Preface

Agam is a group of budding medicos, who are currently doing their under graduation in
various Medical Colleges across Tamil Nadu and Pondicherry. The group was initiated on 18th
November 2017, in the vision of uniting medicos for various social and professional causes.

We feel delighted to present you Agam ENT notes prepared by Agam Divide and Rule 2020
Team to guide our fellow medicos to prepare for university examinations.

This is a reference work of 2017 batch medical students from various colleges. The team
took effort to refer many books and make them into simple notes. We are not the authors of the
following work. The images used in the documents are not copyrighted by us and is obtained from
various sources.

Dear readers, we request you to use this material as a reference note, or revision note, or
recall notes. Please do not learn the topics for the 1st time from this material, as this contain just the
required points, for revision.
Acknowledgement

On behalf of the team, Agam would like to thank all the doctors who taught us Pathology.
Agam would like to whole heartedly appreciate and thank everyone who contributed towards the
making of this material. A special thanks to Taher Hussain, who took the responsibility of leading the
team. The following are the name list of the team who worked together, to bring out the material in
good form.
• 1. Anusha Lakshmi
• 2. Raghunandan
• 3. Saranya B
• 4. Priyadharshini N
• 5. Abhinavi
• 6. Tharangini
• 7. G Vinitha
• 8. R Gokulakrishnan
• 9. Kamal
• 10. Maya Sunder
• 11. Pradakshine S
• 12. Resh Mahesha
• 13. Rasarin
• 14. Mano S
• 15. Harismita R
• 16. Jason Thetravalan T
• 17. Bharathkannan V
• 18. Manasa Sundar
• 19. Satrajit Vijayaram V
• 20. Sneha A
• 21. M Mari Selva Ganesh
• 22. Bhavik shah
• 23. Rajeshwar
• 24. M. Lavanya
• 25. Rajarajan M
• 26. Hiruthick K
• 27. Supriya R
 ANATOMY OF EAR
The external ear
Auricle (or pinna), external acoustic canal and tympanic membrane

Auricle

• Entire pinna except lobule made up cartilage

• No cartilage between tragus and crus of helix (Incisura terminalis)
o Incision in this area is used for endaural approach in EAC or
Mastoid surgery
• Cartilage, perichondrium from tragus and concha
o Used in reconstructive surgery of middle ear.
• Conchal cartilage is used for treatment of depressed nasal bridge
External Acoustic Canal

• Outer Cartilaginous part (8mm in length)

▪ directed upwards, backwards and medially
▪ Fissure of Santorini
• allows the parotid or mastoid infections to reach external ear
▪ presence of ceruminous glands and hair follicles in the outer canal
• vulnerable to furuncles (staphylococcal infection).
o Inner Bony part (16mm in length)
▪ directed downwards, forwards and medially
▪ devoid of ceruminous glands and hair follicles
▪ narrowing in the bony canal (isthmus)
• Foreign bodies, lodged medial to the isthmus are difficult to
remove
▪ Formen of huschkle
• In anteroinferior part of bony canal
• permits infections to and from parotid
RELATIONS OF EXTERNAL ACOUSTIC MEATUS

• Superiorly- Middle cranial fossa

• Posteriorly- Mastoid air cells and the facial nerve
• Inferiorly- Parotid gland
• Anteriorly- Temporomandibular joint
Tympanic Membrane

Consists of three layers:

• Outer epithelial layer
• Inner mucosal layer
• Middle fibrous layer
o Encloses the handle of malleus
o Has three types of fibres—the radial, circular and parabolic

Tympanic membrane – two parts:

1. Pars Tensa
• Peripheral fibrocartilaginous ring called annulus tympanicus
• Central part - tented inwards at the level of the tip of malleus (umbo)
• bright cone of light - in the anteroinferior quadrant

2. Pars Flaccida
• Aka Shrapnell's Membrane
• situated above the lateral process of malleus
• between the notch of Rivinus and the anterior and posterior
malleal folds

Blood supply:

• branches of the external carotid artery

o Posterior auricular artery
o Superficial temporal artery
o Occipital artery
o Maxillary artery
Innervation

• Greater auricular nerve

• Lesser occipital nerve
• Auriculotemporal nerve
o external auditory meatus
o anterior half of lateral surface of TM
• Branches of the facial and vagus nerves
o Auricular branch of Vagus nerve
▪ supplies posterior half of lateral surface of TM
The middle ear
• Mesotympanum- lies opposite the pars tensa
• Epitympanum/attic - lies above the pars tensa but medial to Shrapnell’s
membrane and the bony lateral attic wall
• Hypotympanum- lies below the level of pars tensa
• The portion of middle ear around the tympanic orifice of the eustachian
tube is sometimes called protympanum

The middle ear can be divided into two parts:

• Tympanic cavity
o located medially to the tympanic membrane.
o Contents: the malleus, incus and stapes
• Epitympanic recess
o superior to the tympanic cavity
o lies next to the mastoid air cells
o malleus and incus extend upwards into the this recess.

Borders

• Roof
o formed by a thin bone called tegmen tympani
o separates tympanic cavity from middle cranial fossa

• Floor
o AKA jugular wall
o separate tympanic cavity from jugular bulb

• Lateral wall
o made up of the tympanic membrane and lateral wall of the
epitympanic recess

• Medial wall
o formed by labyrinth
o a prominent bulge called promontory
o oval window which is fixed by footplate of stapes
 o round window (fenestra cochleae) covered by secondary tympanic
membrane.
o The canal for facial nerve is present above the oval window.
o A hook like projection in the medial wall is called processus
chochlearformis.
▪ This marks the first genu of facial nerve (landmark for facial
nerve surgery)

• Anterior wall
o two openings; for the auditory tube and the tensor tympani
muscle
o It separates the middle ear from the internal carotid artery.

• Posterior wall
o lies closely to mastoid air cells
o consists of a bony projection called pyramid(attachment of tendon
of stapedius).
o Facial nerve runs in the posterior wall behind the pyramid.
o Superiorly, there is a hole allowing the attic to communicate with
antrum.
▪ This hole is known as the aditus to the mastoid antrum.
▪ Facial recess/Posterior sinus is a depression in the posterior
wall lateral to the pyramid.

Mastoid Air Cells

• located posterior to epitympanic recess

• collection of air-filled spaces in the mastoid process of
the temporal bone
• The air cells are contained within a cavity called the mastoid antrum
• It is marked externally on the surface of mastoid by suprameatal
(MacEwen’s) triangle.
• The mastoid air cells act as a buffer system of air
• Releasing air into the tympanic cavity when the pressure is too
low.
❖ Three types of mastoid air cells are present
• Well pneumatised or Cellular
• Diploetic
• Sclerotic or Acellular

Muscles

• The tensor tympani originates from the auditory tube and attaches to
the handle of malleus, pulling it medially when contracting.
o It is innervated by the tensor tympani nerve, a branch of
the mandibular nerve.
• The stapedius muscle attaches to the stapes, and is innervated by
the facial nerve.

The inner ear

two main components – the bony labyrinth and membranous labyrinth.

Bony Labyrinth consists of three parts – the cochlea, vestibule and the three
semi-circular canals.

Vestibule

• The vestibule is the central part of the bony labyrinth.

• separated from the middle ear by the oval window and communicates
anteriorly with the cochlea and posteriorly with the semi-circular canals.
• saccule and utricle, are located within the vestibule.

Semi-circular Canals

• There are three semi-circular canals; anterior, lateral and posterior.

• They contain the semi-circular ducts, which are responsible for balance
(along with the utricle and saccule).

Cochlea
 • The bony cochlea is a coiled tube making 2.5 to 2.75 turns around a
central pyramid of bone called modiolus
o producing a cone shape which points in an anterolateral direction
o Branches from the cochlear portion of the vestibulocochlear (VIII)
nerve are found at the base of the modiolus
• Extending outwards from the modiolus is a ledge of bone known
as spiral lamina
• The presence of the cochlear duct creates two perilymph-filled
chambers above and below:
o Scala vestibuli: Located superiorly to the cochlear duct.
o Scala tympani: Located inferiorly to the cochlear duct. It
terminates at the round window.

Membranous Labyrinth

Composed of the cochlear duct, three semi-circular ducts, saccule and the
utricle

Cochlear Duct

• located within the bony scaffolding of the cochlea. It is held in place by

the spiral lamina.
• The presence of the duct creates two canals above and below it –
the scala vestibuli and scala tympani respectively.

Lateral wall

• AKA spiral ligament

• Formed by thickened periosteum

Roof

• Formed by a membrane which separates the cochlear duct from the

scala vestibule (Reissner’s membrane)

Floor

• Formed by a membrane which separates the cochlear duct from the

scala tympani (basilar membrane)
 o The basilar membrane houses the epithelial cells of hearing –
the Organ of Corti.

Saccule and Utricle

• membranous sacs located in the vestibule

• They are organs of balance which detect movement
• The utricle receives the three semi-circular ducts
• The saccule is globular in shape and receives the cochlear duct

Semi-circular Ducts

• Ampullated end of each duct contains a thickened ridge of

neuroepithelium- Crista ampularis

Blood supply:

• Anterior tympanic branch (from maxillary artery)

• Petrosal branch (from middle meningeal artery)
• Stylomastoid branch (from posterior auricular artery).

Membranous labyrinth- labyrinthine artery

Venous drainage of the inner ear is through the labyrinthine vein

Nerve supply: Innervated by the vestibulocochlear nerve

Development of ear
Auricle and External auditory meatus: First branchial cleft

Tympanic membrane It develops from all the three germinal layers. Outer
epithelial layer is formed by the ectoderm, inner mucosal layer by the
endoderm and the middle fibrous layer by the mesoderm.

Middle ear cleft

• The eustachian tube, tympanic cavity, attic, antrum and mastoid air cells
develop from the endoderm
• tubotympanic recess - second pharyngeal pouches.
• Malleus and incus are derived from mesoderm of the first arch
 • stapes develop from the second arch except its footplate and annular
ligament which are derived from the otic capsule.

Membranous Inner Ear Development of the inner ear starts in the 3rd week of
fetal life and is complete by the 16th week.
 PERIPHERAL RECEPTORS AND PHYSIOLOGY OF AUDITORY
AND VESTIBULAR SYSTEM
AUDITORY SYSTEM

Organ of Corti

• sense organ of hearing

• situated in basilar membrane
• components:
o tunnel of corti – contains cortilymph
o hair cells
o supporting cell- Deiters cell, cells of hensen
o tectorial membrane

From cochlear nucleus the main nucleus in the Ascending Auditory pathways is

• Superior Olivary Complex

• Nucleus of Lateral Leminiscus
• Inferior Colliculus
• Medial geniculate body
• Auditory Cortex

Mechanism of Hearing

It is broadly divided into

• Mechanical conduction of sound (conductive apparatus)

• Transduction of mechanical energy to electrical impulses (Sensory
system)
• Conduction of electrical impulses to brain (neural pathway)

Mechanical conduction of sound

• Impedance matching or transformer action is accomplished by

o Lever action of ossicles –
▪ Handle of malleus is 1.3x longer than long process of incus
o Hydraulic action of tympanic membrane
▪ Effective vibratory area of TM to stapes footplate is 14:1
 o Curved membrane effect
• Phase differential between oval and round window
• Natural resonance of external ear (3000Hz) and middle ear (800Hz)

Transduction of mechanical energy to electrical impulses

• Steps in transduction are:
o Movement of stapes footplate
o Vibration of basilar membrane
o Stimulation of the hair cells
o Membrane potential changes in hair cells
Neural Pathways

(Mnemonic: E COLI MA)

Eighth nerve→ Cochlear nuclei→ Superior Olivary complex→ Lateral

leminiscus→ Inferior colliculus→ Medial geniculate body→ Auditory cortex
(Broadmann’s area 41)

COCHLEAR POTENTIAL

• Endocohlear or endolymphatic potential

o Endolymph high K+(135mEq/L).
o + 80mV electrical potential exists between endolymph of scala
media and perilymph of s.vestibuli & s.tympani.
o Depends on the metabolic activity of stria vascularis
▪ High concentration of Na +/K+ ATPase
▪ unique electrogenic K + pump.

• Resting membrane potential of hair cells

o Hair cell has a negative resting potential.
▪ At the lower end: - 70 mV
▪ At the upper end: - 150 mV
o Large negative potential and lack of K+ concentration
difference

• Cochlear microphonic potential

o The sum of receptor potential recorded in apical ends of a
number of hair cells.
 o Recorded by placing 1 electrode in scala media and 1 in scala
tympani extra cellularly.
o Function:
▪ Acts as receptor action potential

• Summating Potential:
o It is the DC Potential that follows the envelope of stimulating
sound
o This is rectified derivative of sound signal.

CN VIII POTENTIAL
• Compound action potential – All or none response of Auditory nerve
fibres.

VESTIBULAR SYSTEM

Peripheral receptors

• Cristae
o Located in ampullated end of semicircular canals
o Angular acceleration
o Hair cells
▪ Type I cells – flask shaped with single large nerve terminal
▪ Type II cells – cylindrical with multiple nerve terminals
• Maculae
o Located in otolith organs
▪ Utricle – lies in horizontal plane
▪ Saccule – lies in its medial wall in vertical plane
o Linear acceleration and gravity

Vestibular Nerve

• Arises from vestibular/scarpa’s ganglion

o Situated in lateral part of internal aucoustic meatus
• Contains bipolar cells
o Distal process innervates sensory epithelium of labyrinth
o Central process aggregate to form vestibular nerve
CENTRAL VESTIBULAR CONNECTIONS

Nucleus:

• Superior
• Medial
• Lateral
• Descending

Afferents:

1. Peripheral vestibular receptors

2. Cerebellum
3. Reticular formation
4. Spinal cord
5. Contralateral vestibular nuclei

Efferents:

1. Nuclei of CN III, IV, VI

2. Motor part of spinal cord
3. Cerebellum
4. Autonomic Nervous System

PHYSIOLOGY OF VESTIBULAR SYSTEM

• Peripheral
o Membranous labyrinth and vestibular nerve
• Central
o Nuclei and fibre tracts in CNS
o Helps in integrate vestibular impulses to other system to maintain
body balance
o Reflexes:
▪ Vestibule-ocular reflex
▪ Vestibulocervical reflex
▪ Vestibulospinal reflex
 AUDIOLOGY AND ACOUSTICS

Intensity of
• Whisper = 30 dB
• Normal conversation = 60 dB
• Shout = 90 dB
• Discomfort of the ear = 120 dB
• Pain in the ear = 130 dB
Noise
It is defined as an aperiodic complex sound. There are three types of noise:
a. White noise: It contains all frequencies in audible spectrum used for
Masking
b. Narrow band noise: It is white noise with certain frequencies, above and
below the given noise, filtered out. It is used to mask the test frequency in
pure tone audiometry.
c. Speech noise: It is a noise having frequencies in the speech range (300–3000
Hz). All other frequencies are filtered out.
Masking
• Phenomenon to produce inaudibility of one sound by the presentation
of another.
• In clinical audiometry, one ear is kept busy by a sound while the other is
being tested.
• Masking of non-test ear is essential in all bone conduction tests, but for
air conduction tests, it is required only when difference of hearing
between two ears exceeds 40 dB
 ASSESSMENT OF HEARINIG

A. Clinical tests of hearing

• Finger friction test
• Watch test
• Speech test
• Tuning fork test
o Rinne test
▪ Positive: AC > BC – seen in normal and SNHL
▪ Negative: BC>AC – seen in conductive hearing loss
▪ False –ve Rinne seen in severe unilateral SNHL
o Weber test
▪ Lateralized to worse ear in Conductive deafness
▪ Lateralized to better ear in sensorineural deafness
o Absolute bone conduction
▪ Patient and examiner hear the fork for same time duration
– conductive deafness
▪ The patient hears the fork for shorter duration compared to
examiner – sensorineural deafness
o Schwabach’s test
▪ Reduced in SNHL
▪ Lengthened in conductive deafness
o Bing test
▪ Binge +ve – hears loud sound when canal is occluded and
soft when canal is open – SNHL and Normal
▪ Binge –ve – conductive hearing loss
o Gelle’s test
▪ Positive – SNHL and Normal
▪ Negative – fixed ossicular chain
B. Audiometric Tests
• Pure Tone Audiometry
o Includes measurement of both air conduction and bone
threshold separately for both ears
o The intensity of audiometer can be increased or decreased in 5
dB steps.
o Air conduction thresholds are measured for 125, 250, 500,
1000, 2000, 4000 and 8000 Hz and bone conduction thresholds
for 250, 500, 1000, 2000 and 4000 Hz.

o Uses of Pure Tone Audiogram

▪ Identify the degree and type of hearing loss.
▪ It essential for prescription of hearing aid.
▪ Helps to find degree of handicap for medicolegal
purposes.
▪ Helps to predict speech reception threshold.

• Speech Audiometry
o Speech reception threshold (SRT)
▪ Minimum intensity at which 50% of words are
repeated correctly by patient
▪ Normal: 10dB of average of speech frequencies 500,
1000, and 2000Hz
o Speech discrimination score
▪ Aka speech recognition/ word recognition score
▪ Phonetically balanced words, said in the patients ear
at 30-40dB above his SRT
▪ Roll Over Phenomenon
✓ Seen in retrocochlear hearing loss.
✓ Increase in speech intensity above a particular
level, the PB word score falls rather than
maintain a plateau as in cochlear type of
sensorineural hearing loss
 • Bekesy Audiometry
o Self-recording audiometry
o Helps to differentiate cochlear from retro cochlear hearing
loss.

