Topic list - ENT

Ear
I.01 – Anatomy and function of the external and middle ear.
I.02 – Anatomy and function of the inner ear.
I.03 – Tunning fork and audiometrical examinations.
I.04 – Otoneurological examinations
I.05 – Malformations and diseases of the external ear
I.06 – Middle ear and pyramid bone traumas
I.07 – Diseases of the Eustachian tube
I.08 – Acute purulent otitis media
I.09 – Chronic mesotympanal otitis media
I.10 – Chronic cholestematous otitis media
I.11 –Intracranial complications of the acute and chronic otitis media
I.12 – Intratemporal complications of the acute and chronic otitis media
I.13 – Indications for antrotomy, mastoidectomy and radical mastoidectomy. What does it mean?
I.14 – Surgical reconstruction of the hearing mechanism
I.15 – Otosclerosis and its surgical treatment
I.16 – Tumors in the external ear and middle ear
I.17 – Toxic damages and circulatory disturbances in the inner ear
I.18 – Acoustic injury
I.19 – Meniere disease
I.20 – Acoustic neuroma and its early diagnosis
I.21 – Hearing loss in childhood
I.22 – Function of the facial nerve and facial palsy
I.23 – Differential diagnosis of the tinnitus
I.24 – Otalgy. Otalgy irradiata. Differential diagnosis. Task of the family doctor.
I.25 – Mastoiditis.

Nose, paranasal sinuses and pharynx

II.01 – Functional anatomy and physiology of the nose and paranasal sinuses
II.02 – Examination of the nose and paranasal sinuses
II.03 – Value and indication of radiological examination in paranasal sinus diseases
II.04 – Diseases of the external nose and its complications
II.05 – Nasal trauma and its treatment
II.06 – Epistaxis
II.07 – Differential diagnosis of nasal obstruction
II.08 – Acute and chronic rhinitis
II.09 – Clinical symptoms, diagnosis and treatment of allergic rhinitis
II.10 –Traumatic lesion of facial cranium
II.11 – Paranasal sinusitis in childhood and adults
II.12 – Treatment of paranasal sinusitis
II.13 – Complications of paranasal sinusitis
II.14 – Tumors of the nose and paranasal sinuses
II.15 – Anatomy and physiology of the pharynx
II.16 – Diseases of the nasopharynx
II.17 – Acute and chronic inflammation of the mesopharynx
II.18 – Acute tonsillitis. Specific angina
II.19 – Chronic tonsillitis and its secondary consequences
II.20 – Indication for adenectomy and tonsilectomy
II.21 – Tumors of the mesopharynx and hypopahrynx.
II.22 – Dysphagia and its management by the family doctor
Larynx
III.01 – Functional anatomy of the larynx
III.02 – Malformations of the larynx
III.03 – Traumas of the larynx. Treatment of laryngeal trauma
III.04 – Functional disorders of the larynx
III.05 – Acute and chronic inflammation of the larynx
III.06 – Acute laryngitis in childhood
III.07 – Benign tumors and precancerous diseases of the larynx. papillomas
III.08 – Malignant tumors of the larynx
III.09 – Treatment of the laryngeal cancer. Surgical procedures for laryngeal carcinoma
III.10 – Dyspnea caused by disorders of the upper respiratory tract
III.11 – Edema in the larynx
III.12 – Indication for conicotomy, tracheotomy and its techniques
III.13 – Intubation or tracheotomy
III.14 – Diagnosis and management of foreign bodies in the upper and lower respiratory tract
III.15 – Differential diagnosis of cervical enlargements and inflammations
III.16 – Ludovic's angina, parapharyngeal and retropharyngeal abscess. Cervical phlegmone
III.17 – Corrosive injury and stenosis of the esophagus. Task of the family doctor
III.18 – Foreign bodies in the pharynx and esophagus. What to do?
III.19 – Diseases of the salivary glands
III.20 – Stenosis in the larynx and upper respiratory tract. Treatment of this disease
III.21 – Differential diagnosis of dysphonia
III.22 – Palpation of the neck and its consequences in the practice.

Practice
Gy.01 – Examination of the external auditory meatus and the ear drum
Gy.02 – Examination of hearing by means of tuning forks
Gy.03 – Audiograms
Gy.04 – Measurement of hearing loss
Gy.05 – Examination of the spontaneous vestibular symptoms
Gy.06 – Cleaning of the external meatus
Gy.07 – Myringotomy. Indications and technique
Gy.08 – Clinical examination of the nose and nasal cavity
Gy.09 – Treatment of epistaxis
Gy.10 – Treatment of the nasal and auricular furuncle. Technique of bandages
Gy.11 – Puncture of the maxillary sinus
Gy.12 – The method of introducing the naso-esophageal nutrition tube
Gy.13 – Ear drops and nasal drops
Gy.14 – X-ray and CT, MRI pictures in ORL
Gy.15 – Removal of the foreign bodies from the external ear, nasal cavity and pharynx
Gy.16 – Examination of the pharynx
Gy.17 – Treatment of the peritonsillar abscess
Gy.18 – Indirect laryngoscopy
Gy.19 – Cleansing of the tracheostomy tube
Gy.20 – Corrosive injuries of the esophagus.
Topic 1. Anatomy and function of the external and the middle ear

External ear
The external ear consists of:
1) Auricle (pinna)
2) External auditory meatus (EAM)

The auricle
Is the outer visible portion, composed of single piece fibroelastic cartilage (connected to skull),
covered with integument, and connected to the surrounding parts by lig. & mm.
 It serves to collect the air vibrations and funnels them in form of sound waves to EAM
 Acts as a resonator to slightly amplify lower frequency sounds
 helps to localize sounds

The pinna larger end is directed upward. Its lateral surface is irregularly concave, directed slightly
forward, and presents numerous eminences and depressions:

The prominent rim of the auricula is called the helix

Where the helix turns downward behind, the auricular tubercle (of Darwin) can be found → very
evident in ~ 6th month of fetal life
The antihelix is another curved prominence, parallel with and in front of the helix→ divides into 2
crura, b/w which is a triangular depression called the fossa triangularis.
The narrow-curved depression b/w the helix and the antihelix is called the scapha
The antihelix describes a curve around a deep, capacious cavity, the concha, which is partially divided
into 2 parts by the crus → cymba (upper part) & cavum (lower part)

The tragus is a small pointed eminence, found in front of the concha, projecting backward over meatus
the antitragus lies opposite to the tragus, and is separated from it by the intertragic notch
Below this is the lobule, composed of tough areolar and adipose tissues, and wanting the firmness and
elasticity of the rest of the auricula.

The cranial (post.) surface of the auricula presents elevations which correspond to the depressions on
its lateral surface and after which they are named eminentia concha & eminentia triangularis.

The skin
Thin, closely adherent to the cartilage, and covered with fine hairs furnished with sebaceous glands,
which are most numerous in the concha and scaphoid fossa.
 On the tragus and antitragus the hairs are strong and numerous.
 The skin of the auricula is continuous with that lining the external acoustic meatus
The ligaments → 2 sets:
1. Extrinsic (ant. and post.) → connecting it to the side of the head
2. Intrinsic → connecting various parts of its cartilage together.

The muscles → 2 sets:

1. Extrinsic → connect it with the skull and scalp and move the auricula as a whole
2. Intrinsic → extend from one part of the auricle to another.

The ext. mm. consist of Auriculares ant. (smallest), sup. (largest) and post.
 These mm. possess very little action
 the Auricularis ant. draws the auricula forward and upward the
 Auricularis superior slightly raises it
 Auricularis posterior draws it backward.

Innervation
 Auriculares ant. & sup. and the intrinsic mm. on lat. surface → temporal branch of the facial n.
 Auricularis post. and the intrinsic mm. on cranial surface → post. auricular branch of same nerve

The sensory nerves are:

 Vagus → Auricular branch
 Mandibular n. → Auriculotemporal branch
 Cervical plexus (C3 and C2) → Lesser occipital & Great auricular

Blood supply
 Post. auricular a. → from external carotid
 Ant. auricular a. → from superficial temporal

Development
The auricle develops from 3 pairs of auricular hillocks that arise in the 5th week, on the lateral faces
of the 1st and 2nd pharyngeal arches.
The hillocks are named for the portions of the auricles to which they give rise.
In the 7th week, the auricular hillocks begin to enlarge, differentiate and fuse, producing the final
shape of the ear, which is gradually translocated from the side of the neck to a more cranial and lateral
site.

Pharyngeal arch
1st → Tragus, Helix, Cymba concha
2nd → Antitragus, Antihelix, Concha

External Auditory meatus (EAM)

The EAM extends from the bottom of the concha to the TM, conducting the vibrations
It is an oval cylindrical canal ~ 4cm length (measured from the tragus) lined by skin
It consists of 2 parts→ cartilage (and mem.) and bone
 The cartilaginous portion (1/3) → ~ 8 mm. in length, it is continuous with the cartilage of the
auricula, and firmly attached to the circumference of the auditory process of the temporal bone.
This part consists a thick subcutaneous tissue in which numerous ceruminous glands secrete ear-
wax.
 The osseous portion (2/3) → ~16 mm. in length, and is narrower than the cartilaginous portion
it is marked, except at its upper part, by a narrow groove, the tympanic sulcus, in which the
circumference of the TM is attached.

The EAM forms an S-shaped curve → 3 parts:

1) Pars externa → directed at first inward, forward, and slightly upward
2) Pars media → passes inward and backward
3) Pars interna → carried inward, forward, and slightly downward (nearly horizontally)

Because of its curvature → canal can be straightened by pulling the auricle backward (for eardrops)

 The EAM presents 2 constrictions, one near the inner end of the cartilaginous portion, and another,
the isthmus, in the osseous portion, ~ 2cm from the bottom of the concha.
 The TM, which closes the inner end of the meatus, is obliquely directed → the floor and ant. wall
of the meatus are longer than the roof and post. wall.

