is no alteration of bone conduction threshold
when the pressure is increased in the EAC itindicates otosclerosis with foot plate fixation.
 Fistula sign: If, following a pressure increase in the external auditory meatus, vertigo and nystagmus
result, a positive fistula sign is said to be present. Such a pressure change can be achieved by simply
compressing the tragus into the Eac-

57. Vestibular Function Test
 Unterberger’s test
 This is modified Romberg’s test wherein the patient is asked to close his eyes
with outstretched hands in front and asked to step up and step down his feet
alternately about 100 times on the point he is standing . The clinician
evaluates the deviation of the patient from his original position after the
test.
 L. Romberg’s test: patient is asked to stand with the feet close together,
and, ifhe can do this and does not sway, he is then asked to close his eyes
and march at a point If Romberg’s sign is present, as soon as his eyes are
closed he begins to sway about or may even fall. If there is defect in the
vestibular apparatus the patient is unable to maintain his original position
and deviates in the course ofexamination.

58. Cochlear function test
 1) whispering btest
 Tuning fork test
 Pure tone audiometry
 Supra threshold test
 Electrocochleogram
 Bera
 Whispering test
1. Normally whispering has to be heard at 6meters
2. Conversation : should heard with in 20meters

59. Pure tone audiometry
 PURE TONE AUDIOMETRY
 Here, a single frequency is used. Single frequency is used because ofthe following reasons:
 Easy to generate,Easy to measure,Easy to calibrate
 Speech is a mixture ofpure tones.
 X-axis: 125 Hz to 8000 Hz in octave. Octave is doubling of frequencies.
 Y-axis is intensity in decibels. From —10 to 120 decibel. Zero level is the level where normal person can
hear at this level. Some can hear better even in —10, hence even this is included. 120 decibel is the upper
limit as this is the discomfort level.
 ‘No response’ only indicates that no response was observed at the highest level that could be produced
within the limits ofthe insüuments used.
 Pure Tone Audiogram,First, properly instruct the patient about what is going to be done.
 Start with air conduction first, because, for air conduction, EAC, middle ear and inner ear are required to
be normal.
 Start with 1 kHz, followed by 2 kHz, 4 kHz and 8 kHz and repeat the 1 kHz again because 1 kHz is the best
frequency to alert the patient and test and retest reliability. 500 Hz and 250 Hz are also tested. Start with
30 dB, ifnormal. Ifthe patient says that he has hearing loss, start with 70

60. Cont..
 The patient responds orally or with signal when he hears the tone. Right ear is plotted with red color
and left with the blue or black color.
 It is repeated with the otherear. Always test the better ear first for air conduction.
 Then perform bone conduction. Here, it is tested only up to 4 kHz, as above this, lot of distortion is
noted.
 Two-rooms setting is necessary when you have to do speech audiometry and free field audiomeåy.
 Air Conduction is Done
 To know whether the patient is deafor normal
 Toknow the degree of impairment
 Bone Conduction is Used
 To know the inner ear status
 To know the type of deafness -
 PTA: Pure tone average is the average of three frequencies — 500 Hz, 1 kHz and 2 kHz. Airbone gap is
the gap between air conduction and bone conduction of all frequencies.

62. Supra threshold test
 Aim ofthe test: to differentiate between cochlear and retrocochlear pathology.
 IndicationsUnilateral SN loss associated with complaints oftinnitus and vertigo.
 Bilateral SN loss with vertigo
 Tests of Recruitment
 Differential liamen test
 50 and 51 decibels given; if patient can still appreciate the difference of 1 decibel difference,
then he has cochlear pathol-
 Short increment sensitivity index
 At normal threshold, the patient will not be able to appreciate the difference of 1 decibel,
hence the tone fortesting is given at 20 decibel above the normal threshold of the patient.
This is the basis of SISI.
 The frequency used is 2 kHz and above. 250, 500 kHz are not reliable.
 First do a basic PTA.
 Next, add 20 decibel to the threshold and set the audiometer in SISI mode where it gives
continuous tone and in between he gets 5 decibel increase. Now 5 decibels is reduced to 4
decibels and 3, 2 and 1 decibel and

63. Cont..
 Each time ask the patient if he can appreciate the difference. 20 interrupted
tone is given at each frequency drop, at 1 decibel difference and ask the
patient to signal each time he hears the interrupted tone.
 SISI Score = number of 1 decibel increment patient heard divided by 20 x 100.
 SISI gram can also be plotted.
 Interpretation
 Jegerclassification
 60—100 It ispositive forrecruitment suggestive ofcochlearpathology
 20-35% ?Coch1ear/RCP
 (0—15% Normal /Conductive /RCP
 Using SISI we can get apredictive value as 91% in cochlear and 48% in RCP.

64. Speech audiometry..
 SPEECH AUDIOMETRY
 Stimulus is speech
 More natural
 Speech reception threshold (speech recognition threshold) Measured in dB.
 —two syllable words with equal stress, e.g., ice cream.
 SRT is the lowest threshold at which the subject can repeat at least 50% of the words.
 Difference between SRT and PTA should not exceed 12 dB. If it exceeds 12 dB, it means the patient is
malingering.
 Speech ,discrimination score (SDC)
 Monosyllables: Phonetically balanced like Man, Van, Tan, Can etc.
 Monosyllables, because it is difficult.
 Used to analyze graphically the percentage of words heard correctly by the sub-
 The test is done 40 dB above the SRT because normally hearing patient should receive 40 dB+ to get
100% score.