• Impedance Audiometry
o Tympanometry
o Acoustic reflex
Tympanometry
• Principle: When a sound strikes tympanic membrane, some of the
sound energy is absorbed while the rest is reflected.
• Types of tympanograms:
o Type A Normal tympanogram
o Type As Compliance is lower at or near ambient air pressure. e.g.
otosclerosis or malleus fixation.
o Type Ad High compliance at or near ambient pressure. Seen in
ossicular discontinuity or thin and lax tympanic membrane.
o Type B No change in compliance with pressure changes. Seen in
middle ear fluid or thick tympanic membrane.
o Type C Maximum compliance occurs with negative pressure in
excess of 100 mm H2O. Seen in retracted tympanic membrane

(b) Acoustic Reflex.

• Tone delivered to one ear and the reflex picked from the same or the
contralateral ear.
• Reflex ARC
o Ipsilateral: CN VIII → ventral cochlear nucleus → CN VII nucleus
ipsilateral stapedius muscle.
o Contralateral: CN VIII → ventral cochlear nucleus →contralateral
medial superior olivary nucleus → contralateral CN VII nucleus →
contralateral stapedius muscle
• USES:
o To test the hearing in infants and young children
o To find malingerers
o To detect cochlear pathology
 o To detect VIIIth nerve lesion
o Lesions of facial nerve
o Lesion of brainstem

C. Special tests of Hearing

o Recruitment
o Ear which does not hear low intensity sound begins to hear
greater intensity sounds as loud or even louder than normal
hearing ear.
o Alternate binaural loudness balance test is used to detect
recruitment in unilateral cases
o Short Increment Sensitivity Index
o used to differentiate a cochlear from a retrocochlear lesion.
o SISI >20% in Conductive deafness
o SISI 70-100% in cochlear deafness
o SISI 0-15% in nerve deafness
o Threshold tone Decay Test
o Measure of nerve fatigue
o Used to detect retrocohlear lesions

o Evoked Response Audiometry

▪ Electrocochleography
✓ It can measure auditory sensitivity to within 20 dB
✓ Invasive procedure - placement of electrodes through
the tympanic membrane.
▪ Auditory brainstem response
✓ It is not a direct test of hearing but correlates highly
with the pure tone thresholds.
✓ ABR provides an ear-specific information as sound
stimulus can be presented to each ear separately by
headphones or ear inserts.
✓ It is an objective test and can be done under sedation
as the latter has no effect on ABR.
 ✓ ABR is used both as a screening test and as a
definitive hearing assessment test in children.
✓ In a screening test, a response to a click stimulus of
less than 40 dB nHL or less is the criterion of passing
the test.

o Auditory Steady State Response

▪ Hearing loss exceeding 80dB can be detected
▪ Helps in selection of children for cochlear implant

o Otoacoustic emissions
▪ OAEs are present when outer hair cells are healthy and are
absent when they are damaged
▪ It helps to test the function of cochlea
▪ Types:
✓ Spontaneous OAEs – healthy normal hearing person
with <30dB hearing loss
✓ Evoked OAEs
❖ Transient Evoked OAEs – preented at 80 – 85dB
❖ Distortion Product OAEs
▪ Uses:
✓ Screening test for neonates
✓ Distinguish cochlear from retrocochlear pathology
✓ Helps in diagnosis of auditory neuropathy

o Central Auditory Tests

▪ Monotic tests
✓ Speech message distorted, hence difficult to
understand the message
▪ Dichotic tests
▪ Binaural tests
✓ Used to identify integration of information from both
ears
 HEARING LOSS
Conductive Hearing Loss

• Process which interferes with the conduction of sound to reach

cochlea
• Lesion present
o External ear and tymphanic membrane
o Middle ear
o Ossicle
o Stapediovestibular joint
• Charracteristics:
o Rinne test –ve
o Weber lateralized to poor ear
o Bone conduction better than air
o loss not more than 60 dB
o Speech discrimination good
• Causes
o Congenital
▪ Meatal atresia
▪ Fixation of stapes foot plate
▪ Fixation of malleus head
▪ Ossicular discontinuity
▪ Congenital cholesteatoma
o Acquired
▪ External ear –ear canal obstruction wax, foreign
body
▪ Middle ear –perforation, fluids, disruption of
ossicles, Eustachian tube blockage
• Management
o Removal of canal obstructions
o Removal of fluid
▪ Myringotomy with or without grommet insertion.
o Removal of mass from middle ear
▪ Tympanotomy can be done
o Stapedectomy, as in otosclerotic fixation of stapes footplate.
 o Tympanoplasty
▪ The procedure may be limited only to repair of
tympanic membrane (myringoplasty), or to
reconstruction of ossicular chain (ossiculoplasty),
or both (tympanoplasty)
o Hearing aid. In cases, where surgery is not possible, refused or
has failed.

Types of tympanoplasty

• Type I Defect is perforation of tympanic membrane which is

repaired with a graft (myringoplasty)
• Type II Defect is perforation of tympanic membrane with
erosion of malleus. Graft is placed on the incus or remnant of
malleus.
• Type III Malleus and incus are absent. Graft is placed on the
stapes head. It is also called myringostapediopexy or
columella tympanoplasty.
• Type IV Only the footplate of stapes is present. It is exposed to
the external ear, and graft is placed between the oval and
round windows
• Type V Stapes footplate is fixed but round window is
functioning. In such cases, another window is created on
horizontal semicircular canal and covered with a graft. Also
called fenestration operation.

Ossicular reconstruction

• Primary ossicular reconstruction can be performed in:

o Traumatic ossicular disruption
o Fixation of ossicles
o Canal wall down procedures when there is no mucosal disease
or cholesteatoma
• Types of Prosthesis
o Incus Prosthesis
o Incus-stapes Prosthesis
o Partial ossicular replacement Prosthesis (PORP)
o Total ossicular replacement Prosthesis (TORP)
Sensoneural Hearing Loss:

• Results from lesions of the cochlea, 8th nerve or central

auditory pathway
• Characteristics
o Rinne test +ve
o Weber lateralised to better ear
o Bone conduction decreased
o Loss may exceed 60dB
o Speech discrimination poor
• Causes
▪ Congenital
o Anamolies of inner ear
▪ Acquired
o Infections of labyrinth
o Trauma to 8th nerve or labyrinth
o Noise induced loss
o Ototoxic drugs
o Presbycusis
o Meniere's disease
o Acoustic neuroma
• Diagnosis is based on
▪ History
▪ Severity
▪ Types of audiogram
▪ Site of lesion
▪ laboratory test (xray, CT scan temporal bone)
• Management
▪ Treatment based on diagnosis
o Syphilitic infection treated with high dose
penicillin
o Hearing loss due to hypothyroidism can be
treated by treatment
▪ Ototoxic drugs should be avoided
▪ Hearing aids
SPECIFIC FORMS OF HEARING LOSS

Inflammation of labyrinth:
• Viral labyrinthitis
Virus → inner ear → stria vascularis → endolymph → organ of
corti
Causes –measles, mumps, cytomegalovirus
• Bacrterial labyrinthitis
Bacteria → middle ear(tympanoganic) or through CSF
(meningoneic)
• Syphilitic –cause sensorial hearing loss both 1 degree+ 2
degree

Familial progressive sensorineural hearing loss:

• Genetic disorder, hearing loss is bilateral
• Progressive degeneration of cochlea
• Basin shaped audiogram

Ototoxicity
Drugs and chemicals can cause damage to inner ear and cause sensorineural
hearing loss, tinnitus and sometime vertigo.
These drugs are:
1) Aminoglycosides
• Streptomycin, gentamicin, tobramicin - These are primarily
vestibulotoxic, selectively destroy type 1 hair cells of crysta-
ampullaris but in high doses also damages cochlea.
• Neomycin, kanamycin, amikacin are chochleotoxic. - They cause
selective destruction of outer hair cells, starting at the basal coil
and progressing onto the apex of cochlea.
Patients at risk of ototoxicity are:
• Having impaired renal function
• Elderly people above 65 years
• People recurrently receiving other ototoxic drugs
• Already received aminoglycoside antibiotics
• Receiving high doses of ototoxic drugs with high serum level of
drug
• Genetic susceptibility to aminoglycoside.
2) Diuretics
• Furosemide, bumetenide , ethavcrynic acid (loop diuretics)
• Causes edema and cystic changes in stria vascularis of the
cochlear duct.
• Mostly reversible damage
• Hearing loss sudden in onset, bilateral and symmetrical.

3) Salicylates
• Symptoms- tinnitus and bilateral sensorineural hearing loss,
particularly affecting higher frequencies.
• Hearing loss due to salicylates is reversible once the drug is
discontinued.

4) Quinine-
• Tinnitus, SNHL, reversible hearing loss.
• High doses irreversible hearing loss.
• Symptoms appear only after prolonged medications.
• Congenital hypoplasia of cochlea and deafness reported in
children whose mother received quinine in 1st trimester

5) Cytotoxic drugs
• Nitrogen mustard, cisplatin, carboplatin
• Affects outer hair cells

6) Desferrioxamine
• High frequency sensorineural hearing loss.
• Children are most commonly affected.

7) Miscellaneous
• Erythromycin
• Ampicillin
• Chloramphenicol
• Indomethacin
• Phenyl butazone
• Propanalol
• Propylthiouracil
• Alcohol, marijuana, tobacco
Noise Trauma
• Sensorineural Hearing Loss
• Occupational hazard in boiler makers, iron- and coppersmiths and
artillery men
a) Acoustic Trauma:
• Permanent damage to hearing caused by single brief
exposure to very intense sound without being preceded by
temporary threshold shift.
• May reach or cross 140 db and may be brief as 0.2 ms.
• Mechanically damage Organ of Corti, tear Reissner’s
membrane, rupture hair cells and allowing mixing of
perilymph and endolymph.
• May damage tympanic membrane and disrupt ossicles
causing conductive loss.

b) Noise-Induced Hearing Loss (NIHL):

• Hearing loss following chromic exposure to less intense
sounds, Usually a hazard of noisy occupations
• Temporary threshold shift(TTS): Hearing is impaired
immediately after exposure to noise but recovers after an
interval of a few minutes to a few hours.
• Permanent threshold shift(PTS): Hearing impairment is
permanent and doesn’t recover at all
• Damage caused by noise trauma depends on:
1. Frequency of 2000-3000 Hz cause more damage
than higher and lower frequencies
2. With increasing intensity, the permissible time for
exposure is reduced
3. Continuous noise is more harmful than
interrupted noise
4. Susceptibility of the individual
5. Pre-existing ear disease
 • NIHL causes damage to hair cells, starting in the basal turn
of cochlea. Outer hair cells are affected before the inner
hair cells
• NIHL is preventable. Pre-employment and annual
audiograms are necessary for early detection. If impaired,
rehabilitation is employed.

c) Non-auditory effects of noise:

• Chronic fatigue and stress by interfering with rest and sleep
• Annoyance and irritability through activation of ANS and
pituitary-adrenal axis
• Hypertension and peptic ulcer
• Laryngeal problems in those who have to speak loudly in
noisy surroundings

Autoimmune Inner ear disease

• Aka autoimmune SNHL
• It is associated with other autoimmune disorders
• Bilateral SNHL ≥30dB
• Investigations:
o Audiogram
o Speech audiogram
o Evoked response audiometry
o Contrast enhanced MRI
o Blood investigations (ESR, Autoimmune antibodies,
complements)
o Western blot assay for anti- Hsp 70 antibodies
• Treatment:
o Prednisolone 1mg/kg/day to 60mg/day X 4 weeks
o Methotrexate 15mg/week

Sudden Hearing Loss

• 30 dB or more of sensorineural hearing loss over atleast three
contiguous frequencies occuring within a period of 3 days or less.
• Mostly unilateral.
• Accompanied by tinnitus or vertigo.
Etiology:

1. Infections
Mumps, herpes zoster, meningitis, encephalitis, syphilis, otitis media.
2. Trauma
Head injury, Ear operations, Noise trauma, Barotrauma,
Spontaneous rupture of cochlear membrane.
3. Vascular
Hemorrhage, embolism or thrombosis of labyrinthine or cochlear
artery, vasospasm
Also associated with diabetes, hypertension, polycythemia, sickle
cell trait.
4. Ear (Otologic)
Meniere's disease, Cogan's syndrome, large vestibular aqueduct
5. Toxic drugs
Ototoxic drugs, insecticides
6. Neoplastic
Acoustic neuroma, metastasis in cerebellopontine angle,
carcinomatous neuropathy
7. Miscellaneous
Multiple sclerosis, hypothyroidism, sarcoidosis
8. Psychogenic

Management:

Detailed history, physical examination and laboratory investigations

INVESTIGATIONS:

• Audiometry
• Vestibular tests
• Imaging studies for temporal bones
• Sedimentation rate
• Test for syphilis, diabetes, hypothyroidism, blood disorders, lipid
profile.
 TREATMENT:

1. Bed rest
2. Steroid therapy : Prednisolone 40 – 60 mg single morning dose
for 1 week and tailed off in 3 weeks.
Use of steroid : Anti-inflammatory and relieves edema
Intratympanic steroids therapy
3. Inhalation of carbogen : 5% CO2 + 95% O2
4. Vasodilator drugs
5. Low molecular weight dextran : Decreases blood viscosity.
6. Hyperbaric oxygen therapy.
7. Low salt diet and a diuretic
Presbycusis
Sensorineural hearing loss associated with physiological aging
process in ear.

PATHOLOGICAL TYPES
1. Sensory
• Characterized by degeneration of organ of corti.
• Speech discrimination remains good.
2. Neural
• Characterized by degeneration of spiral ganglion cells.
• Speech discrimination is poor and out of proportion to the
pure tone loss.
3. Strial / Metabolic
• Characterized by Atrophy of Stria vascularis in all turns of
cochlea.
• Physical and chemical processes of energy production are
affected.
• Speech discrimination is good.
4. Cochlear Conductive
• Characterized by stiffening of the Basilar membrane thus
affecting its movements.
• Audiogram is sloping type.
 NON ORGANIC HEARING LOSS

CAUSES:
• Malingering
• Psychogenic

PRESENTING COMPLAINTS:
• Total hearing loss in one or both ears.
• Exaggerated loss in one or both ears.
MALINGERING CAN BE FOUND OUT BY:
1. High index of suspicion:
• When patient makes exaggerated efforts to hear.
• Frequently making efforts to repeat the question.
• Placing cupped hand to the ear.
2. Inconsistent results on repeat pure tone and speech audiometry tests:
• Normal results: Within 5 dB
• Non organic hearing loss: Greater than 15 dB
3. Absence of shadow curve:
• On testing bone conduction, a shallow curve can be
obtained, if healthy ear is not masked.
• Absence of this curve: Non organic hearing loss.
4. Inconsistency in pure tone average (PTA) and Speech reception
threshold (SRT):
• Pure tone average is the average of hearing threshold
levels of specified frequencies ( eg. 500, 1000, 2000 Hz)
• Normally, PTA < 10 dB of SRT
• Non organic hearing loss = SRT > PTA (by 10 dB)
5. Stenger test:
• Instruments used: Identical tuning forks and double channel
audiometer.
 • Principle: If a time of two intensities, one greater than the other,
is delivered to two ears simultaneously, only the ear which
receives a greater tone of intensity will hear it.
• Procedure: Take tuning forks of two equal frequencies, strike and
keep them 25 cm away from each ear.
Now bring the tuning fork on the side of feigned deafness to
within 8 cm, keeping the tuning fork on normal side at the same
distance.
• Patient should be blindfolded during this test.
True deafness: The patient continues to hear on the
normal side
Feigned deafness: The patient will deny hearing
anything.
6. Acoustic reflex threshold:
• Normal stapedial reflex – elicited at 70 – 100 dB SL.
• If the patient claims deafness and reflex is elicited – Non
organic hearing loss.
SOCIAL AND LEGAL ASPECTS OF HEARING LOSS

• Deaf are those in whom sense of hearing is non-functional for

ordinary purposes of life

Category Hearing acuity

Mild impairment 30 and 45 dB
Serious impairment 45 and 60 dB
Severe impairment 60 and 90 dB

• Degree of hearing loss

1. Mild 26-40 dB
2. Moderate 41-55 dB
3. Moderately severe 56-70 dB
4. Severe 71-91 dB
5. Profund more than 91 dB
 ASSESSMENT OF VESTIBULAR FUNCTIONS
1. Clinical tests
2. Laboratory tests

CLINICAL TESTS OF VESTIBULAR FUNCTION

1. Spontaneous nystagmus -

• Nystagmus is an important sign in the evaluation of vestibular system.