The skin lining the inner bony 2/3 is very thin, with little hair and no glands, well-innervated and very
sensitive to touch, in contrast to the skin of the auricle.
The "fissures of Santorini" are discontinuities in the cartilage of the outer canal → enable infec. or
neoplasm to easily spread down and forward into the adjacent parotid gland.

Anatomical relations of the meatus

 In front of the osseous part → condyle of the mandible
- Frequently separated from the cartilaginous part by a portion of the parotid gland.
- The jaw movements influence to some extent the lumen of this latter portion.
 Behind the osseous part → mastoid air cells, separated from the meatus by a thin layer of bone.

Innervation
The nerves are chiefly derived by auriculotemporal branches of the mandibular n. and vagus.

Blood supply
The arteries supplying the meatus are branches from Post. auricular, Int. maxillary & Temporal aa.

Overall functions of the external ear

 Non acoustic → protection, self cleaning (hairs, wax)
 Acoustic
1. Transmits sounds waves to the sensitive middle ear structures in a discriminating way.
2. alters the amplitude of the incoming sound wave
3. amplifies selected frequency bands (2-4khz)
4. wind-break by creating air turbulence → ↓ constant acoustic effect of moving air.
5. plays a role in the 'spatial' hearing of sounds
6. helps in localization of sound

Examination of the auricule and EAM

 Inspection
 Palpation
 Otoscopy (ear speculum)
 Microscopy
 Audiology (pure tone) → intact hearing, conductive hearingloss, sensorineural hearingloss
The middle ear
The middle ear (tympanic cavity) is an air filled irregular, laterally
compressed space within the petrous part of the temporal bone
 Separated from ext. ear by TM and from inner ear by
the oval window
 Filled with air, which is conveyed to it from the nasal part of
the pharynx through the auditory tube.

The middle ear cavity is consists of:

1) TM
2) Ossicular chain
3) Eustachian (pharyngotympanic) tube
4) Middle ear cavity

Function
1. Keep transmission loss as small as possible and, at certain
frequencies, transmit virtually all the energy of the vibrating air to the inner ear fluid.
2. Equalize static air pressure via the estachian tube.

At 1 kHz – the sound energy transmitted is most effective.

The tympanic membrane

The TM separates the tympanic cavity
from the bottom of the EAM.
 Thin, semitransparent mem.
directed obliquely downward and
inward
 9 - 10 mm. in diameter

Tympanic annulus → fibrocartilaginous ring which is fixed in the tympanic sulcus at the inner end
of the meatus. This sulcus is deficient superiorly at the notch of Rivinus, and from the ends of this
notch two bands, the ant. & post. malleolar folds, are prolonged to the lateral process of the malleus
The small, somewhat triangular part of the membrane situated above these folds is lax and thin, and is
named the pars flaccida (in it a small orifice is sometimes seen)

 The manubrium of the malleus is firmly attached to the medial surface of the membrane
 Cone of light → triangular reflection of light (otoscope)
 Umbo → most depressed center point

The TM is composed of 3 layers:

1. Cutaneous (outer) → derived from the integument lining the meatus
2. Fibrous (middle) → consists of 2 layers
 Radiate → fibers which diverge from the manubrium of the malleus
 Circular → fibers which are plentiful around the circumference but sparse and scattered
near the center
3. Mucosal (inner)
Innervation
 auriculotemporal branch of the mandibular;
 auricular branch of the vagus
 tympanic branch of the glossopharyngeal

Blood supply
 deep auricular branch of the internal maxillary, which ramifies beneath the cutaneous stratum
 stylomastoid branch of the posterior auricular
 tympanic branch of the internal maxillary, which are distributed on the mucous surface.

Auditory ossicles
The ossicles are 3 tiny bones that function to transmit sonic
vibration to inner ear and amplify the force
1) Malleus (hammer)
2) Incus (anvil)
3) stapes (stirrup)

The Ossicles are connected by 2 mm.

 Stapedium → innervated by br. from mandibular n. (V3)
 Tensor tympani → innervated by br. of CN VII

Eustachian (pharyngotympanic) tube

 3.7cm, open into anterior wall of tympanic cavity
 Lat. 1/3 bony → cartilaginous part → membraneous part
 Function to equalize pressure in the mid. ear
 Is closed at rest, open by sphincter nasopharyngeal isthmus & tensor palate
 More horizontal, wider & shorter in infants
Topic 2. Anatomy and function of the inner ear

The inner ear (labyrinth) is located in the petrosal part of the temporal bone. It consists of:
 Acoustic apparatus → cochlea
 Vestibular apparatus → vestibule ( utricle, saccule, semilunar canals)
This vestibule-cochlear organ is responsible for hearing and equilibrium (balance)

The inner ear is divided into 2 cavity sys.:

1) Osseous labyrinth
2) Membranous labyrinth

Osseous labyrinth
The superficial contours of the inner ear are established by a layer of dense bone, that are continuous
with the surrounding temporal bone.

The bony labyrinth can be subdivided into:

1. the vestibule → contains a pair of membranous sacs called saccule and utricle
2. 3 semicircular canals
3. cochlea
It also consists of a fluid called Perilymph which is similar to CSF and within it the membraneous
labyrinth is situated

The vestibule
Is the central portion. Contains both the oval & round windows and an opening (vestibular aqueduct)
which leads to the post. cranial fossa.
The inner surface consists of 3 parts (recesses) separated by a bony crest:
 Utrical → elliptical shaped, give raise to the semicircular canals
 Saccule
 Chochlear recess → from which the cochlea arise

The semicircular canals (ant. post. and lat.)

 The ant. and post. canals are in vertical plane and the lat. canal is in horizontal plane.
 Each canal has 2 cruses → simple and ampulla cruses.
 In the ampulla there is a receptor called crista ampulla → sensitive to angular acceleration!

The cochlea
The bony cochlea is spiral chamber, so called because it is shaped like a snail shell having 2.5 turns.
Bony projections (osseous spiral laminae) divides the cochlea inner surface into 2 parts:
1. Scala vestibuli (sup.) → communicates functionally with the middle ear via the oval window
2. Scala tympani (inf.) → communicated with the middle ear via the round window.
Both scala communicate with each other at a small opening called helicotrema
The cochlea contains the cochlear duct of the membranous labyrinth in which the hearing receptors
are localized → vibration of the foot plate of the stapes vibrates the perilymph in the bony cochlea.
This fluid is essentially incompressible, therefore, there has to be a counter opening in the labyrinth
to allow fluid space to expand when the stapes foot plate moves inwards and in turn to move inwards
when the stapes foot plate moves outwards.

The counter opening is provided by the round window mem. which lies beneath the oval window in
the inner wall of the middle ear. It is covered by a fibrous mem. which moves synchronously but in
opposite phase with the foot plate in the oval window

oval window → scala vestibule → helicoterma → scala tympani → round window

Membranous labyrinth
 Located within the bony labyrinth and is suspended in perilymph.
 It is filled with endolymp (similar to ICF with ↑ K and ↓ Na) and contains the sensory organs.
 Has an outer CT and inner simple cuboidal epi.
 It is divided into 2 parts: vesticular and cochlear labyrinth

Vestibular labyrinth
Responsible for balance and consists of the uticle & saccule → both contain receptors called macula
that detect linear acceleration.

Cochlear labyrinth
Contains the cochlear duct (scala media) and is responsible for hearing
The duct is spiral in shape but looks triangular in cross section → forms 3 walls:
1. Sup. → vestibular mem.
2. Inf. → basilar mem. attached to spiral lamina
3. Stria vasicularis → on the surface of spiral lig.

The receptor that is responsible for sound perception is called Organ of Corti.
 It is located at the top of the basilar mem.
 Waves are passing thought the endolymph stimulate the organ of corti
 Above it, also related to sound perception is a gelatinous tectorial mem.

It composed of inner and outer pillar cell’s rods and divided into an inner and outer parts.
The inner side → contains one row of inner hair cells (IHC) which are the real receptors of hearing
The outer side → contains 3 rows of outer hair cells (OHC)
 regulates the stimulus input to the IHC
 provides a motor function to the organ of corti, responsible for the high sensitivity and sharp
frequency discrimination in hearing

The final structures of the inner ear is the CN VIII and the internal auditory meatus

Internal auditory meatus

Is a bony plate ~1cm in size that separates the cochlear from vestibular organs
CN VIII splits before it into cochlear br. (with spiral ggl.) and vestibular br. (with vestibular ggl.)
 Transmit CN-VII & CN VIII, int. auditory a+v.

Vestibulocochlear nerve (CN VIII)

 Type I fibers → are 1° Afferent and end on dendrites of IHC
 Type II fibers → are efferent and end on OHC
Topic 3. Tuning fork and audiometrical examinations

Hearing of an individual can be tested by clinical and audiometric tests

While assessing the auditory function it is important to find out:

1. Type of hearing loss → conductive, sensorineural or mixed
2. Degree of hearing loss → mild, moderate, moderately severe, severe, profound or total
3. Site of lesion →
Conductive → the lesion may be at external ear, TM, middle ear, ossicles or ET.
If sensorineural → cochlear, retrocochlear or central.
4. Cause of hearing loss → congenital, traumatic, infective, neoplastic, degenerative…

Tuning fork
Represent a clinical test for hearing loss.
It is an acoustic resonator , U-shaped bar of elastic metal (usually steel) with a handle and 2 tines.
It resonates at specific constant pitch when vibrating by striking it against a surface or object
A tuning fork of 512 Hz is ideal

In general, sound is produced by vibrations. Solids can produce sound as either a longitudinal or a
transverse wave (unlike in fluid or gases - only longitudinal).
When the tuning fork is hit, the tines begin to vibrate producing back and forth vibration which
results in longitudinal waves in a direction which is parallel (and anti-parallel) to the direction of
energy transport

Tuning fork is essential for dg. of and diff. b/w conductive and sensorineural hearing loss

It is used to test for:

Air conduction (AC) → a vibrating fork is placed vertically, ~ 2 cm from the opening of EAM.
The sound waves are transmitted through the TM, middle ear and ossicles to the inner ear→ function
of BOTH the conducting mechanism and the cochlea are tested.
Normally, hearing through air conduction is louder and heard twice as long as through the bone
conduction route.