65. Cont..
 Usually groups of 25 words are used at each intensity. Every correctly repeated word scores I and
the total score when multiplied by a factor of 4 is the percentage.
 Normal ear: 100%
 Conductive deafness: 100% discrimination or near is usually reached but at higher intensity
 Sensory deafness: Unable to reach high score
 Neural deafness: Classically very poor discrimination scores
 SDC helps to predict the benefit of amplification with hearing aids.
 Most comfortable levels (MCL)
 Uncomfortable level (UCL)
 Threshold of discomfort (TD) Level at which the patient experiences discomfort. This is usually 100
dB.
 Dynamic range: the differtence between the MCL and TD is called as the dynamic range.
 Dynamic range for a normal person is 100
 In conductive loss, patient is able to hear only at 30 dB, andTDwi11be130dB.
 In cochlear deafness, patient will be able to hear at 30 dB and TD will be 60 dB when he
experiences discomfort due to recruitment.

66. Impedance audiometry
 IMPEDANCE AUDIOMETRY
 Impedance is resistance in the flow of energy. Opposite of impedance is compliance.
 Definition
 Impedance is resistance audiometry is the audiological investigation wherein resistance offered by the
middle ear structures to pressure changes in EAC is measured, which helps us in:
 Assessing the middle ear pressure
 Compliance of middle ear structure
 Ossicularpathology—otosclerosis
 Stapedial reflex
 Estimating the volume of ear canal
 Estimating the volume of middle ear
 Evaluating the ET function
 Normal Curves
 By Liden and Jerger
 Type A Curve
 Seen in
 Normal individuals
 Cholesteatoma confined to the attic.

67. Cont...

68. Stapedial reflex
 Sound delivered Results in stapedial muscle contraction Usually in 70 db
 find the difference in compliance before and after giving the sound. If there is change then the stapedial
reflex is positive.
 The minimum intensity required to evoke the reflex is termed as stapedial reflex threshold (SRT) or
acoustic reflex threshold (ART).
 In normal person and mild to moderate SN loss, the stapedial reflex threshold is 70 dB (fig. 153).
 Conductive deafness: The reflex may be unobtainable due to middle ear pathology.
 In recruitment: the SRT often occurs at levels less than 70dB above the subjective threshold.
 In neural deafness: The SRT occurs at levels in excess of70 dB above the subjective threshold.
 In facial palsy ifthe nerve damage is proximal to the branch to the stapedius muscle the reflex is
unnoticeable.
 Aims of Stapedial Reflex
 Detect middle ear pathology
 Detect cochlear pathology
 Detect retrocochlear pathology
 Detect site of lesion in facial nerve palsy

69. Cont..
 Malingering can be detected —PTA shows 100dB and ifreflex is present at 80 dB then patient
is malingering
 Measurement of the various parameters of the acoustic reflex:
 Threshold
 Latency,Decay,Amplitude
 Provides valuable information in differentiating cochlear, retrocochlear and brainstem lesion.
 Stapedial Reflex Decay It can be detected by presenting the tone continuously and noting
any loss ofamplitude ofcontraction.
 In normal subjects: No decay at 500 Hz anIOOOHz.
 In neural deafness: Reflex decay notedand contarction time halved in about 3sec.
 In Multiple sclerosis: reflex may be absent in one or both side

70. ABR
 Auditory Brainstem Response
 ABR: Auditory brainstem response/BSER (Brain stem evoked response) Introduced by Jewett
 Def: Far field recording of neuroelectric activity of the eighth nerve and brainstem auditory pathways
that occurs over the first 10 milli seconds after a suitable sound stimulus has been delivered to the
ear.
 Wave 1
 - Acoustic nerve
 Wave 11Cochlear nuclei
 Wave 111
 Superior Olivary complex
 Wave IV
 Lateral lemniscus
 Wave V-Inferior colliculus
 Wave VI-Medial geniculate body

71. Oto acoustic emission
 Otoacoustic Emissions
 By Kemp in 1978. Sounds generated by the cochlear outer hair cells which can be picked up by the ear canal—”Kemp’s echos”
or “cochlear echos”.
 Types of OAE
 I. Latency-Time lapse between stimuluS
 Spontaneous OAE: in the absence of any stimuli
 Evoked OAE: these are after the stimulus
 Il. Frequency
 ShortOAE, Long OAE
 111. Stability
 Transient,Distortion
 IV. Based on output limit
 Low-level OAE,High-levelOAE
 Spontaneous OAE
 Seen in only 40 to 60% normal cochlear
 Origin is in the outer hair cell It 2kHz

72. Evoked Oae
 Evoked OAE
 Seen in 98% to 100% normal cochlear
 Types of Evoked OAE
 Transient OAE
 Because they are elicited by transient clicks.
 Distortion OAE
 When two stimuli are presented, FI and F2, the resultant will be interaction ofboth
frequencies as the ear has a non linear fequency of2F1-F2 DP audiogram — 100% of normal
with HL up to 50 dB
 Very highly specific information Relate between DP audiogram and behaviour audiogram
 Advanatages of DP OAE
 Easiest emission, interms of doing and identification of the test. No need for a separate
frequency analyzer.
 DP OAE is free from artifacts.

73. Uses of OAE
 Uses
 Screening neonates for SN loss
 Detect cochlear and retrocochlear pathology Early changes of ototoxicity can
be detected Early cases of noise-induced hearing loss can be detected
 Monitor Meniere’s disease
 Tinnitus — research on
 To R/O malingering
 For intraoperative monitoring
 Infant Screening
 • Optimum time for screening infants is after 24 hours of birth. Transient OAE
is the best for children till one year.

74. Thank you 😊