• may be horizontal, vertical or rotatory
• Vestibular nystagmus has a slow and a fast component,
• the direction of nystagmus is indicated by the direction of the fast
component
• Intensity of nystagmus is indicated by its degree

DEGREE OF NYSTAGMUS
1st degree - It is weak nystagmus and is present when patient looks in
the direction of fast component
2nd degree - It is stronger than the 1st degree nystagmus and is present
when patient looks straight ahead.
3rd degree - It is stronger than the 2nd degree nystagmus and is present
even when patient looks in the direction of the slow component

Vestibular nystagmus:
i. peripheral-due to lesion of labyrinth or VIII-th nerve
✓ peripheral nystagmus can be suppressed by optic fixation by
looking at a fixed point
ii. central-when lesion is in the central neural pathways
✓ cannot be suppressed by optic fixation
Nystagmus Lesion site
torsional nystagmus brainstem/vestibular nuclei

Vertical downbeat nystagmus craniocervical region

Vertical upbeat nystagmus at the junction of pons and medulla

or pons and midbrain.
2. FISTULA TEST
• basis of this test is to induce nystagmus by producing pressure changes
in the external canal which are then transmitted to the labyrinth.
• Normally, the test is negative because the pressure changes cannot be
transmitted to the labyrinth
• Positive: erosion of horizontal semicircular canal as in cholesteatoma
• False negative: cholesteatoma covers the site of fistula and does not
allow pressure changes to be transmitted to the labyrinth.
• False positive: 25% cases of Ménière’s disease due to the fibrous bands
connecting utricular macula to the stapes footplate

3. ROMBERG TEST
• In peripheral vestibular lesions, the patient sways to the side of lesion.
• In central vestibular disorder, patient shows instability.
• sharpened Romberg test performed in few patients who can do romberg
test without a sway.
• In this the patient stands with one heel in front of toes and arms folded
across the chest.

4. GAIT
• In lesion of peripheral vestibular system, with eyes closed, the patient
deviates to the affected side.

5. PAST-POINTING AND FALLING

• If there is acute vestibular failure, on one side, nystagmus is to the
opposite side but the past-pointing and falling will be towards the same
side.

6. DIX-HALLPIKE MANOEUVRE (POSITIONAL TEST)

• This test is particularly useful when patient complains of vertigo in
certain head positions. (BPPV)
• It also helps to differentiate a peripheral from a central lesion.
• Method: Patient sits on a couch.
i. Examiner holds the patient’s head, turns it 45° to the right and then
places the patient in a supine position so that his head hangs 30° below
the horizontal
ii. Patient’s eyes are observed for nystagmus. Four parameters of
nystagmus are observed: latency, duration, direction and fatiguability.
 iii. The test is repeated with head turned to left and then again in straight
head-hanging position.
iv. In BPPV, nystagmus appears after a latent period of2–20 s, lasts for less
than a minute and is always in one direction, i.e. towards the ear that is
undermost.
v. In central lesions nystagmus is produced immediately, as soon as the
head is in critical position without any latency and lasts as long as head
is in that critical position.

7. TEST OF CEREBELLAR DYSFUNCTION

• Disease of the cerebellar hemisphere causes:
1. Asynergia (abnormal finger-nose test)
2. Dysmetria (inability to control range of motion)
3. Adiadochokinesia (inability to perform rapid alternating
movements)
4. Rebound phenomenon (inability to control movement of
extremity when opposing forceful restraint is suddenly released)

• Midline disease of cerebellum causes:

1. Wide base gait
2. Falling in any direction
3. Inability to make sudden turns while walking
4. Truncal ataxia

LABORATORY TESTS OF VESTIBULAR FUNCTION

1. CALORIC TEST
• The basis of this test is to induce nystagmus by thermal stimulation of
the vestibular system.
• Advantage - each labyrinth can be tested separately.
.
A. Modified Kobrak Test.
✓ It is a quick office procedure.
✓ Procedure:
i. Patient is seated with head tilted 60° backwards to
place horizontal canal in vertical position.
ii. Ear is irrigated with ice water for 60 s, first with 5 mL
and if there is no response, 10, 20 and 40 mL.
 iii. nystagmus beating towards the opposite ear will be
seen with 5 mL of ice water.
iv. If response is between 5 and 40 mL, labyrinth is
considered hypoactive.
v. No response to 40mL of water indicates dead
labyrinth.

B. Fitzgerald–Hallpike Test (bithermal caloric test)

i. patient lies supine with head tilted 30° forward so that

horizontal canal is vertical
ii. Ears are irrigated for 40 s alternately with water at 30 °C
and at 44 °C
iii. eyes observed for appearance of nystagmus till its end
point.
iv. Time taken from the start of irrigation to the end point of
nystagmus is recorded and charted on a calorigram
v. If no nystagmus test is repeated with water at 20 °C for 4
min before labelling the labyrinth dead.
vi. A gap of 5 min should be allowed between two ears.
vii. Cold water induces nystagmus to opposite side and warm
water to the same side

• Depending on response to the caloric test, we can find canal paresis or

dead labyrinth, directional preponderance, i.e. nystagmus is more in one
particular direction than in the other, or both canal paresis and
directional preponderance.
a) Canal Paresis.
✓ It indicates that response elicited from a particular canal
(labyrinth), is less than that from the opposite side.

b) Directional Preponderance.
✓ It takes into consideration the duration of nystagmus to the
right or left irrespective of the side elicited from.
✓ If the nystagmus is 25–30% or more on one side than the
other, it is called directional preponderance to that side.
 C. Cold-air Caloric Test.
✓ This test is done when there is perforation of tympanic
membrane because irrigation with water in such a case with
perforation is contraindicated.
✓ The test employs Dundas Grant tube, which is a coiled copper
tube wrapped in cloth.
✓ The air in the tube is cooled by pouring ethyl chloride and then
blown into the ear.

2. ELECTRONYSTAGMOGRAPHY
• It is a method of detecting and recording of nystagmus,which is
spontaneous or induced by caloric, positional,rotational or optokinetic
stimulus.
• useful to detect nystagmus, which is not seen with the naked eye

3. OPTOKINETIC TEST
• Patient is asked to follow a series of vertical stripes on a drum
moving first from right to left and then from left to right.
• produces nystagmus with slow component in the direction of
moving stripes and fast component in the opposite direction.
• Optokinetic abnormalities-brainstem and cerebral
hemispherelesions.
• useful to diagnose a central lesion.

4. ROTATION TEST
• Useful in cases of congenital abnormalities where ear canal has
failed to develop and it is not possibleto perform the caloric test.
• Disadvantage - both the labyrinths are simultaneously stimulated
so cannot be tested individually.
5. GALVANIC TEST
• only vestibular test which helps in differentiating an end organ
lesion from that of vestibular nerve.
 DISORDERS OF VESTIBULAR SYSTEM
Classified into

• Peripheral – involves vestibular end organ, vestibular nerve

• Central – CNS, vestibule-ocular, vestibulospinal pathways

PERIPHERAL VESTIBULAR DISORDERS

• Meniere’s disease
• Benign paroxysmal positional vertigo
• Vestibular neuronitis
• Labyrinthitis
• Vestibulotoxic drugs
• Head trauma
• Perilymph fistula
• Syphilis
• Acoustic neuroma

Benign paroxysmal positional vertigo

Features:
characterized by vertigo when the head is placed in a certain critical position.
i. no hearing loss
ii. no neurologic symptoms
Cause: caused by a disorder of posterior semicircular canal.
Pathogenesis:
Degenerating macula → release otoconial debris, consisting of crystals of
calcium carbonate and floats freely in the endolymph → settles on the cupula
of posterior semicircular canal in a critical head position → causes
displacement of the cupula and vertigo.

Management: treated by performing Epley’s manoeuvre

✓ principle: to reposition the otoconial debris from the

posterior semicircular canal back into the utricle
 ✓ procedure:
i. The doctor stands behind the patient and the
assistant on the side.
ii. The patient is made to sit on the table so that when
he is made to lie down, his head is beyond the edge
of the table
iii. His face is turned 45° to the affected side.

✓ positions: consists of five positions

i. Position 1.- With the head turned 45°, the patient is
made to lie down in head-hanging position.
It will cause vertigo and nystagmus.
ii. Position 2. Head is now turned so that affected ear is
facing up at a 90° rotation.
iii. Position 3. The whole body and head are now rotated
away from the affected ear to a lateral recumbent
position in a 90°-rotation face-down position.
iv. Position 4. Patient is now brought to a sitting position
with head still turned to the unaffected side by 45°.
v. Position 5. The head is now turned forward and chin
brought down 20°

✓ After manoeuvre is complete, patient should maintain an

upright posture for 48 h.
✓ If the patient remains symptomatic, the manoeuvre can be
repeated.

Vestibular Neuronitis

Feature:
• severe vertigo of sudden onset with no cochlear symptoms
• Attacks may last from a few days to 2 or 3 weeks
Cause
• due to a virus that attacks vestibular ganglion.
Management:
• similar to that in Ménière’s disease
• The disease is usually self-limiting.
CENTRAL VESTIBULAR DISORDERS

• Vertebrobasilar insufficiency
o Decrease cerebral blood flow
o Most common cause – atherosclerosis
o Sudden onset of vertigo
• Posterior inferior cerebellar artery syndrome
o AKA Wallenberg syndrome
o Thrombosis of the artery
o Vertigo with diplopia, dysphagia, hoarseness, horner syndrome
o Sensory loss of ipsilateral side
• Basilar migraine
o Occipital headache, visual disturbances, diplopia, severe vertigo
o Common in adolescent and strong menstrual relationship
o Positive family history
• Cerebellar disease
o Acute disease may cause severe vertigo, vomiting and ataxia
o Tumours may produce classical cerebellar disease symptoms
• Multiple sclerosis
o Vertigo and dizziness more common
o Blurring/loss of vision, diplopia,dysarthria, paresthesia and ataxia
o Spontaneous nystagmus present
• Tumours of brainstem and fourth ventricle
o Gliomas, astrocytomas, medduloblastomas etc.
o Positional vertigo and nystagmus present
• Epilepsy
o Vertigo occurs as an aura in temporal lobe epilepsy
o Electroencephalogram is helpful in identifying the attack
• Cervical vertigo
o Occurs 7-10 days after neck injury
o Provoked with movements
o X- rays reveal loss of cervical lordosis

OCULAR VERTIGO
• Seen in Acute extraocular muscle paresis
• High errors of refraction
PSYCHOGENIC VERTIGO
• Seen in Patients suffering from emotional stress, anxiety etc
• Other symptoms of neurosis are seen
• Caloric test shows an exaggerated response
 DISEASES OF EXTERNAL EAR
CONGENITAL DISORDERS OF PINNA

Congenital disorders of pinna

1. Anotia
• Complete absence of
pinna and lobule
• Usually forms part of first
arch syndrome

2. Microtia
• Major developmental
anomaly
• Frequently associated
with anomalies of
external auditory
canal,middle and internal
ear
• May be unilateral or
bilateral. Hearing loss may
be frequent
• Peanut ear is a form of
microtia
3. Macrotia
Exclusively large pinna
4. Bat ear (prominent ear or
protruding ear)
Abnormally protruding ear. Concha is
large with poorly developed antihelix
and scapha.
The deformity can be corrected
surgically any time after the age of 6
years, if cosmetic appearance demands

5. Cup ear or lop ear

• Hypoplasia of the upper
third of the auricle
• Upper portion of helix or
pinna is cupped
• Cockle shell ear or snail
shell war are greater
deformities of cup ear

cup/lop ear corrected ear

6. Cryptotia(pocket ear)
• Upper third of the auricle
is embedded under the
scalp skin.
• It can be corrected by
mobilizing the pinna to
normal position and
covering the raw area by
skin graft.

7. Coloboma

• Transverse cleft in the

pinna in the middle
8. Darwin’s tubercle – pointed
tubercle on the upper part of helix
and represents apex of pinna of
lower animals

9. Stahl's ear(additional fold)- helix

which should normally be folded is
flat and the upper crus of antihelix is
duplicated and reaches rim of helix .
Corrected by a mould in the first
6weeks of life

Stahl’s ear corrected surgically

10. Periauricular tags or appendages
Skin covered tags that appear on a line
drawn from the tragus to the angle of
mouth. They may contain small pieces
of cartilage.

11. Periauricular pits or sinus

Periauricular pit- depression in front of
the crus of helix or above the tragus
Periauricular sinus – epithelial track
and is due to incomplete fusion of
tubercle. May get repeatedly infected
causing purulent discharge. Abscess
may also form.

12. Deformities of ear lobule

Absence of lobule, large lobule ,bifid lobule or a pixed (attached) lobule
TRAUMA TO THE AURICLE

1. Hematoma auris
• Collection of blood between auricular cartilage & its perichondrium due
to blunt trauma in boxers, wrestlers
• Extravasation of blood organise-cauliflower ear (pugilistic stick or
boxer's ear)
• complication: perichondritis
• Treatment :aspiration & pressure dressing

2. Lacerations
• They are repaired as early as possible.
• The perichondrium is stitched with absorbable sutures.
• Prevent stripping of perichondrium from cartilage for fear of avascular
necrosis.
• Skin is closed with fine nonabsorbable sutures.

3. Avulsion of Pinna
• Completely avulsed pinna can be reimplanted by the microvascular
techniques.
• The skin of the avulsed segment of pinna is removed and the cartilage
implanted under the postauricular skin for later reconstruction.

4. Frostbite
Injury due to frostbite varies between erythema and oedema, bullae
formation, necrosis of skin and subcutaneous tissue, and complete necrosis
with loss of the affected part. Treatment
• rewarming with moist cotton pledgets at a temperature of 38–42 °C
• application of 0.5% silver nitrate (soaks for superficial infection)
• analgesics
• protection of bullae from rupture
• systemic antibiotics
• surgical debridement

5. Keloid of Auricle
• It may follow trauma or piercing of the ear. Usual sites are the lobule or
helix.
• Surgical excision of the keloid usually results in recurrence.
INFLAMMATORY DISORDERS

1. Perichondritis
• Infection secondary to laceration, hematoma or surgical incision
(pseudomonas)
• Early stage: red, hot, painful & stiff pinna
Treatment: systemic antibiotics, 4% aluminium acetate (local
application)
• Late stage: abscess between perichondrium and cartilage (NECROSIS)
Treatment: systemic antibiotics (ciprofloxacin), drainage and local
antibiotics based on pus culture, Removal of devitalized cartilage

2. Relapsing Polychondritis
• Rare autoimmune disorder involving cartilage of the ear. Other
cartilages may also be involved.
• The entire auricle except its lobule becomes inflamed and tender.
• External ear canal becomes stenotic.
• Treatment: high doses of systemic steroids.

3. Chondrodermatitis Nodularis Chronica Helicis

• Small painful nodules appear near the free border of helix
• Nodules are tender and the patient is unable to sleep on the affected
side.
• Treatment: excision of the nodule.

DISEASES OF EXTERNAL AUDITORY CANAL

1. CONGENITAL

Atresia of external canal

• It can occur alone or in association with other complications like microtia

• Occur in case of failure of canalisation.

Collaural fistula

• Abnormality of first bronchial cleft.

• It consists of two opening
 o Neck just below the angle of mandible
o external auditory canal or middle ear

2. TRAUMA

Minor laceration of canal skin due to Q-tip injury like scratching of ear with
hairpins etc

Major laceration

• Due to gunshot wound, automobile accident or fights.

• Stenosis of ear canal is the most common complication.

3. INFLAMMATION

Furuncle (Localised acute otitis externa)

• Cause: staphylococcal infection of hair follicle.

• It is localised to outer 1/3 part of external auditory canal (cartilaginous
part).

Clinical presentation: Severe pain tenderness, painful movement of them now,

enlargement of periauricular lymph-node.

Treatment:

• Without abscess formation- systematic antibiotic, analgesic local heat.

• With abscess - incision and drainage.

Diffuse otitis externa

• AKA tropical ear, swimmer's ear, telephonist ear.

• Common organism:
o Staphylococcus aureus
o Pseudomonas pyocyaneus
o Bacillus proteus
o Escherichia coli
• Occurs in immunocompromised patient.

Etiology: Trauma to meatal skin and invasion by pathogenic organisms.

Causes: sweating, changes in pH, itching, aberration and pseudomonas
infection.

Clinical presentation:

• diffuse edema of external auditory canal

• erythema and pain
• discharge

Rarely skin becomes hypertrophic leading to stenosis (chronic stenotic otitis

externa).

Treatment: Antibiotics against pseudomonas, local- ear drops, systemic-

antibiotics, ear toileting before ear drops.

Otomycosis

Organisms: Aspergillus niger, Aspergillus fumigatus, Candida albicans.

Clinical features: intense itching, discomfort, pain, watery discharge with

musty odour and ear blockage.

Otoscope findings:

• Aspergillus niger shows black headed, filamentous growth

• Aspergillus fumigatus shows pale blue or green growth
• Candida shows white or creamy deposit.
• Meatal skin appears edematous.

Treatment:

• Ear toileting done using syringe suction or mopping.

• Antifungal agents like Nystatin, clotrimazole, povidone iodine etc.
• Treatment should be continued for a week even after cure to avoid
recurrence.
Otitis externa haemorrhagica

• Haemorrhagic bullae on tympanic membrane and deep meatus.

• It is a viral infection caused by influenza.

Clinical features: Severe ear pain, blood stained discharge when bullae
ruptures.

Treatment: Analgesic for pain, antibiotics for secondary infection.

Herpes zoster oticus

• formation of vesicles on tympanic membrane, meatal skin, concha and

posterior auricular groove.