Bone conduction (BC) → footplate of vibrating tuning fork is placed firmly on the mastoid bone.
Cochlea is stimulated directly by vibrations conducted through the skull bones → BC is a measure of
the cochlear function ONLY!

The clinical tests

The Weber test
In weber test, sound travels directly to the cochlea via bone.
A vibrating tuning fork is placed in the middle of the forehead or vertex and the pt. is asked if the
sound is heard equally in both ears or better on one side
 Normally → heard equally in both ears (NO lateralization)
 Conductive hearing loss → lateralised to the worse ear (louder in affected ear)
 Sensorineural hearing loss → lateralised to the better ear (quieter in affected ear)

The Rinne test

test air conduction compared with bone conduction in the same ear
A vibrating tuning fork is placed on the patient's mastoid and when he stops hearing, it is brought
beside the meatus and if the pt. still hears → AC > BC.
Finally, the pt. is asked to compare the loudness of sound heard in both cases
 Rinne test is called (+) when AC is longer or louder than BC.
 It is seen in normal ppl. or those having sensorineural deafness.
 A (-) Rinne (BC > AC) is seen in conductive loss → indicates min. air-bone gap of 15-20 dB
False (-) Rinne
Seen in severe unilateral sensorineural hearing loss.
Patient does not perceive any sound of tuning fork by AC but responds to BC testing.
This response to bone conduction is, in reality, from the opposite ear because of transcranial
transmission of sound.

Schwanbach test
It compares pt’s hearing sensitivity with that of an examiner (assuming he has a normal hearing)
The fork is set into vibration, stem is placed alternately against the mastoid process of the pt. and of
the examiner
 Pt. should indicate whether the tone is heard or not each time the fork is placed is pressed against
the mastoid process
 When the pt. no longer hears the tone, examiner immediately places the stem behind his or her
own ear and using a watch, notes the seconds the tone is audible after the pt. stops hearing it

The results
 If the patient stops hearing before the examiner → suggests a sensorineural loss.
 If the patient hears it longer than the examiner → suggests a conductive loss.

Summary of the tuning fork test results

Normal Conductive SN
Rinne AC > BC (+) BC > AC (-) AC > BC
Weber Not lateralised Lateralised to poorer ear Lateralised to better ear
Schwabach Equal Lengthened Shortened

Pure tone audiometry

Audiometry is the term used to describe formal measurement of hearing.
It is a subjective test to which the pts. can respond by pressing a button or raise his hand

The goals of clinical audiometry are:

1. Detect and localize hearing disorder
2. Classify a heading disorder (diagnostic audiometry)
3. Quantify a hearing disorder

An audiometer is an electronic device which produces pure tones (single frequencies)

 Tones intensity can be ↑ or ↓ in 5 dB steps
 Usually AC thresholds are measured for tones of 125, 250, 500, 1000, 2000, 4000 and 8000 Hz
and BC thresholds for 250, 500, 1000 and 2000 and 4000 Hz.

Masking
When diff. b/w the 2 ears is ≥ 40 dB in AC thresholds → the better ear is masked to avoid getting a
shadow curve from the non-test better ear. Similarly, masking is essential in all BC studies
Masking is done by employing narrow-band noise (white noise) to the non-test ear

Air-bone gap
Is the diff. in the thresholds of AC and BC
 The audiometer is calibrated so that the hearing of a normal person for AC and BC, is at zero dB
and there is NO A-B gap
 A-B gap is used to measure the degree of conductive loss.
Pure tone audiometry AC testing
Should be performed to identify any peripheral auditory dysfunction.
Performed by presenting to the pt through earphone, series of tones that are close to the threshold
(the loudness that the person can just barely detect), and keep dropping the intensity in 10 db steps
until the pt. stops responding (raising their hand or pushing a button).
Then the examiner goes back up in 5 db steps until the person starts responding again.

Pure tone audiometry BC testing

Done by placing an oscillator on the mastoid process and measure threshold at the same frequencies.
The threshold of BC is a measure of cochlear function.
 Tone will lateralizes to the poorer ear in case of CHL
 Tone will lateralizes to the better ear in case of SNHL
 Midline or unlaterlization in case of symmetrical loss or normal hearing

Audiogram
The amount of intensity that has to be raised above the normal level is a measure of the degree of
hearing impairment at that frequency → charted in the form of a graph called audiogram.

the reactions of the pt. to the pure tones are

plotted for each ear by using specific symbols

The responses charted on the audiogram define

levels of hearing for each ear.

For adults, normal hearing and degree of hearing loss fall into the following categories:

0 - 20 dB normal hearing
20 - 40 dB mild hearing loss
40 - 60 dB moderate hearing loss
60- 70 dB moderately severe hearing loss
70 - 90 dB severe hearing loss
>90 dB profound hearing loss
>110dB Deafness

Typical patterns
 Noise-induced hearing loss → a notch at 4-6kHz
 Low frequency hearing loss → on the onset of Ménière's disease
 Conductive loss accompanied by a bone conduction notch at intermediate frequencies (Carhart
notch) → in otosclerotic stapes fixation.
Speech Audiometry
In this test, the patient's ability to hear and understand speech is measured.
2 parameters are studied: speech reception threshold and discrimination score.

Speech reception threshold (SRT)

It is the minimum intensity at which 50% of the words are repeated correctly by the patient.
A set of spondee words (2 syllable words with equal stress on each syllable→ baseball, sunlight,
daydream…) is delivered to each ear through the headphone of an audiometer.
The word lists are delivered in the form of recorded tapes or monitored voice and their intensity
varied in 5 dB steps till half of them are correctly heard.
 Normally, SRT is within 10 dB of the average of pure tone threshold of 3 speech frequencies
(500, 1000 and 2000 Hz).
 An SRT better than pure tone average by > 10 dB suggests a functional hearing loss

Speech discrimination score (speech recognition)

It is a measure of patient's ability to understand speech.
Here, a list of phonetically balanced (PB) words (single syllable words → pin, sin, day, bus...) is
delivered to the patient's each ear separately at 30-40 dB above his SRT and the % of words correctly
heard by the patient is recorded.
In normal persons and those with conductive hearing loss a high score of 90-100% can be obtained
(< 40% is considered very poor)

Roll over phenomenon → seen in retrocochlear hearing loss.

With ↑ 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
Impedance Audiometry
Is objective test, widely used in clinical practice and is particularly useful in children. It consists of:
1) Tympanometry
2) Acoustic reflex measurements

Tympanometry
It is based on a simple principle → when a sound strikes TM, some of the sound energy is absorbed
while the rest is reflected.
A stiffer TM would reflect more of sound energy than a compliant one.
By changing the pressures in a sealed EAM and then measuring the reflected sound energy, it is
possible to find the compliance or stiffness of the tympano-ossicular sys. and thus find the healthy or
diseased status of the middle ear

Types of tympanograms

Type A Normal tympanogram.

Type As Compliance is lower at ambient air pressure. Seen in fixation of ossicles →
otosclerosis or malleus fixation.
Type AD High compliance at or near ambient pressure.. Seen in ossicular discontinuity or
thin and lax TM
Type B A flat or dome-shaped graph. Seen in middle ear fluid or thick TM
No change in compliance with pressure changes
Type C Max. compliance occurs with (-) pressure in Seen in retracted TM and may show
excess of 100 mm of H2O. some fluid in middle ear.

Acoustic reflex
based on the fact that a loud sound (70-100 dB above the threshold of hearing of a particular ear)
causes bilateral contraction of the stapedial mm. which can be detected by tympanometry.
Tone can be delivered to one ear and the reflex picked from the same or the contralateral ear.
The reflex arc involved is:

Ipsilateral: CN VIII → ventral cochlear nucleus → CN VII nucleus → ipsilateral stapedius muscle

Contralateral: CN VIII → ventral cochlear nucleus → contralat. medial sup. olivary nucleus →
contralateral CN VII nucleus → contralateral stapedius mm.
Topic 4. Otoneurological examinations

The usual auditory function tests assess the peripheral organ (including both middle and inner ear)
and the cochlear n. → in some pts. these tests result show normal hearing, however they still
complain of listening and understanding disabilities. In these cases, the pts. are said to have auditory
perceptual disorders or, more commonly, central auditory processing disorders (CAPD)

Central auditory processes are the neuronal mechanisms responsible for:

 sound localization and lateralization
 auditory discrimination
 auditory pattern recognition
 temporal aspects of audition → temporal resolution/masking/integration/ordering
 auditory performance with competing acoustic signals and with degraded acoustic signals

CAPD can be defined as abnor. of the basic processes involved in understanding spoken language in
the absence of dysfunction of the peripheral auditory sys. lesion (ear and cochlear nerve).
 They manifest as a deficit in info. processing of the audible signal and/or as an impaired ability
to discriminate, remember, recognize, and comprehend info. presented to normal ears.
 The neuronal abnor. that cause these disorders are localized b/w the cochlear nucleus and
auditory areas of cerebral cortex

Central auditory function tests

Generally are used to characterize abnor. of function rather than to diagnose macroscopic structural
lesions affecting the central auditory pathways
 Lesions can be identified using imaging techniques such as MRI and CT
 Brainstem auditory evoked potentials (BAEP) can help to localize abnor. anatomically
 These types of tests are objective in nature → measure the pts. physiologic involuntary
responses (unlike peripheral tests)

Acoustic reflex (Stapedius reflex)

The efferent auditory system provides feedback control of the volume of sounds reaching the
cochlea.
Loud sounds (> 70 dB) cause reflexive bilat. contraction of the stapedius mm., which limits ossicular
vibration (acoustic-facial reflex arch).

Stapedius Reflex threshold (SRT) is the min. sound pressure level needed to produce a measurable
change in TM impedance.
 Normal: 70-100 dB for pure tones.
 Frequencies b/w 500-4000 Hz are best used.

Pathology:
The acoustic reflex is not considered a strong measure of central auditory function. However, the
reflex may be disturbed by a lesion situated in the lower brainstem (the pons)
 Conductive deafness → fixation of the stapes (SRT is 70-110 dB above the subjective
threshold)
 Recruiting deafness → SRT is < 70 dB above the subjective threshold
 Neural deafness → SRT occurs at levels > 70 dB above the subjective threshold.
Brainstem auditory evoked potentials
Also called Auditory Brainstem response (ABR)
BAEPs are the electrical signals produced by the infra-tentorial auditory sys. in response to transient
auditory stimuli such as clicks or brief tone pips
It is used to differentiate b/w cochlear and retrocochlear hearing loss

The test
Electrodes placed b/w the vertex and the ear or mastoid ipsilateral to the stimulated ear
Stimuli are presented monaurally, and masking noise is presented to the contralateral ear.
The BAEP peaks, which have latencies of less than 10 msec, are typically labeled with roman
numerals

Acoustic clicks → waves obtained → waves can be assign to specific anatomical structures:
I. Cochlear
II. Auditory nerve
III. Cochlear nucleus
IV. Sup. Olivary nucleus
V. Lateral lemniscuses
VI. Inferior colliculus

Vestibular tests
Their purpose is:
1. Determine if there is any abnor. with the vestibular portion of the inner ear.
2. Decide if more expensive tests like MRI are needed.
3. To document objectively vestibular conditions (such as and Perilymph fistula, which
commonly occur after head injury, vestibular neuritis, and Gentamicin ototoxicity, which
commonly is a side effect of medication)

The vestibular tests include:

 electronystagmography (ENG)
 electrocochleography (ECOG)
 rotational chair test
 posturography
 fistula test

Electrocochleography (ECochG)
Measures the potentials arising in the cochlea (cochlear threshold indicator) and CN VIII.
Potentials occurring 1-3ms after stimulus.

Clinical applications:
 Monitoring the Ménière’s disease
 Enhancement of wave I and identification of I-V interweaves interval of the ABR in the
presence of hearing loss
 Monitoring Cochlear and auditory nerve function during surgery
Topic 5. Malformations and diseases of the external ear

Malformations
The pinna is formed from the coalescence of 6 tubercles, and development abnor. are common and
may be just minor variations from the normal or major abnormalities

Minor Malformations (group I)

 Bat ear → The fold of the antihelix is either absent or poorly formed resulting in protruding
ear. corrected b/w ages 4-6
 Anotia → complete absence of pinna
 Microtia → deformity is often associated with EAM atresia and ossicular abnor. result from
abnor. development of the 1st and 2nd branchial arches. may be associated with hypoplasia of
the maxilla and mandible, and eyelid deformities (Treacher–Collins sy.)
 Hypoplastic/atresia EAM → may occur alone or in association with microtia
 Hypoplastic tympanic cavity.
 Congenital aural fistula → incomplete closure of the 1st branchial groove.
 Preauricular sinuses→ commonly seen at the root of helix and is due to incomplete fusion of
tubercles.
It may get repeatedly infected causing purulent discharge. Abscess may also form.
Treatment is surgical excision of the track if the sinus gets repeatedly infected

Moderate Malformations (group II)

 The auricle is usually represented by a rudimentary soft tissue structure.
 The EAM is partially or totally aplastic, it may end blindly with fistulous tract which can be
associated with a cholesteatoma.
 The middle ear structures display malformations of varying degrees.

Severe Malformations (group III)

 The auricle is severely malformed or totally absent.
 The canal is aplastic.
 The antrum and the middle ear may be absent or may be represented by a slitlike lumen.
 The mid. ear ossicles are frequently absent.
 Malformations of the inner ear are frequently represented.

Anomalies of the facial nerve

1. Craniofacial dysostosis (Crouzon’s disease) → cranial synostosis, hypertelorism,
exophthalmus, external strabism.
2. Manibulofacial dysostosis (Treacher Collins and Franceschetti’s disease) → AD inheritance
Antimongoloid slant of the palpebral fissure, coloboma on the lower eyelid, absence of cilia of
the lower eyelid, hypoplasia of the mandibule, micrognathia, macrostomia.).

Management of the malformations

 Plastic surgery or prostheses (in difficult cases)
 In bilat. aural atresia reconstructiv surgery is indicated when the child is > 6-7 yrs old (mastoid
process pneumatized), however, if the atresia is associated with cholesteatoma, correctiv
surgery is indicated regardless of the pts. age.
Diseases of external ear
1) Infection
 Perichondritis auriculae
 Furunculosis
 Otitis externa
 Malignant otitis externa
 Herpes zoster oticus (Ramsay hunt sy.)
2) Trauma → to auricle or eardrum perforation
3) Tumors (topic 16)
4) Other → frost-bite, wax, foreign body

Perichondritis auriculae

Etiology
 infec. 20 to lacerations, haematoma or surgical incisions.
 extension of infe. from diffuse otitis externa or a furuncle of the meatus.
 High Ear Piercing (involving pinna cartilage)

Causative agents: P. aeruginosa, S. aureus, S. Pyogenes

Symptoms and Signs

 Initial symptoms are swollen red, hot and painful pinna which feels stiff.
 Later abscess may form b/w the cartilage and perichondrium with necrosis of cartilage
 TM is NOT involved!!

Treatment
 Early stages → local or sys. AB (Fluoroquinolones) + local 1% aluminium acetate (Burow’s
solution) compresses.
 Abscess → surgical incision, drainage

Furunculosis
A furuncle is a staph. infec. of the hair follicle.
 As the hair are confined only to the cartilaginous part of the meatus, furuncle is seen only in
this part of meatus.
 Usually single but may be multiple

Clinical manifestation
Pts. usually presents with severe pain and tenderness which are out of proportion to the furuncle size.
 Movements of the pinna & jaw are painful
 Swelling of the tragus, mastoid process (pseudomastoiditis)
 Periauricular L.N may be enlarged and tender

Treatment
 Early cases (w/o abscess) → consists of sys. AB, analgesics and local heat.
 Abscess → incision and drainage
 Recurrent furunculosis → DM should be excluded
External otitis
Infla. of meatal skin which may spread to involve the pinna and epidermal layer of TM
 Disease is commonly seen in hot and humid climate and in swimmers.
 Excessive sweating changes the pH of meatal skin from that of acid to alkaline which favours
growth of pathogens.
 Types: Diffuse OR circumscriptive external otitis

Etiology
1. Trauma to the meatal skin → scratching the ear canal with hair pins…
2. Invasion by pathogenic MO → S
3. Some cases are 20 to infec. of the middle ear, or allergic sensitisation to the topical ear drops
used for chr. suppurative otitis

Causative agents
 Bacteria → S. aureus, B. proteus, E. coli and P. pyocyanus
 fungi → Candida albicans, Aspergillus niger
 infec. is often mixed

Clinical features
Diffuse otitis externa may be acute or chronic with varying degrees of severity

Acute phase
Characterised by hot burning sensation in the ear, followed by pain which is aggravated by
movements of jaw.
 Ear starts oozing thin serous discharge which later becomes thick and purulent.
 Meatal lining is inflamed and swollen.
 Collection of debris and discharge accompanied with meatal swelling gives rise to conductive
hearing loss.
 Severe cases → regional L.N become enlarged & tender with cellulitis of surrounding tissues

Chronic phase
Characterised by irritation and strong itching sensation.
 This is responsible for acute exacerbations and reinfection.
 Discharge is scanty and may dry up to form crusts.
 Meatal skin which is thick and swollen may also show scaling and fissuring.
 Rarely, the skin becomes hypertrophic leading to meatal stenosis (chr. stenotic otitis externa).

Therapy: Burow solution strip, local AB, antimycotics, steroid, anti-infla. drugs

Malignant (necrotizing) external otitis

Is an infla. condition caused by pseudomonas infec. usually in the elderly diabetics, or in those on
immunosupp. drugs.
 Its early manifestations resemble diffuse otitis externa but there is excruciating pain and
appearance of granulations in the meatus.
 Facial paralysis is common.
 Infection may spread to the skull base and jugular foramen causing multiple cranial nerve
palsies.
 Anteriorly, infection spreads to temporomandibular fossa, posteriorly to the mastoid and
medially into the middle ear and petrous bone.
 CT scan is useful, to know the extent of disease

Treatment: high doses of IV antibiotics directed against pseudomonas (tobramycin, ticarcillin or 3rd
gen. cephalosporins).
Herpes zoster oticus (Ramsay hunt sy.)
It is characterised by formation of vesicles (Herpetic eruptions) on the TM, meatal skin, concha and
postauricular groove.
 CN VII and VIII may be involved
 Organism: chickenpox virus (VZV)

Symptoms
 fever, severe neuralgic pain
 erythema, vesicles on the auricle and the external meatus,
 peripheral facial nerve paralysis 60–90%
 sensorineural hearing loss, vestibular disorders (vertigo,nyst)
 paresis of glossopharyngeal and vagus nerve
 regional lymphadenitis
 serous meningitis

Complications
 Sensorineural hearing loss (vestibular organ might be affected)
 Ramsay-Hunt sy. → acute peripheral facial neuropathy associated with erythematous
vesicular rash of the skin of the ear canal, auricle and/or mucous mem. of the oropharynx.