Malignant (Necrotising) otitis externa

• caused by pseudomonas infection.

• Most commonly seen in elderly with diabetes.

Clinical features:

• excruciating pain, appearance of granulation in ear canal, facial paralysis.

• Spread anteriorly to temporomandibular fossa, posteriorly to mastoid
and medially into the middle ear and petrous bone.

Treatment: Control of diabetes. Toilet of ear canal and antibiotics for

pseudomonas infection like gentamicin and 3rd generation cephalosporins.

Eczematous otitis externa

It is a hypersensitivity reaction to infective organisms or topical ear drops.

Seborrheic otitis externa

Associated with seborrheic dermatitis of scalp.

Neurodermatitis

It is caused by compulsive scratching and intense itching due to psychological

factors.
MISCELLANEOUS

Foreign Body

Small children often put beads, pips, paper and other objects into their own
ears. Adults may get a foreign body stuck in an attempt to clean the ear, e.g.
with match sticks, or cotton buds.

Management:

• Syringing is usually successful in removing a foreign body.

• Clumsy attempts to remove the foreign body and rupture of the
tympanic membrane may result.
• If the child (or adult) is uncooperative, resort to general anaesthesia.

Insects

• Live insects,such as moths or flies,in the outer meatus produce dramatic

‘tinnitus’.
• Peace is restored by the instillation of spirit or olive oil
• corpse can then be syringed out

WAX

• Wax or cerumen is produced by the ceruminous glands in the outer

meatus and migrates laterally along the meatus.
• Impacted wax may cause some deafness or irritation of the meatal skin
and removed by syringing.

KERATOSIS OBTURANS

• Collection of a pearly white mass of desquamated epithelial cells in the

deep meatus
• Clinical features: Presenting symptoms may be pain in the ear, hearing
loss, tinnitus and sometimes ear discharge.
• Examination: ear canal may be full of pearly white mass of keratin
material disposed in several layers
• Treatment: Keratotic mass is removed either by syringing or
instrumentation
DISEASES OF TYMPANIC MEMBRANE

Retracted tympanic membrane

• Due to negative intratympanic pressure when the eustachian tube is

blocked.
• It appears dull and lustreless. Cone of light is absent or interrupted.
• Handle of malleus appears foreshortened. Lateral process of malleus
becomes more prominent.
• Anterior and posterior malleal folds become sickle shaped.

Myringitis bullosa

• Small, fluid-filled blisters form on the eardrum.

• It is a painful condition characterized by formation of haemorrhagic
blebs on the tympanic membrane and deep meatus.
• Caused by a virus or Mycoplasma pneumoniae.

Herpes Zoster oticus

• Involves geniculate ganglion of facial nerve.

• Characterized by appearance of vesicles on the tympanic membrane,
deep meatus, concha and retroauricular sulcus.
• It involves VIIth (more often) and the VIIIth cranial nerves.

Myringitis granulosa.

• Nonspecific granulations form on the outer surface of tympanic

membrane.
• Associated with impacted wax, long-standing foreign body or external
ear infection.
Tear in tympanic membrane

• Traumatic perforation of the tympanic membrane

• Ragged perforation with blood in the external auditory canal.

Symptoms:

• Pain, acute at time of rupture, usually transient.

• Deafness, not usually severe, conductive in type. Cochlear damage may
occur from excessive movement of the stapes.
• Tinnitus, may be persistent—this is cochlear damage.
• Vertigo, rarely.

Signs:

• Bleeding from the ear

• Blood clot in the meatus.
• A visible tear in the tympanic membrane.

Treatment:

• Do not clean out the ear.

• Do not put in drops.
• Do not syringe.
• Injury by direct trauma, treat with prophylactic antibiotics.

Tympanosclerosis.

• Hyalinization and calcification in the fibrous layer of tympanic

membrane.
• Chalky white plaque
• Seen in cases of serous otitis media as a complication of ventilation tube.
• Asymptomatic

Perforations

They may be associated with chronic otitis media.

 EUSTACHIAN TUBE AND IT’S DISORDERS

• nasopharynx with tympanic cavity

• Length - 36mm long.
• Runs downwards, forwards and medially at 45 degree angle.
• It is divided into
o bony - posterolateral- 1/3rd ( 12mm )
o Fibrocartilaginous- anteromedial-2/3rd ( 24mm ) both meets at
isthmus ( narrowest part of tube )
• muscles: tensor veli palatine, Levator veli palatine,
Salpingopharnlyngeus.
• Elastic hinge Ostmann's pad of fat.

Histology: lined by pseudostratified ciliated columnar epithelium.

Nerve supply:
• Tympanic branch of IX nerve - sensory and parasympathetic supply.
• Mandibular branch of III nerve- tensor veli palatini.
• Motor supply through pharyngeal plexus- levator veli palatini and
salpingophryngeus

Physiological functions of eustachian tube-

• Ventilation and regulation of middle ear pressure

• Protective function- protects ear from reflux of nasopharyngeal
secretion.
• Clearance of middle ear secretion.
 DISORDERS OF EUSTACHIAN TUBE

Tubal blockage

• Normally Eustachian tube is closed except during yawning, swallowing,

and sneezing where it opens intermittently by contraction of Tensor Veli
Palatini muscle.
• Thus middle ear is filled by air containing oxygen, carbon dioxide,
nitrogen and water vapour.
• When tube is blocked, at first OXYGEN is absorbed and later other gases
also diffuse into the blood

This results in negative pressure and RETRACTION OF TYMPANIC MEMBRANE.

• On further retraction, it results in locking of the tube with collection of

exudate and transudate and even haemorrhage.

Effects of Acute tubal blockage:

Acute tubal blockage

Absorption of middle ear gases

Negative pressure in middle ear

Retraction of tympanic membrane

Transudate in middle ear / haemorrhage

EFFECTS OF PROLONGED TUBAL BLOCKAGE:

Prolonged tubal blockage/dysfunction

Otitis media with effusion

Atelectatic ear/ perforation

Retraction pocket/ cholesteatoma

Erosion of incudostapedeal joint.

Types of Eustachian tube obstruction :

1. Mechanical

a) Intrinsic cause: allergy, inflammation

b) extrinsic cause: tumour in nasopharynx or adenoids.

2. Functional

• It is caused by the collapse of the tube due to increased cartilage

compliance which resists opening of tube or due to poor function of
Tensor veli palatini muscle.

CLINICAL CONDITIONS OF TOTAL TUBAL OBSTRUCTION:

• Upper respiratory tract infection

• Sinusitis
• Nasal polyps
• Deviated nasal septum
• Hypertrophic androids
• Cleft palate
• Down Syndrome
SYMPTOMS OF TUBAL OCCLUSION:

• Otalgia
• Hearing loss
• Popping sensation
• Tinnitus
• Disturbance of equilibrium
• Vertigo

SIGNS OF TUBAL OCCLUSION (depends on severity):

• Retracted Tympanic membrane

• Congestion along the handle of malleus and pars tensa
• Transudate behind the tympanic membrane imparting it an amber
colour
• In severe cases, tympanic membrane is severely retracted with
haemorrhage in sub epithelial layer.

ADENOIDS

Adenoids cause tubal dysfunction by

• Mechanical obstruction of tubal opening

• Acting as a reservoir for pathogenic organisms
• In cases of allergy, mast cells of adenoids release inflammatory mediator
which cause tubal blockage.

CLEFT PALATE AND TUBAL DYSFUNCTION:

• Abnormalities of torus tubarius

• shows high elastin density thus making tube difficult to open.
• Tensor veli palatini muscle does not insert into the torus tubarius
DOWN SYNDROME AND TUBAL DYSFUNCTION:

1. Poor tone of Tensor veli palatini muscle

2. Abnormal shape of nasopharynx

RETRACTION POCKETS AND EUSTACHIAN TUBES

• In ventilation of middle ear cleft,

o air passes from Eustachian tube to Mesotympanum
o Mesotympanum to Attic
o Attic to Aditus and then Antrum
o Finally to Mastoid air cell system

Any obstruction in pathway of ventilation can cause retraction pockets. Eg:

• Obstruction of Eustachian tube →Total atelectasis of tympanic

membrane
• Obstruction in middle ear→retraction in posterior part of middle ear
whole anterior part is ventilator.
• Obstruction in isthmi →Attic retraction pocket
• Obstruction at aditus→cholesterol granuloma and collection of mucous
discharge in mastoid air cells.

PATULOUS EUSTACHIAN TUBE:

• Eustachian tube is abnormally patent.

• It occurs in conditions like pregnancy, rapid weight loss, multiple
sclerosis.
 DISEASES OF THE MIDDLE EAR

Acute Suppurative Otitis Media

• An acute inflammation of middle ear by pyogenic organisms.

• Causative organisms :
o Streptococcus pneumonia
o Haemophilus influenza
o Moraxella catarrhalis
❖ Etiology :
o ASOM, follows viral infection of Upper Respiratory Tract.
o Common in infants and children
❖ Routes of Infection :
o Via Eustachian Tube
o Via External Ear
o Blood borne
❖ Pre Disposing Factors :
o Recurrent infections of common cold, Upper Respiratory
Tract infections
o Infection of Tonsils and Adenoids
o Chronic rhinitis and sinusitis etc.,
❖ Pathology and Clinical features :

5 stages :

i. Stage of Tubal Occlusion :

Nasopharyngeal end of Eustachian tube blocked by edema and hyperaemia.

Negative Tympanic pressure

Retraction of Tympanic Membrane

 ▪ Symptoms :
a. Ear ache
b. Hearing Loss

▪ Signs :
a. Retraction of Tympanic membrane
b. T.M – looks dull and non-shiny
c. Loss of Light reflex
d. Tuning fork test - Conductive type of Hearing Loss

ii. Stage of Presuppuration

Prolonged Tubal occlusion

Invasion of pyogenic organisms in Tympanic cavity

Inflammatory exudates in middle ear (Sterile secretions)

Congestion of Tympanic Membrane

▪ Symptoms :
a. Increased Earache
b. Increased Hearing loss
c. Tinnitus
d. High degree fever (in children)
▪ Signs :
a. Congestions of Pars Tensa
b. CARTWHEEL APPEARANCE
c. Tuning fork test : Conductive type of Hearing loss
iii. Stage of Suppuration :

Marked formation of Pus in the middle ear and to some

extent in Mastoid air cells

Bulging of Tympanic Membrane to the point of rupture

▪ Symptoms :
a. Severe Ear ache
b. Further increase in Hearing Loss
c. High grade Fever accompanied by Vomiting and
convulsions (in children)
▪ Signs :
a. T.M – Red, congested and bulging with loss of
landmarks
b. A yellow spot on Tympanic Membrane
c. Tenderness over Mastoid antrum

*X-Ray of Mastoid – Clouding of Air cells (due to exudates)*

iv. Stage of Resolution:

Tympanic Membrane ruptures with release of pus.

Inflammatory process begins to resolve.

Perforation heals within 3-6 weeks

Hearing comes back to normal

 ▪ Symptoms:
a. Earache relieved
b. Fever comes down
▪ Signs:
a. Blood tinged discharge in External auditory canal
which later becomes mucopurulent.
b. Perforation of Tympanic membrane

*(Most common site of Perforation – Antero inferior part of Pars Tensa)

*Healed T.M is dimeric i.e., has only two layer (Fibrous layer is lost)
*Light house sign - positive

v. Stage of Complication :
If virulence of organism is high, resolution may not take place
leading to following complications,

a. Acute Mastoiditis
b. Subperiosteal abscess
c. Facial Paralysis
d. Labyrinthitis
e. Petrositis
f. Extra Dural abscess
g. Meningitis

❖ Treatment :
✓ Stage i & ii - Antibiotics + Analgesics + Nasal decongestants
✓ Stage iii - Myringotomy (in Postero inferior part of Pars Tensa)
✓ Stage iv - No Treatment required (90% heels of its own)

Antibiotics commonly used:

• Ampicillin (50mg/kg/day)
• Amoxicillin (40mg/kg/day)

*Antibiotic therapy continued for min. 10 days, till hearing returns to normal.*
Nasal Decongestants :

Drops – Ephedrine or Oxymetazoline or Xylometazoline

Oral – Pseudoephedrine

Analgesics/Antipyretics: Paracetamol can be given.

OTITIS MEDIA WITH EFFUSION

• AKA Serous OM, Secretory OM, Mucoid OM, Glue Ear

• Accumulation of non purulent effusion in the middle ear cleft.

▪ Symptoms :
o Hearing loss (upto 40dB)
o Delayed and defective speech
o Mild ear aches
▪ Otoscopic findings :
o T.M – dull and opaque, blue/yellow coloured, Bulging with
fluid behind T.M
o CART-WHEEL APPEARANCE
o Air bubbles may be seen.
o Mobility of T.M – Restricted

❖ Hearing Tests :
o Tuning fork test – Conducting type of hearing loss
o Pure Tone Audiometry : A-B gap – 20 to 40dB
o Tympanometry : Type B Curve

❖ Treatment :
• Medical :
a. Antibiotics
b. Decongestants
 c. Anti allergics
d. Middle ear aeration ( by Valsalva manoeuvre)
• Surgical :
a. Myringotomy and Aspiration of Fluid with Grommet
Insertion ( 2 incisions made on AI and AS part of T.M –
Beer Can Principle)

BAROTRAUMA (AERO-OTITIS MEDIA)

• Nonsuppurative condition resulting from failure of eustachian tube to

maintain middle ear pressure at ambient atmospheric level.

MECHANISM:
• When atmospheric pressure is higher than that of middle ear by critical
level of 90 mm Hg, eustachian tube gets locked.
• In the presence of eustachian tube oedema, even smaller pressure
differentials cause “locking” of the tube.

CLINICAL FEATURES:
• Severe earache, hearing loss and tinnitus are common complaints.
• Vertigo is uncommon.
• Tympanic membrane appears retracted and congested. It may get
ruptured.
• Middle ear may show air bubbles or haemorrhagic effusion.
• Hearing loss is usually conductive but sensorineural type of loss may also
be seen.

TREATMENT:
• Catheterization or politzerization.
• In mild cases, decongestant nasal drops or oral nasal decongestant with
antihistaminics.
• In the presence of fluid, myringotomy may be performed to “unlock”
the tube and aspirate the fluid.
 CHOLESTEATOMA AND CHRONIC OTITIS MEDIA
CHOLESTEATOMA
• Keratinizing squamous epithelium presence in the middle ear or mastoid
that constitutes a cholesteatoma.

THEORIES-
ORIGIN OF CHOLESTEATOMA

• Presence of congenital cell rests

• Witt maack’s theory - Invagination Of Tympanic Membrane

o from the attic or posterosuperior part of pars tensa in the form of
retraction pockets

• Ruedi ’s theory-Basal cell hyperplasia

o The basal cells of germinal layer of skin proliferate under the
influence of infection and lay down keratinizing squamous
epithelium.

• Habermann’s theory-Epithelial invasion

o The epithelium from the meatus grows into the middle ear
through a pre-existing perforation.

• Sade’s theory-Metaplasia
o Middle earmucosa, undergoes metaplasia due to repeated
infections and transforms into squamous epithelium.

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

1.Congenital cholesteatoma

• Arises from Embryonic epidermal cell rests in the middle ear cleft or
temporal bone
 • Symptoms are based on its location
• Three important sites:
o Middle ear
o Petrous apex
o Cerebellopontine angle(CP angle)

2. Primary Acquired Cholesteatoma

• No history of previous otitis media or a pre-existing perforation

Theories on its genesis are:

o Invagination of pars flaccida
o Basal cell hyperplasia
o Squamous metaplasia

3. Secondary Acquired Cholesteatoma

• A pre-existing perforation in pars tensa

• Asociated with posterosuperior marginal perforation or sometimes large
central perforation

Theories on its genesis include:

o Migration of squamous epithelium
o Middle ear mucosa undergoes metaplasia due to repeated infections of
middle ear through the pre-existing perforation.

EXPANSION OF CHOLESTEATOMA AND DESTRUCTION OF BONE

An attic cholesteatoma extension,

1. Backwards into Aditus ad antrum and mastoid

2. Downwards into the mesotympanum

3. Medially it surrounds ossicles-Incus& head of malleus.

Bone destruction in cholesteatoma by enzymatic destruction

• Enzymes liberated by osteoclasts and mononuclear inflammatory cells

• Enzymes involved,
o collagenase,
o acidphosphatase
o proteolytictic enzymes

CHRONIC SUPPURATIVE OTITIS MEDIA

• It is a long-standing infection of a part or whole of the middle ear cleft

characterized by
o Ear discharge
o Permanent perforation

• Permanent perforation is
o Edges are covered by squamous epithelium
o It does not heal spontaneously.