Therapy: analgesics, antiviral ointment

Trauma
 Minor lacerations of canal skin result from Q-tip injury (hair pins, needles or match stick) or
unskilled instrumentation by physician. They usually heal W/O sequelae
 Major lacerations result from GSW, automobile accidents or fights.
- The condyle of mandible may force through the ant. canal wall.
- These cases require careful treatment
- Stenosis of the ear canal is a common complication

Haematoma of the auricle (othaematoma)

Direct blow to the head – extravasation of blood and serum beneath the perichondrium.
Symptoms → auricle enlargement, bluish swelling, the outline of the conchal folds is lost pain

Treatment:
 aspiration – repeated daily
 firm pressure dressing
 antibiotic
 incision – drainage
Topic 6. Middle ear and pyramid bone traumas

The middle ear and temporal bone are often involved in accidents involving trauma to the head.
The accidents are most frequently those involving motor vehicles, however, industrial and athletic
injuries may also present potential lesions to these structures.
 The temporal bone and middle ear are composed of very dense bone → source of the injury
must be of intense force.
 The type of injury seen with trauma to the head is classified as blunt and penetrating

Blunt trauma
Most frequently occurs as the result of the head being thrown against a solid or semisolid object, or an
object being thrown directly at the head.
 Fractures of the EAM, middle ear structures, otic capsule and its surrounding structures may
occur from blunt trauma.
 The fractures can be divided into longitudinal (most common) and transverse

Longidutinal fractures
The line of the fracture runs along the pyramidal axis extending into the middle ear.
These fractures most commonly result from direct lateral blunt trauma to the skull in the parietal
region.
The most frequently involved structures are:
1. TM
2. Roof of middle ear
3. Ant. portion of the petrous apex.
Fracture line may involve a portion of the Eustachian canal, most frequently in the tympanic portion.

Consequences of longitudinal fractures

1) Longitudinal fractures most frequently traverse at some point through the middle ear and
commonly may cause disruption of the middle ear ossicles, creating a conductive hearing loss.
2) Sensory neural hearing loss is a relatively UNcommon finding.
3) The vestibular involvement is relatively mild and thought to be related to concussive effects
rather than direct involvement of the vestibular labyrinth.
4) Bleeding in the middle ear presents with bleeding from the external canal (unlike in transverse
fractures in which bleeding is confined behind the eardrum!)
5) Spinal fluid leak may occur but is less common than in a transverse fracture.

Transverse fractures
Fracture line runs across the pyramidal axis extending into bony labyrinth and the int. auditory canal
 Are far less common than longitudinal ones.
 Most frequently occur by a severe blow to the occipital portion of the calvarium, however, they
may also occur from a direct frontal blow.
 Requires a far more intense blow to the skull.

The fracture most often begins at the jugulare foramen and extends across the petrous pyramid.
The fracture may actually traverse the otic capsule or may traverse the structures of the lateral most
end of the internal auditory canal

Consequences of transverse fractures

1) Severe sensorineural hearing loss
2) Loss of vestibular function → due to direct injury to inner ear or fracture through the otic capsule.
3) Facial paralysis → caused by interruption of the facial n.
4) Bleeding in middle ear (TM is often intact!)→ hemotympanum may be seen w/o ext. bleeding.
5) CSF leakage → detected by clear fluid draining from the eustachian tube into the nasopharynx.
Mixed fractures
Due to the skull anatomy, fractures are often mixed in nature → fracture line extending in almost any
direction across the basal portion of the skull.

Treatment of pyramidal fractures

Generally conservative. Prophylactic antibiotics.

Indications for early otologic intervention:

 early meningitis treated by mastoidectomy
 bleeding from the sigmoid sinus – ligatura of the sinus
 persistent CSF otorrhea – repair of the dura
 progressive facial nerve paresis . decompression
 depressed fracture of the external auditory canal – reconstruction

Indications for late otologic intervention:

 antibiotic resistant traumatic otitis media
 chronic mastoiditis
 late facial nerve paralysis – decompression
 posttraumatic deafness – tympanoplasty
 posttraumatic cholesteatoma – radical mastoidectomy

Summary of the diff. b/w the fractures:

Feature Longitudinal Fractures Transverse Fractures

Incidence ~ 80% ~ 20%

Mechanism Temporal or parietal trauma Frontal or occipital trauma
CSF otorrhea Less frequent common
TM perforation Common Rare
Facial nerve damage 20% 50%
most often temporary and frequently severe, usually permanent, and
delayed in onset immediate in onset
Hearing loss conductive severe sensorineural or mixed
Hemotympanum associated with otorrhagia not associated with otorrhagia
Nystagmus  usually spontaneous  spontaneous
 less intense (1st or 2nd degree)  intense (3rd degree)
 positional  fast component beating to the
 may be absent opposite ear
 long lasting
Vertigo Common Common
less intense, and/or positional intense, usually associated in the
absence is also possible acute phase with N&V
Penetrating trauma
Penetrating trauma to the middle ear and temporal bone may be relatively minor, such as a laceration
of the ear canal (Q-tips injury), to rather severe, including GSW to ear and temporal bone.

The most common penetrating injury to the middle ear and temporal bone is a self inflicted
instrumentation of the ear canal, such as a Q-tip injury, or the introduction of a foreign object, such as
a branch or other solid structure, stone or other foreign body

Consequences
The penetrating injury may create only a supf. flap laceration of the ext. canal, may penetrate the TM,
and may involve the ossicular chain in the middle ear.
The ext. canal penetration may also involve the facial nerve in its tympanic portion and may effect
direct injury to the auditory and vestibular system.

Traumatic eardrum perforation

Etiology
 compression injury → slap, blast from shot-fireing or gunfire
 Instrumental injury → hairpin, Q-tip, matches
 Petrous bone fracture

Symptoms
 pain, bleeding
 conductive hearing loss
 localization of the perforation: pars tensa → stellate shape

Treatment
 cleaning of the ear canal by suction using operating microscope
 reposition of the edges of the ear drum- covering by silicone or
 gelfoam patch
 antibiotic, TETANUS toxoid
 Urgent tympanotomy: facial nerve injury or subluxation of the Stapes (vertigo, nystagmus,
sensorineural hearing loss)

Traumatic disconnection of the ossicular chain

Occurs due to head injury, foreign body, or failed myringotomy.
 The incudo-stapedial joint is a common site of dislocation.
 Dg: absence of stapedial reflex and conductive deafness.
 Treatment: surgery

Baro-traumatic otitis media

When the pressure in the eardrum is lower than the atmospheric pressure.
 The TM retracts inwards, causing edema, pain, deafness, and tinnitus
 Treatment: decongestants to open the eustachian tube, and myringotomy if needed.
Topic 7. Diseases of the Eustachian tube

Anatomy
Eustachian tube (auditory or pharyngotympanic tube), connects nasopharynx with the tympanic
cavity.
In an adult, it is ~ 36 mm long and runs downwards, forwards and medially from its tympanic end,
forming an angle of 45° with the horizontal.

It is divided into 2 parts:

1. Bony (tympanic end) → is posterolateral, forms 1/3 of the total length
2. Fibrocartilaginous → anteromedial, forms 2/3
The 2 parts meet at isthmus which is the narrowest part of the tube

Innervations
 Tympanic branch of CN IX supplies sensory innervation to the tubal mucosa.
 Tensor veli palatini is supplied by mandibular branch of trigeminal (V3) nerve.
 Levator veli palatini and salpingopharyngeus receive motor nn. supply through pharyngeal
plexus (Cranial part of CN XI through vagus)

Function
1) Ventilation and regulation of middle ear pressure.
2) Protection against nasopharyngeal sound pressure and reflux of nasopharyngeal secretions.
3) Middle ear clearance of secretions.

Examination of the ET
 Pharyngeal end → post. rhinoscopy, rigid nasal endoscope or flexible nasopharyngoscope.
- The extrinsic causes which obstruct this end can be excluded
 Tympanic end → microscope or endoscope, if there is a preexisting perforation.
- Eustachian tube endoscopy or middle ear endoscopy can be done with very fine flexible
endoscopes.
- Exam. of TM with otoscope or microscope may reveal retraction pockets or fluid in mid.
ear.
- Movements of TM with respiration point to patulous ET

Further assessment of function of the tube can be made by:

 Valsalva, politzerisation, Toynbee and other tests
 Nasal exam. → endoscopy, tests of allergy, CT scan of temporal bones and paranasal sinuses.
 MRI may be required to exclude MS in patulous eustachian tube

Disorders of the ET

Tubal blockage
Normally, ET is closed. It opens intermittently during swallowing, yawning and sneezing through the
active contraction of Tensor veli palatini mm.
Air, composed of O2, CO2, nitrogen and water vapour, normally fills the middle ear and mastoid→
when tube is blocked, first O2 is absorbed, but later other gases, CO2 and nitrogen also diffuse out into
the blood → results in (-) pressure in the middle ear and retraction of TM.
If (-) pressure is still further ↑, it causes "locking" of the tube with collection of transudate and later
exudate and even haemorrhage
ET obstruction can be mechanical, functional or both.
1) Mechanical → can result from intrinsic causes (such as inflammation or allergy) or extrinsic
causes (such as tumour in the nasopharynx or adenoids).
2) Functional → caused by collapse of the tube due to ↑ cartilage compliance which resists
opening of the tube or failure of active tubal-opening mechanism due to poor function of tensor
veli palatine

Overall etiology
1. URTI (viral or bacterial) 6. Nasopharyngeal tumour/mass
2. Allergy 7. Cleft palate → inadequate tensor palati function
3. Sinusitis 8. Tumour - nasopharyngeal CA (adults)
4. Nasal polypi 9. barotrauma (sudden changes in air pressure)
5. Hypertrophic adenoids 10. Abnor. spatial orientation of ET → Down's sy.
(horizontal position)
Clinical presentation
Symptoms
 Otalgia → mild to severe
 hearing loss
 popping sensation, cracking noise on swallowing
 tinnitus
 disturbances of equilibrium or even vertigo

Signs → vary and depend upon the acuteness of the condition and severity.
 Retracted TM
 Radial vascularization of the eardrum
 Amber discoloration of the pars tensa
 Fluid level and air bubbles in the middle ear
 Congestion along the handle of malleus and the pars tensa
 Conductive hearing loss
 In severe cases (barotraumas) → TM is markedly retracted with haemorrhages in subepithelial
layer, haemotympanum or sometimes a perforation

Treatment
Elimination of the infla. in the paranasal sinuses and nasopharynx (nasal drop, antihistamine,
antibiotic)
adenotomy – later

Patulous Eustachian Tube

ET is abnor. patent.
It is mostly idiopathic but rapid weight loss, pregnancy especially 3rd trimester, or MS can also cause
it.

S&S
 Chief complaint is hearing the pts. own voice (autophony), and breath sounds.
 Due to abnormal potency→ pressure changes in the nasopharynx are easily transmitted to the
middle ear → the movements of tympanic can be seen with inspiration and expiration (these
movements are further exaggerated if pt. breathes after closing the opposite nostril)

Treatment
 Acute condition of patulous tube is self-limiting and does not require treatment.
 In others → weight gain, potassium iodide P.O is helpful
 In some long-standing cases → cauterisation of the tubes or insertion of a grommet
Topic 8. Acute purulent otitis media

Acute otitis media is an acute infla. of middle ear by pyogenic MO.

Refers to infla. of ET, mid. ear, attic, aditus, antrum and mastoid air cells Diseases of middle ear
 More common in infants and children. 1) Acute/chr. otitis media
 Typically, the disease follows viral infec. of URT but soon the 2) Mastoiditis
pyogenic MO invade the mid. ear 3) Osclerosis
4) Aero-Otitis
Causative agents 5) Trauma
Most common organisms in infants and young children are
 S. pneumoniae (30%)
 H. influenzae (20%)
 Moraxella catarrhalis (12%).
 Other → S. pyogenes, S. aureus and sometimes P. aeruginosa.

Risk factors
Anything that interferes with normal functioning of ET predisposes to middle ear infec. It could be:
1. Recurrent attacks of common cold, URTI, and exanthematous fevers (measles, diphtheria,
whooping cough).
2. Infec. of tonsils and adenoids.
3. Chr. rhinitis and sinusitis.
4. Nasal allergy
5. Tumours of nasopharynx
6. packing of nose or nasopharynx for epistaxis.
7. Cleft palate

Route of infec.
1. Via ET → most common. Infec. travels via the lumen of the tube or along peritubal
lymphatics.
 ET in infants and young children is shorter, wider and more horizontal → may account for
higher incidence of infec. in this age group.
 Breast or bottle feeding in a young infant in horizontal position may force fluids through
the tube into the middle ear → need to keep the infant propped up with head a little higher.
 Swimming and diving can also force water through the tube into the middle ear.
2. Via external ear → traumatic perforation of TM due to any cause open a route to mid ear infec
3. Hematogenous spread → uncommon route

Clinical presentation → 5 stages

1) Stage of tubal occlusion
 edema and hyperemia of nasopharyngeal end of ET → tube blocks → absorp. of air and
(-) intratympanic pressure → retraction of TM with some degree of effusion in the middle
ear but fluid may not be clinically visible
 Symptoms: deafness and earache (not marked). no fever
 Signs: TM is retracted, loss of light reflex.
 Tuning fork tests show conductive deafness
 2) Stage of pre-suppuration
 If tubal occlusion is prolonged → pyogenic MO invade tympanic cavity → hyperaemia of
its lining, infla. exudate appears in the middle ear. TM becomes congested
 Symptoms: marked ear pain which may disturb sleep and is of throbbing nature.
Deafness and tinnitus (complained by adults). Usually, child has high fever and is restless
 Signs: congestion of pars tensa. Later, whole of TM becomes uniformly red
 Tuning fork tests will again show conductive type of hearing loss

3) Stage of suppuration
 marked by formation of pus in the middle ear and to some extent in mastoid air cells.
 TM starts bulging to the point of rupture
 excruciating ear pain. Deafness ↑, higher fever. +/- vomiting & convulsions
 TM appears red and bulging with loss of landmarks.
 Yellow spot may be seen on the TM where rupture is imminent.
 X-rays of mastoid will show clouding of air cells because of exudates

4) Stage of resolution
 TM ruptures with release of pus and subsidence of symptoms.
 Infla. process begins to resolve.
 If proper tr. is started early or if infec. was mild, resolution may start even w/o TM
rupture
 With evacuation of pus, earache is relieved, fever comes down and child feels better
 EAM may contain bloody discharge which later becomes mucopurulent.
 Usually, a small perforation is seen in antero-inferior quadrant of pars tensa.
 Hyperaemia of TM begins to subside with return to normal colour and landmarks

5) Stage of complication
 If virulence of MO is high or resistance of pt. is poor → resolution may not take place and
disease spreads beyond the confines of middle ear.
 It may lead to acute mastoiditis, subperiosteal abscess, facial paralysis, labyrinthitis,
petrositis, extradural abscess, meningitis, brain abscess or lateral sinus thrombophlebitis

Diagnosis
Otoscopy exam. shows hyperaemic TM, maleus can’t be seen because of the thickness of the mem.
Also there are fistula, discharges, and scar formation.

Treatment
 Antibiotics → indicated in all cases with fever and severe earache. As the most common
organisms are Strept. pneumoniae and H. influenzae, the drugs which are effective in acute
otitis media are ampicillin or amoxicillin and in case of allergy- erythromycin
 Decongestant nasal drops (Ephedrine)
 Analgestic, antipyretic
 Myringotomy → incising the drum to evacuate pus and is indicated when
1. drum is bulging and there is acute pain
2. there is an incomplete resolution despite antibiotics when drum remains full with
persistent conductive deafness
3. there is persistent effusion > 12 weeks
Topic 9. Chronic mesotympanal otitis media

Chronic mesotympanal (mucosal) otitis media is a chr. mucosal infla.of the middle ear.
It is one of the most common infectious diseases in children worldwide.
Usually it is due to recurrent infections in childhood, Re-infections from the nasopharynx, ear drum
perforation, and ET disorders.

Pathogenesis
The disease is basically the end result of several diff. 10 disease processes.
The infla. remains confined to the mucosa but in some cases may lead to osteitis → chr. infla.
destruction of the ossicles.
Unlike cholesteatoma, the destructive bone process is unusual and less likely to extend and progress.
Vascular obliteration can occur due to heavy scar tissue deposits, leading to aseptic bone necrosis

Predisposing factors
 ↓ mucosal imm. Competence
 Causative agent virulence
 Anatomic conditions in mid. ear
 Impaired ET function (cleft lip)
 Generalized disease (allergy, immunedef...)

Clinical features
The infec. is associated with symptoms free periods alternating with acute exacerbations
 There is a chr. discharge of mucoid purulent odourless exudates
 The exudates may be creamy and purulent during acute phase and become mucoid as infec.
resolves
 The pt. has conductive hearing loos.
 No pain, general condition is good

Complications
 Exacerbations can occur due to exogenous infec. (bathwater)
 Progression to cholesteatoma & Progressive hearing loss

Diagnosis
History shows chr. recurrent aural discharge with reduced hearing
 Otoscopic exam. shows central defect of TM, scarring of pars tensa +/- aural polyps
 CT may reveal opacity of the cell sys. +/- signs of bone destruction
 Audiogram → conductive hearing loss

Differential diagnosis
1. Cholesteatoma
2. Aural tuberculosis
3. Mid. ear carcinoma

Treatment
Antibiotic eardrops should be the first step in treating COM, and surgery the last when optimal medical
treatment has failed.
 Conservative methods for drying the ear → periodic cleaning..
 In acute phase → sys. & local antibiotics
 Aural polyps should be surgically removed
 Mastoidectomy → to eliminate infec. foci
 Tympanoplasty → reconstructing the conductive sound apparatus
Topic 10. Chronic cholestematous otitis media

Cholesteatoma is a "skin in the wrong place".

The term is a misnomer, because it neither contains cholesterol crystals nor is it a tumour to merit
the suffix "oma", however, the term has been retained because of its wider usage
Normally, middle ear cleft is lined by diff. types of epi. in diff. regions:
 Ciliated columnar → in anterior and inferior part
 Cuboidal → in middle part
 Pavement-like → in attic.
Keratinising squamous epi. is NOT a part of the normal lining → the presence of this epi. type in
the middle ear or mastoid, constitutes a cholesteatoma.
Cholesteatoma consists of 2 parts
1) Matrix → made up of keratinising squamous epi. on a thin stroma of fibrous tissues
2) Central white mass → consisting of keratin debris produced by the matrix.
Pathogenesis
The exact genesis of cholesteatoma is unclear, however some theories exist:
1. Presence of congenital cell rests.
2. Invagination of TM (most popular) → from the attic or postero-superior part of pars tensa in
the form of retraction pockets → outer surface of TM is lined by stratified squamous epi.
which after invagination forms matrix and lays down keratin in the pocket.
3. Basal cell hyperplasia → basal cells of germinal layer of skin prolif. due to infec
4. Epithelial invasion → from the meatus or outer drum surface
5. Metaplasia → cubic cell of mucosa undergoe metaplasia to squmous due to repeated infec.
Classification
1) Congenital
2) Acquired, primary
3) Acquired, secondary
Congenital cholesteatoma
It arises from the embryonic epidermal cell rests in the middle ear cleft or temporal bone.
Occurs at 3 important sites: middle ear, petrous apex and cerebellopontine angle → symptoms
depends on the location

In the middle ear → white mass behind an intact TM and conductive hearing loss.
 May be discovered on routine examination of children or at the time of myringotomy
 May spontaneously rupture the TM and present with a discharging ear indistinguishable from a
case of chronic suppurative otitis media (CSOM).