TYPES OF CSOM

1. Tubo tympanic type/Safe/Benign type:

It involves anteroinferior part of middle ear cleft:
• Middle ear
• Eustachiantube
• Mesotympanum
• Central perforation
There is no risk of serious complications

2. Attico antral/unsafe/dangerous type:

It involves posterosuperior part of the cleft:
• Attic
• Antrum
• Mastoid
• Associated with an attic or a marginal perforation.
• Boneerosion by cholesteatoma, granulations or osteitis
Risk of complications is high
PATHOLOGY OF TUBOTYMPANIC TYPE

1. Perforation of pars tensa

2. Middle ear mucosaPolyps
3. Ossicular chain
4. Tympanosclerosis
5. Fibrosis and adhesions
.
Aerobic organisms:

• Pseudomonas aeruginosa
• Proteus
• Escherichia coli
• Staphylococcus aureus

Anaerobes:

• Bacteroides fragilis
• Anaerobic Streptococci

CLINICAL FEATURES OF SAFE TYPE CSOM

• Ear discharge:
o Non offensive
o Mucoid or mucopurulent
o Constant or intermittent
o Profuse

• Hearing loss: Conductive type hearing loss

• Perforation: Central perforation involving pars tensa

• Middle ear mucosa: Inflammed, red, edematous

ROUND WINDOW SHIELDING EFFECT

• Patient hears better in the presence of discharge rather than dry ear
• Effect is produced by discharge, by maintaining phase differential
 • In dry ear, sound waves strike both the Oval and Round windows
simultaneously, thus cancelling each other's effect with no movement of
perilymph

TREATMENT OF SAFE TYPE CSOM

1. Aural toilet-Dry mopping, Suction of discharge and Debris

2. Ear drops
3. Systemic antibiotics
4. Treatment of contributory causes
5. Surgical treatment
6. Reconstructive surgery
Precautions-
• Avoid water entering in ear during bathing
• Avoid hard nasal blows

• ATTICO ANTRAL TYPE OF CSOM (Unsafe type/Dangerous type CSOM)

• Pathology similiar to cholesteatoma
• Osteitis and granulation tissue seen
• Ossicular necrosis
• Cholesterol granuloma and CHOLESTEATOMA associated
• Foul smelling Purulent blood stained discharge
• More Complications

SIGNS OF UNSAFE TYPE CSOM

1. Perforation:
It is either attic or posterosuperior marginal type.

2. Stagesof tympanic membrane retraction:

o Stage I-
Tympanic membrane is retracted
Does not contact the incus

o Stage II
Tympanic membrane is retracted deep
Contacts the incus
 Middle ear mucosa is not affected.

o Stage III-Also called MIDDLE EAR ATELECTASIS

o Stage IV-called ADHESIVE OTITIS MEDIA POCKETS.

INVESTIGATIONS
• Examination under microscope -Note the Pathological changes
• Tuning fork testsand audiogram:
o They are essential for preoperative assessment and to confirm
the degree and type of hearing loss.
• X-ray mastoids/CT scan temporal bone-
o Degree of Bony destruction and mastoid pneumatisation noted
• Culture and sensitivity of ear discharge –Selection of Antibiotics

TREATMENT OF ATTICO ANTRAL CSOM

1. Surgical management-
• It is the mainstay of treatment
• Canal down procedure is done-
o Radical mastoidectomy and Modified Radical Mastoidectomy

2. Reconstructive surgery-
Hearing can be restored by myringoplasty or tympanoplasty.

Tubercular Otitis Media :

Etiology :

a) Secondary to Pulmonary TB.

b) Common in children and young adults.

Pathological Changes :

a) Tubercles in submucosal layers of miidle ear cleft.

b) Painless necrosis of T.M
c) Mutiple perforations coalesce to single large perforations
d) Middle ear & Mastoid – filled with pale granulations
Complications :

a) Mastoiditis
b) Facial paralysis
c) Post aurucular fistula
d) Osteomyelitis
e) Profound hearing loss

Clinical features :

a) Painless ear discharge

b) Multiple Perforations in Pars Tensa
c) Severe hearing loss – Conductive type

Treatment :

a) Anti Tuberculosis Drugs

b) Mastoid Surgery in case of any complications
 COMPLICATIONS OF SUPPRATIVE OTITIS MEDIA
INTRATEMPORAL/EXTRACRANIAL COMPLICATION

• Mastoiditis
• Petrositis
• Facial paralysis
• Labyrinthitis

INTRACRANIAL COMPLICATIONS

• Extradural abscess
• Subdural abscess
• Meningitis
• Lateral sinus thrombophlebitis
• Otitic hydrocephalus

INTRATEMPORAL/EXTRACRANIAL COMPLICATION

1. MASTOIDITIS:( most common)

• Inflammation of mucosal lining of antrum and mastoid air cell
system.
• Infection spreads from-mucosa lining the mastoid air cells→ bony
walls of the mastoid air cell system.
ETIOLOGY:
• High virulence of organisms
• Beta-hemolytic streptococcus -most common causative organism.
• Anaerobic organisms are also associated with mastoiditis
PATHOLOGY:
1. Production of pus under tension.
2. Hyperemic decalcification and osteoclastic resorption of bony walls.
CLINICAL FEATURES:
o Symptoms:
1. Pain behind the ear
2. Fever:
3. Ear discharge:
o Signs:
1. Mastoid tenderness:
2. Ear discharge:
3. Sagging of posterosuperior meatal wall:
4. Perforation of tympanic membrane:
5. Swelling over the mastoid:
6. Hearing loss: Conductive type of hearing loss

7. General findings:

• Patient appears ill and toxic with low grade fever.

• In children, fever is high with a rise in pulse rate.

INVESTIGATIONS:
• Blood Counts →show ‘Polymorphonuclear Leukocytosis’
• ESR→ is usually raised.
• X-Ray Mastoid:
• CT scan temporal bone→ clouding of air cells due to collection of
Exudate.
• Bony partitions between air cells become indistinct, but the sinus
plate – seen as distinct outline.
• In later stages, a cavity- seen.
• Ear Swab: for culture and sensitivity.

DIFFERENTIAL DIAGNOSIS:

1.Suppuration of Mastoid Lymph Nodes:

2. Furunculosis of Meatus.
3. Infected Sebaceous Cyst
Treatment:

1. Hospitalization of the Patient.

2. Antibiotics.
3. Myringotomy.
• When pus is under tension it is relieved by wide myringotomy.
4. Cortical Mastoidectomy.
• It is indicated when there is:
o Subperiosteal abscess.
o Sagging of posterosuperior meatal wall.
o “Positive reservoir sign”→ meatus immediately fills with pus
after it has been mopped out.
o No change in condition of patient or it worsens in spite of
adequate medical treatment for 48 h.
o Mastoiditis
.
Complications of Acute Mastoiditis:

• Subperiosteal abscess
• Labyrinthitis
• Facial paralysis
• Petrositis
• Extradural abscess
• Subdural abscess
• Meningitis
• Brain abscess
• Lateral sinus thrombophlebitis
• Otitic hydrocephalous

Abscesses in Relation to Mastoid Infection:

1. Postauricular Abscess :(commonest abscess)

• abscess forms over the “Mac Ewen’s triangle”→pus travels along
the vascular channels of “lamina cribrosa”.

2. Zygomatic Abscess:
• Due to infection of zygomatic air cells situated at the posterior
root of zygoma.
• Swelling appears in front of and above the pinna
3. Bezold Abscess:
• Occurs following “acute coalescent mastoiditis”
• The abscess may:
(i)Lie deep to SCM, pushing the muscle outwards,
(ii) follow the posterior belly of digastric - present as a swelling
between the tip of mastoid and angle of jaw
(iii)be present in upper part of posterior triangle
(iv) reach the parapharyngeal space; or
(v) track down along the carotid vessels

• Clinical features:
o Onset is sudden.
o There is pain, fever, a tender swelling in the neck and torticollis.
o Patient gives history of purulent otorrhea.

• Investigation: A computed tomography (CT) scan of the mastoid and

swelling of the neck may establish the diagnosis.

• Treatment:
o Cortical mastoidectomy for coalescent mastoiditis
o Drainage of the neck abscess through a separate incision
and putting a drain in the dependent part.
o Administration of intravenous antibiotics by the culture and
sensitivity report of the pus taken at the time of surgery.

4. Meatal Abscess (Luc Abscess):

• Pus breaks through the bony wall between the antrum and external
osseous meatus.

5. Behind the Mastoid (Citelli’s Abscess):

• Abscess is formed behind the mastoid more towards the occipital bone.
• Abscess of the digastric triangle
6. Parapharyngeal or Retropharyngeal Abscess.

• Result of infection of the “peri tubal cells” due to acute coalescent

mastoiditis.
MASKED (LATENT) MASTOIDITIS:
• slow destruction of mastoid air cells but without the acute signs and
symptoms often seen in acute mastoiditis.
• ‘No pain, no discharge, no fever and no mastoid swelling’
• In Mastoidectomy: ‘destruction of the air cells with granulation tissue’
and ‘dark gelatinous material filling the mastoid’ is seen.
• Erosion of the tegmen tympani and sinus plate with an extradural or peri
sinus abscess seen.

Etiology:

• Inadequate antibiotic therapy

• Use of oral Penicillin

Clinical Features:
• Usually affects children
• Mild pain behind the ear but with persistent hearing loss.
• Tympanic membrane appears thick with loss of translucency.
• Slight tenderness may be elicited over the mastoid.
• Audiometry shows conductive hearing loss of variable degree.

Investigation:
• X-ray of mastoid will reveal clouding of air cells with loss of cell outline.

Treatment:

• Cortical mastoidectomy with full doses of antibiotics -the treatment of

choice.
• This may cause tympanic membrane to return to normal with
improvement in hearing.

PETROSITIS:

• Spread of infection from middle ear and mastoid to the petrous part of
temporal bone is called petrositis.
Clinical Features:
• Gradenigo syndrome:
o It is the classical presentation.
o Triad:
a) External rectus palsy (VIth nerve palsy),
b) Deep-seated ear or retro-orbital pain (Vth nerve involvement)
c) Persistent ear discharge.

• Persistent ear discharge with or without deep-seated pain in spite of an

adequate cortical or modified radical mastoidectomy also points to
petrositis.
• Fever, headache, vomiting, neck rigidity
• Facial paralysis and recurrent vertigo- due to involvement of facial and
statoacoustic nerves.

Diagnosis:
• CT scan of temporal bone: will show bony details of the petrous apex
and the air cells
• MRI: helps to differentiate diploic marrow-containing apex from the
fluid or pus.

Treatment:

• Cortical, modified radical or radical mastoidectomy

• The fistulous tract should be found out -then curetted and enlarged to
provide free drainage.
• Tract of posterosuperior cells starts in the ‘Trautman’s
triangle’ or the attic.
• Tract of anterior cells is situated near the’ tympanic opening
of eustachian tube’
• intravenous antibacterial therapy

FACIAL PARALYSIS:

It can occur as a complication of both acute and chronic otitis media.

• Acute Otitis Media:

- When the bony canal is dehiscent;

 ▪ The nerve lies just under the middle ear mucosa;
▪ Inflammation of middle ear spreads to epi- and perineurium
causing facial paralysis.

- Facial nerve function fully recovers if acute otitis media is controlled

with systemic antibiotics.
- Myringotomy or cortical mastoidectomy may sometimes be required.

• Chronic Otitis Media:

o Results either from ‘cholesteatoma’ or ‘penetrating granulation
tissue’.
o Cholesteatoma- destroys bony canal -then, causes pressure on the
nerve- aided by edema of associated inflammatory process.
o Facial paralysis is insidious but slowly progressive.

o Treatment-
▪ Immediate exploration of the middle ear and mastoid.

LABYRINTHITIS:
CIRCUMSCRIBED ETIOLOGY CLINICAL FEATURE TREATMENT
LABYRINTHIS/ 1. Chronic 1.Transient vertigo -pressure on tragus,
cleaning the ear or while performing 1.In chronic
FISTULA OF suppurative Suppurative otitis
LABYRINTHITIS: otitis media ‘Valsalva maneuver’.
media or
with Cholesteatoma-
2.It is diagnosed by “fistula test” which
Thinning or cholesteatoma
can be performed in 2 ways.
“Mastoid
is the most exploration” is often
erosion of Pressure on tragus: required to
common cause.
bony capsule • Sudden inward pressure is eliminate the cause.
of labyrinth- applied on the tragus→ This
2. Neoplasms of increases air pressure in the 2.Systemic
usually of the middle ear, e.g. ear canal and stimulates the antibiotic therapy
horizontal carcinoma or labyrinth→Patient will should
glomus tumor. complain of vertigo; be instituted before
semicircular and after operation
canal. 3. Surgical or • Nystagmus may also be
to prevent spread
of infection into the
accidental induced with quick labyrinth.
trauma to component towards the ear
labyrinth. under test.

Siegel’s speculum:
• When positive pressure is
applied to ear canal→ patient
complains of vertigo usually
with nystagmus.

• The quick component of

nystagmus would be towards
the affected ear;(ampullopetal
displacement of cupula).

• Ampullopetal flow of
endolymph (as also
ampullopetal displacement of
cupula) whether in rotation,
caloric or fistula test causes
nystagmus to same side.

• If “negative pressure is
applied”, again it would induce
vertigo and nystagmus but
this time- the quick
component of nystagmus
“would be directed to the
(opposite) healthy side due to
ampullofugal displacement of
cupula”.
DIFFUSE SEROUS ETIOLOGY CLINICAL FEATURE TREATMENT

LABYRINTHITIS: • Medical:
1. Most often it 1.Mild cases -vertigo and nausea 1. Patient is put to
It is diffuse intra arises from pre- bed, his head
labyrinthine existing 2.Severe cases- vertigo is worse with immobilized with
affected ear above.
inflammation circumscribed marked 2. Antibacterial
without pus labyrinthitis nausea, vomiting and even spontaneous therapy is given in full
formation and is a associated with nystagmus. doses to control
reversible condition chronic middle infection.
if treated early. ear suppuration 3.Quick component of nystagmus is 3. Labyrinthine
sedatives, e.g.
or towards the affected ear. prochlorperazine
cholesteatoma. (Stomatal) or
4.As the inflammation is diffuse, cochlea dimenhydrinate
2. In acute is also affected with some degree of (Dramamine), given
infections of sensorineural hearing loss. for symptomatic relief
of vertigo.
middle ear clef-, 4. Myringotomy -if
inflammation 5.Serous labyrinthitis, if not checked→ labyrinthitis has
spreads through suppurative labyrinthitis with total loss followed acute otitis
annular ligament of vestibular and cochlear function. media and the drum
or the round is bulging.
5.Pus is cultured for
window. specific antibacterial
therapy.
3. It can follow • Surgical:
stapedectomy or 1.Cortical
fenestration mastoidectomy (in
acute mastoiditis)
operation. 2.Modified radical
mastoidectomy (in
chronic middle ear
infection or
cholesteatoma)
3.This is diffuse
pyogenic infection of
the labyrinth with
permanent loss of
vestibular and
cochlear functions.
DIFFUSE ETIOLOGY CLINICAL FEATURES TREATMENT
SUPPURATIVE It usually follows: 1.There is severe vertigo with nausea
LABYRINTHITIS: “serous and vomiting- due to acute vestibular failure. 1.It is same as for
labyrinthitis”- serous
2.Spontaneous nystagmus will be observed
This is diffuse pyogenic labyrinthitis.
with its quick component towards the
pyogenic infection Organisms-
healthy side.
of the labyrinth entering through 2.Rarely, drainage
with a pathological or 3.Patient is markedly toxic. of the labyrinth is
permanent loss of surgical fistula. required- if
vestibular and 4.There is total loss of hearing. ‘intralabyrinthine
cochlear functions. Suppuration’ is
5.Relief from vertigo is seen after acting as a source
3-6 weeks due to adaptation. of intracranial
complications,
e.g. meningitis or
brain abscess.

INTRACRANIAL COMPLICATIONS OF OTITIS MEDIA

LATERAL SINUS THROMBOPHLEBITIS/ SIGMOID SINUS THROMBOSIS:

It is an inflammation of inner wall of lateral venous sinus with formation of an

intrasinus thrombus.
Etiology:
• Complication of acute coalescent mastoiditis, masked mastoiditis or
chronic suppuration of middle ear and cholesteatoma.
Pathology:
The pathological process – 4 stages:
• Formation of Peri sinus Abscess
• Endophlebitis and Mural Thrombus Formation
• Obliteration of Sinus Lumen and Intrasinus abscess
• Extension of Thrombus

CLINICAL FEATURES:

• Hectic Picket-Fence Type of Fever with Rigors

• Headache
• Progressive Anemia and Emaciation
• Griesinger’s Sign
o This is due to “thrombosis” of ‘mastoid emissary vein’→”Edema”
over the ‘posterior part of mastoid’.
• Papilloedema
• Tobey-Ayer Test
 o This is to record CSF pressure by manometer
• Crowe-Beck Test
o Pressure on jugular vein of healthy side produces engorgement of
retinal veins (seen by ophthalmoscopy) and supraorbital veins.
• Tenderness Along Jugular Vein

Investigations:
1. Blood Smear: done to rule out malaria.

2. Blood Culture:
• Done to find causative organisms.
• Culture should be taken at the time of chill when organisms enter the
blood stream.

3. CSF Examination-CSF: - normal -except- for rise in pressure- also helps to

exclude meningitis.

4. X-Ray Mastoids: may show clouding of air cells (acute mastoiditis) or

cholesteatoma

5. Imaging Studies:
• Contrast-enhanced CT scan shows- sinus thrombosis- delta sign.
• “Delta sign” may also be seen on contrast-enhanced MRI.

6.Culture and Sensitivity: Ear swab

Complications:

• Septicemia and pyemic abscesses in lung, bone, joints or subcutaneous

tissue.
• Meningitis and subdural abscess.
• Cerebellar abscess.
• Thrombosis of jugular bulb and jugular vein with involvement of IXth, Xth
and XIth cranial nerves.
• Cavernous sinus thrombosis.
• Otitic hydrocephalus, when thrombus extends to sagittal sinus via
confluence of sinuses.
Treatment:

1. Intravenous Antibacterial Therapy

2. Mastoidectomy and Exposure of Sinus

• A “complete cortical or modified radical mastoidectomy” is performed;
• Depends on :
--Whether sinus thrombosis has complicated acute or chronic middle ear
disease.

3. Ligation of Internal Jugular Vein

It is indicated when antibiotic and surgical treatment has failed to control-
embolic phenomenon and rigors, or tenderness and swelling along jugular vein
is spreading.

4. Anticoagulant Therapy
Used when thrombosis is extending to cavernous sinus.

5. Supportive Treatment
Repeated blood transfusions may be required to combat anemia and improve
patient’s resistance.

MENINGITIS:

• It is inflammation of leptomeninges (pia and arachnoid) usually

with bacterial invasion of CSF in subarachnoid space.
• Most common intracranial complication
• In infants and children, otogenic meningitis usually follows acute
otitis media
• In adults it is due to chronic middle ear infection.

Mode of Infection
▪ Blood-borne infection- infants and children;
▪ Chronic ear disease- in adults
▪ Retrograde thrombophlebitis -extradural abscess or
granulation tissue
 Clinical Features
o Symptoms and signs of meningitis are due to:
(i) Presence of infection,
(ii) Raised intracranial tension, and
(iii)Meningeal and cerebral irritation.
o Their severity will vary with the extent of disease.
1. There is rise in temperature (102-104 °F) often with
chills and rigors.
2. Headache.
3. Neck rigidity.
4. Photophobia and mental irritability.
5. Nausea and vomiting (sometimes projectile).
6. Drowsiness which may progress to delirium or coma.
7. Cranial nerve palsies and hemiplegia.

Examination will show:

(i) Neck rigidity,
(ii) Positive Kernig’s sign
(iii) Tendon reflexes are- initially exaggerated - later become sluggish or
absent.
(iv) Papilloedema

Diagnosis:
• CT or MRI with contrast will help to make the diagnosis.
• Lumbar puncture and CSF examination establish the diagnosis.
• CSF - turbid
-cell count is raised and may even reach 1000/mL with predominance of
polymorphs
-protein level is raised,
- sugar is reduced
- chlorides are diminished
• CSF is always cultured to find the causative organisms and their antibiotic
sensitivity.
Treatment:

MEDICAL
• Antimicrobial therapy directed against aerobic and anaerobic
organisms should be instituted.
• Culture and sensitivity of CSF -aid in the choice of antibiotics.
• Corticosteroids combined with antibiotic therapy -helps to reduce
neurological or audiological complications

SURGICAL

• Myringotomy or Cortical Mastoidectomy

• With cholesteatoma- will require Radical or modified radical
mastoidectomy.

OTOGENIC BRAIN ABSCESS:

• In adults - follows chronic suppurative otitis media with cholesteatoma,
• In children-result of acute otitis media.
• Cerebral abscess is seen twice as frequently as cerebellar abscess.

Pathology:
Brain abscess develops through 4 stages:

1. Stage of Invasion (Initial Encephalitis).

• Headache, low-grade fever, malaise and drowsiness.

2. Stage of Localization (Latent Abscess).

• no symptoms.
• pus localized by formation of a capsule
• lasts for several weeks.
3. Stage of Enlargement (Manifest Abscess).
• Abscess begins to enlarge.
• A zone of edema appears round the abscess - responsible for
aggravation of symptoms.
 • Clinical features at this stage are due to:
(a) Raised intracranial tension.
(b) Disturbance of function in the cerebrum or cerebellum,
causing focal symptoms and signs.
4. Stage of Termination (Rupture of Abscess).
• Expanding abscess in the white matter of brain→ ruptures into the
ventricle or subarachnoid space →fatal meningitis.

HEADACHE NOMINAL APHASIA

NAUSEA AND
VOMITING

HOMONYMOUS
HEMIANOPIA

Raised LEVEL OF CONTRALATERAL

MOTOR
IntracranialTension CONSCIOUSNESS
PARALYSIS

EPILEPTIC FITS
PAPILLOEDEM
SLOW PULSE A
AND PUPILARY CHANGES AND
SUBNORMAL OCCULULOMOTOR PALSY
TEMPERATURE
TEMPORAL
LOBE
ABSCESS
HEADACHE
CLINICAL FEATURES

SPONTANEOUS
NYSTAGMUS

IPSILATERAL
HYPOTONIA AND
WEAKNESS

IPSILATERAL
ATAXIA

Localizing
PAST-POINTING
Features AND INTENTION
TREMOR

CEREBELLAR
ABSCESS

DYSDIADOCHOKINESIA
1. Symptoms and Signs of Raised Intracranial Tension:

(a) Headache- worse in the morning.

(b) Nausea and vomiting. -usually projectile- more often in cerebellar lesions
(c) Level of consciousness. Lethargy →drowsiness→confusion→stupor→coma
(d) Papilloedema-Appears late when raised intracranial tension has persisted
for2-3 weeks
(e) Slow pulse and subnormal temperature.

2. Localizing Features

(a) Temporal lobe abscess:

(i) Nominal aphasia: If abscess involves dominant hemisphere-patient fails to

tell the names of common objects such as key, pen, etc. but can demonstrate
their use.

(ii) Homonymous hemianopia.

• This is due to pressure on the optic radiations.
• Visual field, opposite to the side of lesion, is lost.
• The defect is usually in the upper, but sometimes in the lower
quadrants.

(iii) Contralateral motor paralysis.

• In the usual upward spread of abscess, face → arm→leg.
• Inward spread, towards internal capsule, involves the leg→arm →face.

(iv) Epileptic fits.

• Involvement of uncinate gyrus causes hallucinations of taste, and smell
and involuntary smacking movements of lips and tongue.
• Generalized fits may occur.
(v) Pupillary changes and oculomotor palsy.
• It indicates trans tentorial herniation.
(b) Cerebellar abscess:
(i) Headache: involves suboccipital region and may be associated with neck
rigidity.
(ii) Spontaneous nystagmus: is common and irregular and generally, to the side
of lesion.
(iii) Ipsilateral hypotonia and weakness.
(iv) Ipsilateral ataxia: Patient staggers to the side of lesion.
(v) Past-pointing and intention tremor: can be elicited by finger nose test.
(vi) Dysdiadochokinesia: Rapid pronation and supination of the forearm shows
slow and irregular movements on the affected side.

Investigations:
1. Skull X-Rays.
• Useful to see midline shift, if pineal gland is calcified
• Reveals gas in the abscess cavity
• They have been replaced by CT scan.

2. CT Scan
• Helps to find the site and size of an abscess
• It also reveals associated complications such as extradural abscess,
sigmoid sinus thrombosis, etc.

3. X-ray Mastoids or CT Scan. of the temporal bone - evaluation of associated

ear disease.

4. Lumbar Puncture.
• There is risk of coning.
• CSF:
▪ rise in pressure,
▪ increase in protein content
▪ normal glucose level
▪ white cell count of CSF is raised
▪ contains polymorphs or lymphocytes depending on the acuteness of
lesion.
TREATMENT:

MEDICAL
• High doses of antibiotics are given parenterally.
• Chloramphenicol and third generation Cephalosporins
• Metronidazole -Bacteroides fragilis, in brain abscess
• Aminoglycoside antibiotics, e.g. gentamicin- pseudomonas or proteus
• Culture of discharge from the ear may be helpful in the choice of
antibiotic.
• Raised intracranial tension can be lowered by dexamethasone, 4 mg i.v.
6 hourly or mannitol 20% in doses of 0.5 g/kg body weight.
• Discharge from the ear should be treated by suction clearance and use
of topical ear drop.

NEUROSURGICAL

• Abscess is approached through a sterile field.

• Options include:

(i)Repeated aspiration through a burr hole

(ii)Excision of abscess

(iii) Open incision of the abscess and evacuation of pus.

• If abscess is treated by aspiration, it should be followed by repeat CT or

MRI scans to see if it diminishes in size.
• An expanding abscess, or one that does not decrease in size, may
require excision.
• Pus recovered from the abscess should be cultured and its sensitivity
discovered.
• Penicillin can be instilled into the abscess after aspiration.

OTOLOGIC

• Acute otitis media might have resolved with the antibiotics given for the
abscess.
• Chronic otitis media -Radical Mastoidectomy- to remove the irreversible
disease and to exteriorize the infected area.
 • Surgery of the ear is undertaken only after the abscess has been
controlled by antibiotics and neurosurgical treatment.

OTOSCLEROSIS/OTOSPONGOSIS

• Irregularly laid Spongy bone in bony labyrinth

• Common focus: SATPES REGION
• 50% patients have positive family history
• Females have twice the incidence of males
• Age of onset: 20 – 30 years

Pathology
GROSS:

• Lesion – white/grey/yellow
• If red – increased vascularity

MICROSCOPY

• Increased spongy bone content in normally dense enchondral layer of

the otic capsule
1. Endosteal
2. Enchondral ➔ site of otosclerosis
3. Periosteal

TRIAD
Van der Hoeve syndrome

• Blue sclera
• Osteogenesis imperfect
• Otosclerosis

Types of otoscelrosis

1. Stapedial otosclerosis
 2. Cochlear otosclerosis
3. Histologic otosclerosis

Stapedial otosclerosis
• Most common type
• Site- fissula ante fenestrum (in front of oval window)
• Causes Stapes fixation→ conductive hearing loss

Focuses in stapedial otosclerosis

• Anterior focus
• Posterior focus – behind oval window
• Circumferential – around margin of foot plate of stapes
• Biscuit type – around margin of foot plate of stapes
• Obliterative type – complete obliteration of oval window

Cochlear otosclerosis
• Site: Round window
• Sensorineural hearing loss (due to toxic material in inner ear fluid)

Histologic otosclerosis
• Asymptomatic
• No hearing loss

Symptoms

❖ Presenting symptom
➢ Hearing loss: Common type → bilateral conductive type
▪ Onset: insidious
▪ Progressive
▪ Painless
➢ PARACUSIS WILLISH
▪ Person hears better in noisy surroundings than normal surroundings
➢ Tinnitus
▪ In cochlear otosclerosis
➢ Vertigo
➢ Speech
Signs

❖ Tympanic membrane, Eustachian tube – normal

❖ Schwartz sign – reddish spot seen on the promontory through tympanic
membrane
❖ Rinne’s test ➔ -ve (BC>AC)
❖ Weber test ➔ lateralized to ear of more conductive loss
❖ Absolute bone conduction – normal/ may decrease in cochlear type
❖ Pure tone audiometry → loss of air conduction for lower frequency
❖ Bone conduction normal
➢ Carhart’s notch: the dip in bone conduction(max at 2000Hz) → called
Carhart’s notch
❖ Mixed hearing loss also possible
❖ Speech audiometry – normal/except in cochlear type
❖ Tympanometry – early: normal / later: ossicular stiffness
❖ Stapedial stiffness – absent

Differential diagnosis

Other causes of conductive deafness

• Serous otitis media

• Adhesive otitis media
• Tympanosclerosis
• Stapes fixation(congenital)

Treatment

• No pharmacological agent
• Sodium fluoride = hasten maturity and arrest further events

Surgical
Stapedectomy/Stapedectomy with placement of prosthesis (local anasthesia)

• Teflon piston
• Stainless steel
• Platinum Teflon
 • Titanium Teflon

Brief steps of stapedectomy

• Meatal incision
• Exposure of stapes area and removeits superstructure
• Create hole in stapes foot plate(stapedectomy) / removal part of foot
plate(stapedectomy)
• Place prosthesis
• Close the structures

Complications
• Later perforation of tympanic membrane
• Injury to chorda tympani nerve, facial nerve
• Incus dislocation/erosion
• Prosthesis dislocation
• Dead ear (2%)

Contraindications
• If it is the only hearing ear
• Associated meniere’s disease
• Young children (recurrent Eustachian tube dysfunction)
• Professional athletes, divers, frequent air travelers
• Otitis externa, TM perforation
 FACIAL NERVE AND ITS DISORDERS

ANATOMY AND FUNCTIONS OF FACIAL NERVE:

• Facial nerve runs from pons to parotid.

• It is a mixed nerve having motor and a sensory root.
• There are two efferent and two afferent pathways.

NUCLEUS OF FACIAL NERVE:

• Motor nucleus of the nerve is situated in the pons. It receives fibres from
the precentral gyrus.

• Upper part of the nucleus which innervates forehead muscles receives

fibres from both the cerebral hemispheres, whereas the lower part of
nucleus which supplies lower face gets only crossed fibres from one
hemisphere.

• The function of forehead is thus preserved in supranuclear lesions because

of bilateral innervation.

• The emotional movements such as smiling as it also receives fibres from

the thalamus by alternate routes, thus providing involuntary control to
facial muscles.

COURSE OF FACIAL NERVE:

The course of the nervecan thus be divided into three parts:

1. Intracranial Part. From pons to internal acoustic meatus (15–17 mm).

2. Intratemporal Part. From internal acoustic meatus to stylomastoid

foramen. It is further divided into:

(a) Meatal segment (8–10 mm) -Within internal acoustic meatus.

(b) Labyrinthine segment (4.0 mm) -From fundus of meatus to the geniculate
ganglion
(c) Tympanic or horizontal segment (11.0 mm) -From geniculate ganglion to
just above the pyramidal eminence

(d) Mastoid or vertical segment (13.0 mm) -From the pyramid to stylomastoid
foramen.

3. Extracranial Part -From stylomastoid foramen to the termination of its

peripheral branches.

BRANCHES OF FACIAL NERVE

• Greater superficial Petrosal Nerve.

• Nerve to Stapedius. It arises at the level of second genu
• Chorda Tympani
• Communicating Branch
• Posterior Auricular Nerve
• Muscular Branches- To stylohyoid and posterior belly of digastric.
• Peripheral Branches upper temporofacial and a lower cervicofacial, which
further divide into smaller branches. –
o These are the temporal, zygomatic, buccal, mandibular and
cervical and together form pes anserinus (goose-foot). They
supply all the muscles of facial expression.

BLOOD SUPPLY OF FACIAL NERVE:

• Anterior-inferior cerebellar artery - supplies cerebellopontine angle

• labyrinthine artery - internal auditory canal
• superficial petrosal artery - geniculate ganglion and the adjacent region
• stylomastoid artery - mastoid and tympanic segment.

• All the arteries form an external plexus which lies in the epineurium and
feeds a deeper intra neural internal plexus

VARIATION AND ANOMALIES OF FACIAL NERVE

1. Bony dehiscence (absence of bony cover)

 • This is the most common anomaly.

• Dehiscence occurs most commonly in tympanic segment over the oval

window.

• A dehiscent nerve is prone to injury at the time of surgery or gets easily

involved in mastoid and middle ear infections.

2. Prolapse of nerve

• The dehiscent nerve may prolapse over the stapes and make stapes
surgery or ossicular reconstruction difficult.

3. Hump

• The nerve may make a hump posteriorly near the horizontal canal
making it vulnerable to injury while exposing the antrum during mastoid
surgery.

4. Bifurcation and trifurcation

• The vertical part of facial nerve divides into two or three branches, each
occupying a separate canal and exiting through individual foramen.

5. Bifurcation and enclosing the stapes

• The nerve divides proximal to oval window—one part passing above and
the other below it and then reuniting.

6. Between oval and round windows

• Just before oval window the nerve crosses the middle ear passing
between oval and round windows.

SEVERITY OF NERVE INJURY:

• Neurapraxia - a conduction block

• Axonotmesis -injury to axons.
• Neurotmesis - injury to nerve.

Sunderland classification (based on anatomical structure of the nerve)

1°= Partial block to flow of axoplasm; no morphological changes are seen.
Recovery of function is complete (neurapraxia).

2°= Loss of axons, but endoneurial tubes remain intact. During recovery,
axons will grow into their respective tubes, and the result is good
(axonotmesis).

3°= Injury to endoneurium. During recovery, axons of one tube can grow into
another. Synkinesis can occur (neurotmesis).

4°= Injury to perineurium in addition to above. Scarring will impair

regeneration of fibres.

5°= Injury to epineurium in addition to above.

The first three degrees are seen in viral and inflammatory disorders while
fourth and fifth are seen in surgical or accidental trauma to the nerve or in
neoplasms.

ELECTRODIAGNOSTIC TESTS:

These tests are useful to differentiate between neurapraxia and degeneration

of the nerve.

• Minimal Nerve Excitability Test

• Maximal Stimulation Test (MST)
• Electroneuronography (ENoG)
• Electromyography (EMG)

CAUSES OF FACIAL PARALYSIS (central or peripheral)

Peripheral lesions are more common and about two-thirds of them are of
the idiopathic.

A. IDIOPATHIC

1. Bell’s Palsy (paresis of acute onset)

• 60-75% of facial paralysis is due to Bell’s palsy.

• Risk of Bell palsy is more in diabetics (angiopathy) and pregnant women
(retention of fluid).