Primary acquired cholesteatoma

Called primary as there is no history of previous otitis media or a pre-existing perforation.

Secondary acquired cholesteatoma

these cases, there is already a pre-existing perforation in pars tensa.
Often associated with posterosuperior marginal perforation or sometimes large central perforation.

Clinical manifestation
 Conductive deafness
 Malodorous otorrhoea
 Perforation (pars flaccida/pars tensa)
 Headache, earache
 Vertigo
 facial paralysis
Expansion of Cholesteatoma and Destruction of Bone
Once cholesteatoma enters the middle ear cleft, it invades the surrounding structures, first by
following the path of least resistance, and then by enzymatic bone destruction.

An attic cholesteatoma may extend

 backwards into the aditus, antrum and mastoid
 downwards into the mesotympanum
 medially, it may surround the incus and/or head of malleus

Cholesteatoma may cause destruction of ear ossicles, erosion of bony labyrinth, canal of facial n.,
sinus plate or tegmen tympani and thus cause several complications.
Bone destruction has been attributed to various enzymes (for ex. collagenase) liberated by
osteoclasts and mononuclear infla. cells, seen in association with cholesteatoma.

Treatment (surgery)
 Radical mastectomy (conservative / canal wall up technique)
 2nd step surgery → tympanoplasy (if there are no symptoms for one year)
Topic 11. Intracranial complications of the acute and chronic otitis media

Factors influencing development of complications

1) Age → most complications occur in the 1st decade of life or in elderly
2) Poor socio-economic → limited access to health care
3) Presence of MDR organisms → ineffective treatment
4) Immunocompromised host → AIDS, DM, Tx, immunosuppressive drugs
5) Preformed pathways → Infec. can easily travel beyond the middle ear cleft if preformed
pathways exist, (previous ear surgery, fracture of temporal bone, perilymph fistula...)
6) Cholesteatoma → osteitis or granulation tissue destroy the bone & help infec. to penetrate
deeper.

Classification of complications

Intratemporal Intracranial
1. Mastoiditis 1. Extradural abscess
2. Petrositis 2. Subdural abscess
3. Facial paralysis 3. Meningitis
4. Labyrinthitis 4. Brain abscess (otogenic)
5. Lateral sinus thrombophlebitis
6. Otitic hydrocephalus

Intracranial complications

Extradural Abscess
Collection of pus b/w the bone and dura, may occur in both acute and chr. infec.:
 In acute OM → bone over the dura is destroyed by hyperaemic decalcification
 In chr. OM → bone is destroyed by cholesteatoma and pus comes directly in contact with dura.
Spread of infec. can also occur by venous thrombophlebitis → bone over the dura remains intact.

An extradural abscess may lie in relation to dura of middle or post. cranial fossa or outside the dura
of lateral venous sinus (perisinus abscess).
The affected dura may be covered with granulations or appear discoloured

Clinical Features
Most of the time, extradural or perisinus abscesses are asymptomatic and silent, and are discovered
accidently during cortical or modified radical mastoidectomy
 Persistent headache on the side of otitis media.
 Severe ear pain.
 General malaise with low-grade fever.
 Pulsatile purulent ear discharge.
 Disappearance of headache with free flow of pus from the ear (spontaneous abscess drainage)

Treatment
 Cortical/modified radical/radical mastoidectomy → often required to deal with causative
process.
 Extradural abscess → evacuated by removing overlying bone till the limits of healthy dura.
 Antibiotic → should be provided for a min. of 5 days
Subdural Abscess
Collection of pus between dura and arachnoid.
 Infec. spreads from the ear by erosion of bone and dura or by thrombophlebitic process
 Pus rapidly spreads in subdural space and comes to lie against the convex surface of cerebral
hemisphere causing pressure symptoms.
 With time, the pus may get loculated at various places in subdural space

Clinical Features
S&S of subdural abscess are due to:
1. meningeal irritation → headache, fever, malaise, drowsiness, neck rigidity, (+) Kernig's sign
2. thrombophlebitis of cortical veins of cerebrum → aphasia, hemiplegia, hemianopia
3. ↑ ICP → papilloedema, ptosis and dilated pupil

Diagnosis
 Lumbar puncture should NOT be done as it can cause herniation of the cerebellar tonsils.
 CT scan or MRI are required for diagnosis

Treatment
 Series of burr holes or a craniotomy is done to drain subdural empyema.
 IV antibiotics
 Mastoidectomy

Meningitis
Infla. of leptomeninges (pia and arachnoid) usually with bact. invasion of CSF in subarachnoid
space.
 Most common intracranial complication of otitis media.
 Can occur in both acute and chronic otitis media.
 In infants and children, otogenic meningitis usually follows acute otitis media while in adults it
is due to chr. middle ear infection

Clinical presentation
S&S severity will vary with the extent of disease
 Fever, headache, neck rigidity, photophobia, mental irritability, N&V, drowsiness, delirium,
coma
 (+) Kernig's & Brudzinski's signs
 Papilloedema

Diagnosis
 Contrast CT or MRI → may also reveal another associated intracranial lesion
 Lumbar puncture → CSF is turbid, ↑ cell count (predominance of NG-s), ↓ glucose, ↑ protein
 CSF culture

Treatment
 Antimicrobial therapy against aerobic and anaerobic organisms
 Corticosteroids
 Surgical → myringotomy or cortical mastoidectomy.
Otogenic Brain Abscess
50% of brain abscesses in adults and 25% in children are otogenic in origin.
 In adults → abscess usually follows chr. suppurative OM with cholesteatoma
 In children → usually the result of acute otitis media.
 Cerebral abscess is seen 2X more than cerebellar abscess

Pathogenesis
Cerebral abscess develops as a result of direct extension of mid. ear infec. through the tegmen or by
retrograde thrombophlebitis (in which case the tegmen is intact).
Often it is associated with extradural abscess

Cerebellar abscess also develops as a direct extension through the Trautmann's triangle or by
retrograde thrombophlebitis.
Often associated with extradural abscess, perisinus abscess, sigmoid sinus thrombophlebitis or
labyrinthitis

Causative agents
 Aerobic → S. pyogen, S. pneumoniae, S. haemolyticus, Proteus mirabilis, E. Coli, P.
aeruginosa.
 Anaerobic → Peptostreptococcus and Bacteroides fragilis.

Brain abscess develops through 4 stages:

Stage of invasion Often asymptomatic

(initial encephalitis) headache, low-grade fever, malaise and drowsiness
Stage of localisation no symptoms during this stage
(latent abscess) may last for several weeks
Stage of enlargement Abscess begins to enlarge
(manifest abscess)  Raised intracranial tension.
 Disturbance of function in the cerebrum or
cerebellum
Stage of termination fatal meningitis
(rupture of abscess)

Clinical features can be divided into:

1. ↑ ICP → Headache, N&V (projectile), ↓ LOC, confusion, stupor, papilloedema
2. Area of brain affected→ localising features

Localising features
Temporal lobe abscess
 Nominal aphasia→ if abscess involves dominant hemisphere
 Homonymous hemianopia → due to pressure on the optic radiations. Visual field, opposite to
the side of lesion, is lost.
 Contralateral motor paralysis
- upward spread of abscess→ face is involved first followed by the arm and leg.
- Inward spread (towards int. capsule) → first involves legs followed by arm and face.
 Epileptic fits → involvement of uncinate gyrus causes hallucinations of taste, and small and
involuntary smacking movements of lips and tongue.
 Pupillary changes and oculomotor palsy → indicates transtentorial herniation.
Cerebellar abscess
 Headache → involves suboccipital region and may be associated with neck rigidity.
 Spontaneous nystagmus → common, generally to the side of lesion.
 Ipsilateral hypotonia and weakness.
 Ipsilateral ataxia
 Intention tremor
 Dysdiadokokinesia

Diagnosis
X-rays → reveals midline shift, pineal gland calcification, gas in the abscess cavity
CT → the single most important tool and helps to find the site and size of an abscess & associated
complications

Treatment
 High doses of antibiotics (Chloramphenicol and 3rd gen. Cephalosporins)
 Discharge from the ear should be treated by suction clearance and use of topical ear drops
 Neurosurgical abscess drainage

Lateral Sinus Thrombophlebitis (Syn. Sigmoid Sinus Thrombosis)

Infla. of inner wall of lateral venous sinus with formation of a thrombus, occurs as a complication of
acute coalescent mastoiditis, masked mastoiditis or chronic suppuration of middle ear and
cholesteatoma
 S&S: fever, headache, anemia, papilloedema, Tenderness along jugular vein..
 Diagnosis: blood smear & culture, CSF, imaging studies
 Complications: septicaemia, meningitis, cerebellar abscesses, jagular thrombosis
 Treatment: antibiotic and mastoidectomy, anticoagulants, jagular ligation

Otitic Hydrocephalus
Characterised by ↑ ICP with normal CSF findings.
Seen in children and adolescents with acute or chr. middle ear infections
Lateral sinus thrombosis accompanying mid. ear infec. causes obstruction to venous return.
If thrombosis extends to superior sagittal sinus→ impede the function of arachnoid villi to absorb
CSF.