Aetiology

• Viral Infection - herpes simplex, herpes zoster or the Epstein–Barr virus.

Other cranial nerves may also be involved.

• Vascular Ischaemia

▪ Primary ischaemia is induced by cold or emotional stress.

▪ Secondary ischaemia is the result of primary ischaemia which causes

increased capillary permeability

• Hereditary. The fallopian canal is narrow. 10% of the cases of Bell palsy
have a positive family history.

• Autoimmune Disorder. T-lymphocyte changes have been observed.

Clinical Features of Bell’s palsy

• Onset is sudden. Patient is unable to close his eye.

• On attempting to close the eye, eyeball turns up and out (Bell
phenomenon).
• Saliva dribbles from the angle of mouth. Tears flow down from the eye
(epiphora).Face becomes asymmetrical.
• Paralysis may be complete or incomplete.
• Bell palsy is recurrent in 3–10% of patients.

Diagnosis.

• Diagnosis is always by exclusion i.e, All other known causes of peripheral

facial paralysis should be excluded.
• This requires careful history, otological and head and neck examination, X-
ray studies, blood tests.
Treatment

General:

• Reassurance.
• Relief of ear pain by analgesics.
• Care of the eye. Eye must be protected against exposure keratitis.
• Physiotherapy or massage of the facial muscles gives psychological support.

Medical management:

• Steroids
▪ Prednisolone is the drug of choice.
▪ Contraindications to use of steroids include pregnancy, diabetes,
hypertension, peptic ulcer, pulmonary tuberculosis and glaucoma.
▪ Steroids have been found useful to prevent incidence of synkinesis,
crocodile tears and to shorten the recovery time of facial paralysis

Surgical Treatment

Nerve decompression relieves pressure on the nerve fibres and thus improves
the microcirculation of the nerve. Vertical and tympanic segments of nerve are
decompressed.

Prognosis

• 85-90% of the patients recover fully.

• Ten to fifteen per cent recover incompletely.
• Recurrent facial palsy may not recover fully.
• Prognosis is good in incomplete Bell palsy (95% complete recovery)

2. Melkersson Syndrome

• It is also an idiopathic disorder consisting of a triad of

o facial paralysis
o swelling of lips
o fissured tongue

Paralysis may be recurrent. Treatment is the same as for Bell palsy.

B. INFECTIONS

1. Herpes Zoster Oticus (Ramsay–Hunt Syndrome)

o There is facial paralysis along with vesicular rash in the external auditory
canal and pinna
o There may also be anaesthesia of face, giddiness and hearing
o impairment due to involvement of Vth and VIIIth nerves.
o Treatment is the same as for Bell palsy (add acyclovir)

2. Infections of Middle Ear

3. Malignant Otitis Externa

C. TRAUMA

1. Fractures of Temporal Bone

➢ Fractures of temporal bone may be longitudinal, transverse or mixed.

➢ Paralysis is due to intraneural haematoma, compression by a bony spicule

or transection of nerve.

2. Ear or Mastoid Surgery

3. Parotid Surgery and Trauma to Face

⚫ Facial nerve may be injured in surgery of parotid tumours or deliberately

excised in malignant tumours.

D. NEOPLASMS

1. Intratemporal Neoplasms

• Carcinoma of external or middle ear, glomus tumour,

rhabdomyosarcoma and metastatic tumours of temporal bone, all result
in facial paralysis.
• Facial nerve neuroma occurs anywhere along the course of nerve and
produces paralysis of gradual or sudden onset.
2. Tumours of Parotid

• Facial paralysis with tumour of the parotid almost always implies

malignancy.

E. SYSTEMIC DISEASES AND FACIAL PARALYSIS

diabetes, hypothyroidism, leukaemia, sarcoidosis, periarteritis nodosa,

Wegener’s granulomatosis, leprosy, syphilis and demyelinating disease.

TOPODIAGNOSTIC TESTS FOR LESIONS IN INTRATEMPORAL PART

(useful in finding the site of lesion in paralysis of lower motor neuron.)

1. Schirmer Test.

• It compares lacrimation of the two sides.

• A strip of filter paper is hooked in the lower fornix of each eye and the
amount of wetting of strip measured.
• Decreased lacrimation indicates lesion proximal to the geniculate
ganglion as the secretomotor fibres to lacrimal gland leave at the
geniculate ganglion via greater superficial petrosal nerve.

2. Stapedial Reflex.

• Stapedial reflex is lost in lesions above the nerve to stapedius.

• It is tested by tympanometry.

3. Taste Test.

• It can be measured by a drop of salt or sugar solution placed on one side

of the protruded tongue, or by electrogustometry.
• Impairment of taste indicates lesion above the chorda tympani.

4. Submandibular Salivary Flow Test.

• It also measures function of chorda tympani.

 • Polythene tubes are passed into both Wharton ducts and drops of saliva
counted during one minute period.
• Decreased salivation shows injury above the chorda.

COMPLICATIONS FOLLOWING FACIAL PARALYSIS:

Peripheral facial paralysis due to any cause may result in any of the
following complications:

• Incomplete Recovery
• Exposure Keratitis
• Synkinesis (Mass Movement)
• Tics and Spasms
• Contractures
• Crocodile Tears (Gustatory Lacrimation)
• Frey’s Syndrome (Gustatory Sweating)
• Psychological and Social Problems

HYPERKINETIC DISORDERS OF FACIAL NERVE

They are characterized by involuntary twitching of facial muscles on one or

both sides.

1. Hemifacial Spasm - characterized by repeated, uncontrollable twitchings of

facial muscles on one side.

Types

(i) idiopathic, where cause is not known

(ii) secondary, where cause is acoustic neuroma, congenital cholesteatoma or

glomus tumour

⚫ Many cases of hemifacial spasm are due to irritation of the nerve because
of a vascular loop at the cerebellopontine angle.

⚫ Microvascular decompression through posterior fossa craniotomy has met

with high success rate in these cases.
⚫ Botulinum toxin has been used in the affected muscle. It blocks the
neuromuscular junction by preventing release of acetylcholine.

2.Blepharospasm.

⚫ Twitchings and spasms are limited to orbiculars oculi muscles on both

sides.

⚫ Botulinum-A toxin injected into the periorbital muscles gives relief for 3–6
months. Injection can be repeated, if necessary

SURGERY OF FACIAL NERVE:

• Decompression
• End-to-End Anastomosis
• Nerve Graft (Cable Graft)
• Hypoglossal-Facial Anastomosis
• Plastic Procedures
 MÉNIÈRE’S DISEASE

• Aka endolymphatic hydrops

• Disorder of inner ear
• Cause – distended endolymphatic system with endolymph
Etiology
i. defective absorption by endolymphatic sac
ii. vasomotor disturbance
iii. allergy
iv. sodium water retention
v. hypothyroidism
vi. autoimmune or viral infections
Pathology :
Dilated ducts completely fill the scala vestibuli & cause marked bulging of
Reissner’s membrane which herniate through the helicotrema into apical part
of scala tympani

Clinical features:
➢ age : 35 to 6 yrs
➢ sex : males are affected more
➢ usually unilateral
➢ cardinal symptoms
• episodic vertigo
• fluctuating sensorineural hearing loss
• tinnitus
• aural fullness
Examination
1. Otoscopy: no abnormality in tympanic membrane
2. Nystagmus: seen during acute attacks. It is towards the
unaffected ear.
3. Tuning fork test: indicates sensorineural hearing loss.
Investigations
o pure tone audiometry
 o speech audiometry
o special audiometry test
o electrocochleography
o caloric test
o glycerol test
Management
A. General Measures
1. Reassurance: reduce patients anxiety by reassuring and
explaining the true nature of the disease
2. Cessation of smoking: nicotine causes vasospasm so
smoking should be stopped completely.
3. Low salt diet: salt free diet is recommended. Intake should
not exceed 1.5-2.0 g/day
4. Avoid excess intake of water
5. Avoid coffee, tea & alcohol.
6. Avoid stress &&change lifestyle
7. Avoid activities needing good balancing

B. Management of acute attacks

During acute attacks there is severe vertigo with nausea and
vomiting.
patient is apprehensive.

1. Reassurance
2. Bed rest : head supported with pillow to prevent
movements
3. I.V fluids and electrolytes: to combat the loss due to
vomiting
4. Vestibular sedatives :
✓ to stop vertigo.
✓ administered intramuscularly or intravenously
✓ drugs used: dimenhydrinate(Dramamine) ,
promethazine theoclate(Avomine) or
prochlorperazine(Stemetil)
✓ diazepam 5-10mg given i.v
✓ some are given 0.4mg of atropine s.c
 5. Vasodilators: Carbogen (5% CO2 with 92% O2) is good
cerebral vasodilator,improves labyrinthine circulation.

C. Management of chronic phase

1. Vestibular sedatives: prochlorperazine(Stemetil) 10mg TDS

for 2 months later reduced to 5mgTDS for a month.
2. Vasodilators
3. Diuretics: Furosemide 40mg
4. Propantheline bromide
5. Elimination of allergen
80% of the patients are effectively managed with medical therapy
Methods used:
1. Intratympanic gentamicin therapy
2. microwick
Surgical treatment
✓ Used only when the medical treatment fails
• Conservative procedures
✓ Used in cases where vertigo is disabling but hearing is still
usefully and need to be preserved
A) Decompression of endolymphatic sac
B) Endolymphatic shunt operation
C) Sacculotomy (ficks operation
D) Section of vestibular nerve
E) Ultrasonic destruction of vestibular labyrinth

• Destructive procedures
✓ Totally destroy cochlear and vestibular functions so used
only when cochlear function is not serviceable
✓ Labyrinthectomy: membranous labyrinth is completely destroyed
by opening through the lateral semicircular canals by
transmastoid route or through oval windows are Bu transcanal
approach

• Intermittent low pressure pulse therapy (Meniett device

therapy)
 TUMORS OF EXTERNAL EAR
Tumours of Auricle

Benign tumors

• Preauricular sinus or cyst

o Due to faulty union of hillocks of 1st and 2nd branchial
arches.
o Surgery indicated if there is swelling or infection.
• Sebaceous cyst
o Common site post auricular sulcus
o Surgical excision recommended
• Dermoid cyst
o Round mass over upper part of mastoid
• Keloid
o Following trauma
o Rx– surgical excision with injection of triamcinolone
• Hemangioma
o Capillary hemangioma
o Cavernous hemangioma
• Papilloma
• Cutaneous horn
• Keratocanthoma
o Benign tumour resembling malignant
• Neurofibroma
o Firm swelling
o Associated with von Recklinghausen disease

Benign Tumours Of External Auditory Canal

• Osteoma
o It arises from cancellous bone
o arising from the posterior wall of the osseous meatus.
o Surgical removal by fracturing through its pedicle or
removal with a drill.
• Exostoses
 o multiple and bilateral, smooth, sessile, bony swellings
o They arise from compact bone.
o removed with high speed drill to restore normal sized
meatus.
• Ceruminoma
o It is a tumour of modified sweat glands which secrete
cerumen.
o It obstructs the meatus leading to retention of wax and
debris.
o Wide surgical excision should be done and patient regularly
followed up.
o Postoperative radiotherapy should be given in case of
suspicion of malignancy.
• Sebaceous adenoma
o It arises from sebaceous glands of the meatus
o Smooth, skin-covered swelling in the outer meatus.
o Treatment: is surgical excision.

Malignant Tumors

• Squamous cell carcinoma

o It is seen in cases of long-standing ear discharge.
o It may arise primarily from the meatus
o secondary extension from the middle ear carcinoma.
o Symptoms: blood staining of hitherto mucopurulent
discharge
o Ulcerated area in the meatus or a bleeding polypoid mass or
granulations
o En bloc wide surgical excision with postoperative radiation.
• Basal cell and adenocarcinomas
o They can rarely arise from the meatus.
o Diagnosis is made only on biopsy.
o Wide surgical excision and postoperative radiation.
• Malignant ceruminoma
o Malignant type is twice as common as benign.
• Malignant melanoma – Rare tumour
 TUMOURS OF MIDDLE EAR
GLOMUS TUMORS

• Chemodectomas /non chromaffin paragangliomas

• Arise from GLOMUS BODIES along parasympathetic nerves in
skull base, thorax, neck.
• Glomus TYMPANICUM for tumor in middle ear PROMONTRY
• Glomus JUGULARE from JUGULAR FORAMEN
• Glomus VAGALE from HIGH IN THE NECK
• CAROTID BODY TUMORS from CAROTID BODY

PATHOLOGY:

• Most common BENIGN TUMOR within temporal bone

• Simple swelling/ marked bone erosion / marked expansion with cranial
nerve paralysis.
• All these tumors secrete catecholamines but only few become clinically
evident.

CLINICAL FEATURES:

Incidence: Middle age, Female to male 3:1 Familial (auto-dominant)

SYMPTOMS

• hearing loss
• Bloody discharge
• PULSATILE TINITUS
• Ear fullness
• Ear pain
• Cranial N palsy: facial nerve
• May include 6 9 10 11 12 nerves.
SIGNS: RISING SUN APPEARANCE: red blue mass behind tympanum.

BROWN’S SIGN: dark red middle ear mass BLANCHES ON SEIGELIZATION.

DIAGNOSIS:

• AUDIOGRAM initially conductive later profound sensorineural hearing

loss.
• MRI: for tumor extension; T1 weighted shows salt and pepper
appearance.
• CT scan: absent plate of bone btw jugular foramen and carotid canal in
Glomus JUGULARE called PHELP’S SIGN
• 24-hour URINE VMA may be increased.
TREATMENT:

• Surgical approaches
o Transcanal approach
o Hypotympanic approach
o Extended facial recess approach
o Mastoid neck approach
o Infratemporal fossa approach of FISCH
o Transcondylar approach
• Radiation
• Embolization
ACOUSTIC NEUROMA: (NEURILEMMOMA OR NEURINOMA)
• BENIGN SCHWANOMA OF 8TH cranial nerve
• 10% of all intracranial tumors and 80% of cerebellopontine tumors

Course of disease:

• Arises from the vestibular nerve in the internal auditory meatus

• Grows into the cerebellopontine angle cistern
• Compress the nerves, brainstem and cerebellum there
• Increases the intra cranial pressure flowed by death if untreated
Symptoms:

• Gradual unilateral sensorineural hearing loss

• Tinnitus: unilateral high-pitched and continuous
• Vertigo: abrupt and early in onset
• Trigeminal involvement: Hypesthesia of facial region
• 7th nerve:
o Sensory fibres affected early
o Palsy can occur late in large tumors
• 9th 10th 11th 12th nerves can be affected: Leads to Dysphagia dysphonia
• Brainstem involvement: Weakness and numbness of limbs
• Cerebellum involvement: Ataxia and disequilibria
• Raised ICP: Headache nausea vomiting diplopia
Signs:

• Loss of sensation in posterior superior meatal wall; HOUSE AND

HITSELBERGER’S SIGN
• Cerebellar function tests positive; Romberg’s positive – falls towards
affected side
• Loss of corneal reflex (5th Nerve)
Investigations:

• Audiological tests.
• Stapedial reflex decay test
• Vestibular tests- Caloric test
• Neurological tests.
 • Radialogical tests:
o Plain X-rays
o Computed tomography (CT) scan.
o MRI WITH GADOLINIUM CONTRAST. It is superior to CT scan and
is the GOLD STANDARD for diagnosis of acoustic neuroma.
• Evoked response audiometry (BERA).

TREATMENT

• Surgical removal of the tumour is the treatment of choice. Surgical

approach will depend upon the size of tumour.
• The various approaches are:
o Middle cranial fossa approach.
o Trans labyrinthine approach.
o Suboccipital (retro sigmoid) approach.
o Combined trans labyrinthine-suboccipital approach.
• RADIOTHERAPY
o X-knife or Gamma knife surgery
 THE DEAF CHILD
People with profound (> 90 dB loss) or TOTAL DEAFNESS fail to develop speech
, termed as DEAF MUTE or DEAF and DUMB.

• No defect in speech producing apparatus.

• Main defect is deafness.
• Never heard speech thus failed to develop it.
• Period of speech development: 0-5 years.
• Thus , early assessment and identification of hearing loss is required.
AETIOLOGY

PRENATAL CAUSES
• Infant :
o Scheibe dysplasia
o Alexander dysplasia
o Bing Siebenmann dysplasia
o Michael Aplasia
o Mondini dysplasia
o Enlarged vestibular aqueduct

• Maternal
o Infections during pregnancy (TORCH Infections)
o Drugs during pregnancy (Streptomycin , Gentamycin , Quinine ,
Amikacin)
o Radiations
o Nutritional deficiencies
o Diabetes
o Maternal alcoholism
PERINATAL CAUSES
• Anoxia
• Premature baby
• Birth injury
• Neonatal jaundice
• Neonatal meningitis
• Sepsis
 • Ototoxic drugs
POSTNATAL CAUSES
• Genetic: Alport syndrome , Hurler’s , Familial progressive sensorineural
deafness
• Non genetic: viral infection, secretory otitis media , trauma

EVALUATION

Suspicion of hearing loss

• Child sleeps through loud noises.
• Fail to startle for sounds
• Fail to develop speech between 1 to 2 years.
• Defective speech – if partially hearing.
Risk factors
• Family history
• Prenatal, postnatal aetiology.

ASSESSMENT

1) SCREENING PROCEDURES
• OAE - Oto Acoustic Emissions
• ABR – Audio Brainstem response.
2) BEHAVIOUR OBSERVATION AUDIOMETRY
• Auditory signals that brings change in behaviour of infant. Ex.
Alertness, Cessation of an activity , Widening of eyes and facial
grimacing.
• Moro's reflex: Movement of limb and extension of head with
sound of 80-90 dB
• Cochleopalpebral reflex : Blink to loud sounds.
• Cessation reflex : Infants stop activity or cries on sound of
90dB.
3) DISTRACTION TECHNIQUES:
• Turns head on direction of sounds.
4) CONDITIONING TECHNIQUES:
 • Visual Audiometry
• Play audiometry
• Speech Audiometry
5) OBJECTIVE TESTS :
• Evoked response audiometry
1. Electrocochleography: Measure auditory sensitivity.
2. Auditory Brainstem response
• Oto Acoustic Emissions
• Impedance Audiometry
o OAE and ABR used in both screening procedures of deaf mute
and hearing evaluation.
MANAGEMENT

• Parental Guidance
• Hearing aids
• Cochlear implants
• Development of speech and language
o Communication: Two way process. Need receiver and
transmitter. Auditory faculty is poor in hearing impaired people.
o Auditory oral communication: Hearing aids and Speech therapy
o Manual communication: Sign language
o Total communication : All modalities of sensory input to
auditory .Develop oral speech , lip reading. Vibro tactile aids.
o Education of deaf: Residential or day schools for children of
impaired hearing.Use of Radio hearing aids.
o VOCATIONAL GUIDANCE
 REHABLITATION OF THE HEARING IMPAIRED

All Hearing impaired Individuals require aural rehabilitation for

communication.
Types:
• CONVENTIONAL HEARING AIDS
• BONE ANCHORED HEARING AIDS
• IMPLANTED HEARING AIDS

CONVENTIONAL HEARING AIDS

• Used to amplify sounds reaching the ear

• Three parts :
Microphone : Picks sound and converts into electrical impulse.
Amplifier : Magnifies electrical impulse.
Receiver : Converts electric impulse back into sound.
• TYPES :
a. AIR CONDUCTION HEARING AIDS
b. BONE CONDUCTION HEARING AIDS

AIR CONDUCTION HEARING AIDS

• Amplified sound is transmitted to tympanic membrane through ear
canal
TYPES:
1. BODY WORN TYPE:
→Commonest type
Indications: Deaf persons, Children with congenital disease.

2. BEHIND THE EAR TYPES:

Indications: Slight to moderate hearing loss of high frequency ones.

3. SPECTACLE TYPES OF HEARING AIDS

Indications: People require both eye glasses and hearing aid
 4. IN THE EAR TYPES:
Indications: Mild to moderate hearing losses with flat configuration.

5. Canal types ( In The Canal and Completely In the Canal )

Indications: Mild to moderate cases of hearing loss of high frequency
(1-4 kHz)

INDICATIONS OF HEARING AIDS:

Persons with hearing problem that cannot be helped by medical or

surgical means need hearing aid.

SENSORINEURAL HEARING LOSS

DEAF CHILDREN

CONDUCTIVE DEAFNESS

BONE CONDUCTION HEARING AIDS

• Bone vibrator is fitted on mastoid.
• Stimulate cochlea.
• Useful in persons of draining ears , otitis externa , atresia of ear canal
when ear inserts cannot be worn.

DISADVANTAGES OF CONVENTIONAL HEARING AIDS :

• Poor Cosmetic appeal.

• Acoustic feedback.
• Spectral distortion.
• Occlusion of auditory canal.
• Collection of wax in canal , blockage of insert.
• Sensitivity of canal skin to ear mould.
• Cannot be used in discharged ears.
 BONE ANCHORED HEARING AIDS
• Principle : Bone conduction
Indications: Conductive hearing loss, Unilateral hearing loss , People cannot
wear “ In the ear” or “ behind the ear” hearing aids.

• Three components :
TITANIUM FIXTURE
TITANIUM ABUTEMENT
SOUND PROCESSOR

Indications:

• Chronic inflammation or infection of ear canal.

• cannot wear “in the ear ”hearing aids.
• Malformed/ absence of outer ear or ear canal
• single sided deafness
• Otosclerosis
• tympanosclerosis

IMPLANTED HEARING AIDS

• Direct drive principle.

• These systems use mechanical vibrations delivered directly to the
ossicular chain, leaving ear canal completely open.
TYPES

a. Piezoelectric devices
b. Electromagnetic hearing devices

a. Piezoelectric devices
• Operate by passing electric current into piezo ceramic crystal.
• Change volume, produce vibratory signal.
• Piezoelectric transducer attached to ossicles, drive vibrations
• Examples: Envoy , MET , Rion, TICA.

b. Electromagnetic devices:
• Function by passing electric current into a coil, creates magnetic flux
that drives adjacent magnet.
 • Small magnet is attached to one of the ossicles of middle ear to convey
vibrations to the cochlea.
• Examples: Vibrant sound bridge devices (symphonix device)
VIBRANT SOUNDBRIDGE DEVICE:

• Semi implantable device

• Two components: Internal and External.
Internal component

• Vibrating ossicular prosthesis

• Three parts: receiver, floating mass transducer, conductor link
between the two.
• FMT connected to incus.
External component

• Audio processor
• It has microphone, picks up sound and transmit across skin by
radio frequency waves to internal receiver

Indications: Adults aged 18 years

Older with moderate to severe sensorineural hearing loss

DISADVANTAGES:

• Discomfort due to occlusion effect of canal.

• Wax occluding hearing aid mould and wax impaction of hearing aid
canal.

ADVANTAGES :

• Bypass of ear canal and tympanic membrane , thus eliminate Occlusion ,

feedback , discomfort , wax related problems.
• Better than conventional hearing aids.
• Improved sound quality.
 COCHLEAR IMPLANTS

Components of cochlear implants:

• External:
o External speech processor(microphone present)
o Transmitter
• Internal
o Electronic array
o Receiver/stimulant package

Candidacy profile

Used in both children and adults

1) B/L severe or profound sensorineural hearing loss
2) Little/no benefit from hearing aids
3) No material contraindication dor surgery
4) Good family and social support towards habilitation
5) Adequate cognitive function to be able to use the service

Candidates with hearing impairments:

A) Prelingual candidates
• Deafened before acquisition of speech and language
B) Postlingual candidates
• Deafened after acquisition of speech and language

Outcomes of Cochlear Implantation:

• Successful outcome
o Prior use of hearing aids /post lingual patients - previous auditory
experience
o Younger age implantation(specially for prelingual patients)
o Short duration deafness
o Neural patients within auditory system
• Factors limit benefit of cochlear implantation:
• Implantation of patients with auditory implantation and
degeneration in central auditory pathway limit speech and
language acquisition in patients
COCHLEAR IMPLANTS

Pre lingual candidates :

Children → Speech and language acquisition good after few years
Recognize speech: constant
Auditory- verbal training method
Early age infants (<13mnths age) better results
Adult → No/little prior auditory impulse limited benefit
Sound awareness achieved

Post lingual candidates:

Children → Very good benefits
&Adults can use telephone eventually
Recognize speech with minimal lip reading (or) visual cues

Complications of cochlear implants:

EARLY COMPLICATIONS

• Facial paralysis
• Wound infection
• Wound dehiscence
• Flap necrosis
• CSF leak
• Meningitis
• Postoperative dizziness/Vertigo
LATE COMPLICATIONS

• Exposure of device and extrusion

• Pain at the site of implant
• Migration/displacement of the device
• Late device failure
• Otitis media
 OTALGIA
LOCAL CAUSES

• External:
→ Furncle
→ Impacted ear wax
→ Otitis external
→ Otomycosis
→ Myringitis bullosa
• Middle ear:
→ Acute otitis media
→ Eustachian tube
→ Mastoiditis
→ Extra dural abscess
→ Aero –otitis

REFERRED CAUSES

• Via the 5th cranial nerve

→ Dental -caries teeth , apical abscess, costen syndrome
→ Oral cavity- benign or malignant ulcerative lesion of oral cavity
or tongue
→ TM Joint disorders
→ Sphenopalantine neuralgia
• Via 9th cranial nerve :
→ Oropharynx : acute tonsillitis , peritonsillar abscess ,
tonsillectomy
→ Base of tongue - tuberculosis or malignancy
→ Elongated styloid process
• Via 10th cranial nerve: malignancy or ulcerative lesion of
vallecula, epiglottis, larynx
• Via C2+C3 spinal nerve - cervical spondylitis, injuries of cervical
spine + caries spine

PSHYCOGENIC CAUSES

• no cause has been discovered, Pain may be functional

 TINNITUS
Tinnitus is ringing sound or noise in the ear.

FEATURES: Origin of the sound is within the patient.

• It may unilateral or bilateral.
TYPES
1. Subjective Can be heard only by the patient.
2. Objective Can be heard by the patient and the doctor
with the help Stethoscope.
CAUSES
Subjective Tinnitus Objective Tinnitus
OTOLOGIC VASCULAR
Impacted Wax, Fluid in Middle Ear, Congenital AV Malformation, Glomus
Chronic Otitis media, Presbycusis, Tumor of middle ear, Carotid Stenosis,
Noise induced hearing loss. Carotid Aneurysm, Dehiscent Jugular
Bulb.
METABOLIC
Obesity, Hyperthyroidism, Patulous Eustachian Tube
Hypothyroidism, Vitamin B12
deficiency, Hyperlipidaemia.
NEUROLOGIC
Temporal Bone Fractures, Brain Palatal Myoclonus
Haemorrhage, Brain infarct,
Labyrinthine Concussion,
Postmeningitic.
CARDIOVASCULAR
Hypertension, Hypotension, Anaemia, Idiopaphic Stapedial / Tensor Tympani
Arteriosclerosis, Cardiac Arrhythmias. Myoclonus.
PHARMACOLOGIC All Ototoxic drugs. Dental Causes
PSYCHOGENIC
Anxiety, Depression Clicking of Temporomandibular Joint.
TREATMENT
Tinnitus is a symptom and not a disease and cause should be discovered
and treated.
Management Includes
• Reassurance and Psychotherapy: Patient should learn to live
with Tinnitus.
• Techniques of relaxation and Biofeedback.
• Sedation and Tranquillizers: Needed during the initial stages.
• Tinnitus Maskers:
1 They are worn like earing aid.
2 It provides symptom free period for several hours due to the
phenomenon of residual inhibition.

TINNITUS INSTRUMENT: Hearing aid + Masker

TINNITUS RETRAINING THERAPY (TRT):

Jastreboff’s Neurophysiologic Therapeutic Model aims to attenuate
connections between auditory, limbic and autonomic nervous systems and
thus create Tinnitus habituation.
TRT Therapy needs a long period of 18 to 24 months, but gives significant
improvement.

It occurs at two levels.

• Habituation of Reaction: It is uncoupling of brain and body from
negative reactions to Tinnitus.

• Habituation of Tinnitus: With this therapy patient suffering from

Tinnitus lose awareness of Tinnitus.

Counselling - It is important to educate the patient about Tinnitus,

Mechanism, Perception, Plasticity of Brain which
can habituate any sensory stimuli.

Sound Therapy - Patient should avoid silent environment.

Sound generators are used which produce
continuous low level broadband noise for 8 hours
a day for habituation.
 MYRINGOTOMY
Incision on tympanic membrane with the purpose to drain suppurative or non suppurative
effusion of the middle ear or to provide aeration in malfunctioning eustachian tube

INDICATIONS

• Acute suppurative otitis media.

• Otitis media with effusion.
• Aero-otitis media
• Atelectatic ear

STEPS OF OPERATION

• Ear canal is cleaned of wax and debris. Operation is ideally performed under
operating microscope using a sharp myringotome and a good suction apparatus.
• In acute suppurative otitis media, a circumferential incision is made in the
posteroinferior quadrant of tympanic membrane, midway between handle of
malleus and tympanic annulus, avoiding injury to incudostapedial joint.
• In otitis media with effusion, a small radial incision is made in the posteroinferior or
anteroinferior quadrant and all the effusion sucked out.
POSTOPERATIVE CARE In serous otitis media, just leave a wad of cotton wool for 24–48 h.
Drum incisions usually heal rapidly. No water should be permitted to enter the ear canal
for at least 1 week, and if a grommet has been inserted, entry of water is prevented so
long as grommet is in position.

COMPLICATIONS

a) Injury to incudostapedial joint or stapes.

b) Injury to jugular bulb with profuse bleeding, if jugular bulb is high and bony floor of
the middle ear dehiscent.
c) Middle ear infection.
GROMMET

It is a ventilation tube placed in the tympanic membrane for drainage or ventilation of the
middle ear. It has also been called pressure-equalizing or tympanostomy tube and is made
of Teflon or medical-grade silicon which is biocompatible. Complications of ventilation tube
include:

i. Blockage due to blood or secretions

ii. Middle ear infection
iii. Extrusion
iv. Persistent perforation after extrusion or removal.
v. Granuloma formation.
 MASTOIDECTOMY
TYPES:

1. CORTICAL/SIMPLE/COMPLETE MASTOIDECTOMY (SHWARTZ OPERATION)

➢ Mastoid: Complete exenteration of all accessible mastoid air cells
(converting them into single cavity)
➢ Posterior meatal wall: Intact
➢ Middle ear structures: Not disturbed

2. RADICAL MASTOIDECTOMY
➢ To eradicate disease from the middle ear and mastoid (without any attempt
to reconstruct hearing)
➢ Posterior meatal wall: Removed – entire area of middle ear, attic, antrum,
and mastoid is converted into a single cavity
➢ Middle ear structures: All remnants of tympanic membrane, ossicles(except
stapes footplate), and mucoperiosteal lining are removed; Eustachian tube is
obliterated(by a piece of muscle or cartilage)

3. MODIFIED RADICAL MASTOIDECTOMY

➢ Modification of radical mastoidectomy where hearing mechanism is
preserved.
➢ Disease localized to attic and antrum is removed
➢ Both posterior meatal wall and lateral attic wall are removed.

ANAESTHESIA: General anaesthesia (preferred); Local anaesthesia (in selected cases)

POSITION: Patient lies supine with face turned to one side and the ear to be operated
uppermost.

INCISION:

Cortical - Postaural

Radical - Endaural/Postaural
 CORTICAL
INDICATIONS 1. Acute mastoiditis
2. Incompletely resolved
acute otitis media with
reservoir
sign
3. As an initial step to
perform:
a. endolymphatic sac
surgery
b. decompression of facial
nerve
c. trans labyrinthine or
retro labyrinthine
procedures for acoustic
neuroma.
COMPLICATIONS 1. Injury to facial nerve.
2. Dislocation of incus.
3. Injury to horizontal semi-
circular canal.
(Postoperative giddiness
and nystagmus.)
4. Injury to sigmoid sinus
with profuse bleeding.
5. Injury to dura of middle
cranial fossa.
6. Postoperative wound
infection and wound
breakdown.
RADICAL MODIFIED RADICAL
1. Recurrent 1. Cholesteatoma
cholesteatoma that confined to the attic
cannot be safely and antrum.
removed
(that invading 2. Localized chronic
Eustachian tube) otitis media.
2. As an approach to
petrous apex.
3. Removal of
glomus tumour.
3. Carcinoma middle
ear
1. Facial paralysis. ‘Same as radical’
2. Perichondritis of
pinna.
3. Injury to dura or
sigmoid sinus.
4. Labyrinthitis, if
stapes gets
dislocated.
5. Severe conductive
deafness of 50 dB or
more.
6. Cavity problems.
 MYRINGOPLASTY
❖ Closure of perforation of pars tensa of the tympanic membrane
❖ Advantages:
✓ restoring the hearing loss
✓ to check repeated infection (from external auditory canal and Eustachian
tube)
✓ to prevent aeroallergens reaching the exposed middle ear mucosa
❖ Myringoplasty can be combined with ossicular reconstruction when it is called
tympanoplasty.

ANAESTHESIA: General (preferred)/Local anaesthesia

POSITION: Patient lies supine with face turned to one side and the ear to be operated
uppermost.

INCISION: Depends on the size of ear canal – Endomeatal/Endaural/Postaural

GRAFT MATERIALS used are:

• Temporalis fascia (most common)

• Areolar fascia overlying the temporal fascia
• Perichondrium from the tragus
• Cartilage
• Vein
• Periosteum

TECHNIQUE:

1. UNDERLAY TECHNIQUE(Graft is under the anterior annulus, supported by gelfoam)

2. OVERLAY TECHNIQUE(Graft placed on the outer surface of tympanic membrane)

COMPLICATIONS:
❖ UNDERLAY TECHNIQUE
1. Middle ear becomes narrow.
2. Graft may get adherent to the promontory.
3. Anteriorly, graft may lose contact from the remnant of tympanic membrane
leading to anterior perforation.
❖ OVERLAY TECHNIQUE
1. Blunting of the anterior sulcus.
2. Epithelial pearls (epidermal cysts - squamous epithelium buried under the graft)
3. Lateralization of graft (Graft loses contact from the malleus handle)