Clinical Features
Symptoms → headache, diplopia (CN VI paralysis), blurring vision (papilloedema or optic atrophy)
Signs → Papilloedema, Nystagmus

Diagnosis
CSF pressure > 300 mm H2O (normal: 70-120 mm H2O).
It is otherwise normal in cell, protein and sugar content and is bacteriologically sterile

Treatment
Aim is to reduce CSF pressure to prevent optic atrophy and blindness.
 Acetazolamide and corticosteroids
 Repeated lumbar puncture or placement of a lumbar drain or lumboperitoneal shunt
 Mid. ear infec. may require antibiotics and mastoid exploration to deal with sinus thrombosis
Topic 12. Intratemporal complications of the acute and chronic otitis media

1) Mastoiditis → see topic 25

2) Petrositis
3) Facial paralysis
4) Labyrinthitis

Petrositis
Spread of infec. from middle ear and mastoid to the petrous part of temporal bone is called petrositis.
It may be associated with acute coalescent mastoiditis, latent mastoiditis or chr. mid. ear infec.
Like mastoid, the petrous bone may be of 3 types:
1. pneumatised with air cells extending to the petrous apex
2. diploic containing only marrow space
3. sclerotic.
Pneumatisation of petrous apex occurs in only 30% of cases with cells extending from the mid. ear or
mastoid to the petrous apex. Usually 2 cell tracts are recognized:
1) Posterosuperior tract → which starts in the mastoid and runs behind or above the bony
labyrinth to the petrous apex.
2) Anteroinferior tract → which starts at the hypotympanum near the ET runs around the cochlea
to reach the petrous apex
Infective process runs along these cell tracts and reaches the petrous apex.
Pathological process is similar to that of coalescent mastoiditis forming epidural abscess at the
petrous apex involving CN VI and trigeminal ggl.
Clinical presentation
Gradenigo's sy. is the classical presentation, and consists of a triad of:
1) External rectus palsy (CN VI palsy)
2) Deep-seated ear or retro-orbital pain (CN V involvement) It is uncommon to see the
3) Persistent ear discharge full triad these days!!!

Fever, headache, vomiting and sometimes neck rigidity may also be associated.
In some pts. → facial paralysis and recurrent vertigo (involvement of facial and statoacoustic nn.)

Diagnosis
Requires both CT and MRI.
 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 fluid or pus

Treatment
 Cortical, modified radical or radical mastoidectomy
 The fistulous tract should recognized than curetted and enlarged to provide free drainage.
 IV antibiotcs should precede and follow surgical intervention.

Facial Paralysis
Can occur as a complication of both acute and chr. otitis media.

Acute Otitis Media

Facial nerve is normally well protected in its bony canal. Sometimes, the bony canal is dehiscent, and
the n. lies just under the middle ear mucosa.
It is in these cases that infla. of middle ear spreads to epi- and perineurium, causing facial paralysis.
 Facial n. function fully recovers if AOM is controlled with sys. antibiotics.
 Myringotomy or cortical mastoidectomy may be required
Chronic Otitis Media
Facial paralysis in chronic otitis media either results from cholesteatoma or from penetrating
granulation tissue.
 Facial paralysis is insidious but slowly progressive.
 Treatment is urgent exploration of the middle ear and mastoid.
 If a segment of the nerve has been destroyed by granulation tissue, resection and grafting

Labyrinthitis → 3 types:
1) Circumscribed
2) Diffuse serous
3) Diffuse suppurative

Circumscribed Labyrinthitis (Fistula of Labyrinth)

Thinning or erosion of bony capsule of labyrinth, usually of horizontal semicircular canal.
Can occur due to:
 Chr. suppurative OM with cholesteatoma (most common cause)
 Neoplasms of mid. ear → carcinoma or glomus tumour.
 Surgical or accidental trauma to labyrinth

Clinical presentation
 Part of mem. labyrinth is exposed and becomes sensitive to pressure changes.
 Transient vertigo induced by pressure on tragus, cleaning the ear or during Valsalva maneuver

Diagnosis
It is diagnosed by "fistula test" which can be performed in two ways
1. Pressure on tragus → ↑ air pressure in ear canal and stimulates the labyrinth → vertigo.
2. Siegle's speculum → When (+) pressure is applied to ear canal, patient complains of vertigo
usually with nystagmus. The quick component of nystagmus would be towards the affected ear.

Treatment
 In chr. suppurative OM or cholesteatoma, mastoid exploration is often required
 Sys. AB → before and after operation to prevent spread of infection into the labyrinth

Diffuse Serous Labyrinthitis

Diffuse intra-labyrinthine infla. W/O pus formation. Reversible if condition treated early
Can occur due to:
 pre-existing circumscribed labyrinthitis associated with chr. mid. ear infec. or cholesteatoma
 In acute infec. of mid. ear → cleft infla. spreads through annular ligament or the round window.
 Follows stapedectomy or fenestration operation.

Clinical presentation
 Mild → vertigo and nausea
 Severe → worse vertigo, N&V, spontaneous nystagmus (quick component towards affected ear).
 As the infla. is diffuse → cochlea is also affected with some degree of sensorineural hearing loss

Treatment
 Antibacterial therapy.
 Labyrinthine sedatives → prochlorperazine or dimenhydrinate (sympt. relief of vertigo).
 Myringotomy → if labyrinthitis has followed AOM and the drum is bulging.
 Cortical mastoidectomy (in acute mastoiditis) or modified radical mastoidectomy (in chr. infec.
or cholesteatoma)
Diffuse Suppurative Labyrinthitis
Diffuse pyogenic infec. of the labyrinth with permanent loss of vestibular and cochlear functions
 Usually follows serous labyrinthitis, pyogenic MO entering via a pathological or surgical fistula
 Severe vertigo with N&V due to acute vestibular failure
 Spontaneous nystagmus will be observed with its quick component towards the healthy side.
 Total loss of hearing.
 Treatment → is same as for serous labyrinthitis. Rarely, drainage of the labyrinth is required
Topic 13. Indications for antrotomy, mastoidectomy and radical mastoidectomy. What does it
mean?

Antrotomy
The mastoid antrum is a cavity b/w the middle ear and temporal bone in the skull
An antrotomy is a transcortical exposure of antrum through the tunnel by drilling the cortical bone at
the Macewen triangle

Macewen triangle
A triangle used as a guide in mastoid operations, formed by:
 Root of the zygomatic arch,
 Posterior wall of the bony EAM,
 Line connecting the extremities of the first 2.

It is carried out in infants and young children whose mastoid process is incompleteley pneumatised
(basically its the mastoidectomy in kids)
The infected part of the mastiod process is cleared via incision through the wall of the mastoid antrum.
 The antrum and aditus are widely opened from the mastoid cortex to improve aeration while
leaving the post. wall to the ear canal intact.
 Only in a portion of the air cell sys. is exenterated

Indication
1. Mastoid evaluation in setting of tympanoplasty for chr. mesotympanic OM with significant
drainage
2. Persistent otitis media with effusion
3. Depending on findings → extending the procedure to cortical mastoidectomy

Mastoidectomy
A mastoidectomy is a surgical procedure that removes an infected mastoid air cells resulting from ear
infec, such as mastoiditis or chr. otitis, or by infla. disease of the mid. ear (cholesteatoma) when
medical treatment is not effective.
 The primary goal of the surgery is to completely remove infec. foci and eliminate the ear infec.
 Mastoidectomies are also performed sometimes to repair paralyzed facial nerves.

Types of mastoidectomy

Cortical Mastoidectomy (Simple Mastoidectomy or Schwartz Operation)

Exenteration of all accessible mastoid air cells preserving the post. meatal wall
The aim of this procedure is to remove mastoid air cells and define the limits of pneumatisation.
Indications
1. Acute coalescent mastoiditis.
2. Incompletely resolved AOM with reservoir sign.
3. Masked mastoiditis.
4. As an initial step to perform:
 endolymphatic sac surgery
 decompression of facial nerve
 translabyrinthine or retro-labyrinthine procedures for acoustic neuroma.
Modified Radical Mastoidectomy
Is an operation to eradicate disease of the attic and mastoid, both are exteriorised into the EAM, by
removal of the post. meatal and lateral attic walls.
Irreversibly damaged tissues are removed, preserving the rest (TM remnant, functioning ossicles and
the reversible mucosa and function of the ET) to conserve or reconstruct hearing mechanism

Indications
1. Cholesteatoma confined to the attic and antrum.
2. Localised chronic otitis media

Radical Mastoidectomy
Is an operation to eradicate disease of the middle ear and mastoid in which mastoid, middle ear, attic
and the antrum are exteriorised into the external ear by removal of posterior meatal wall.
 All remnants of TM, malleus, incus (NOT stapes) chorda tympani and the mucoperiosteal lining
are removed
 The opening of ET closed by packing a piece of muscle or cartilage into the ET

Indications
1. When all cholesteatoma cannot be safely removed → invading ET, round window niche,
perilabyrinthine or hypotympanic cells.
2. If previous attempts to eradicate chr. infla. disease or cholesteatoma have failed.
3. As an approach to petrous apex.
4. Removal of glomus tumour.
5. Carcinoma middle ear → radical mastoidectomy followed by radioth. is an alternative to en bloc
removal of temporal bone.
Topic 14. Surgical reconstruction of the hearing mechanism

Myringoplasty
It is repair of TM.
Graft materials of choice are temporalis fascia or the perichondrium taken from the patient.
Sometimes, homografts such as dura, vein, fascia or cadaver TM are also used.
Repair can be done by 2 techniques: the underlay or the overlay.
1) Underlay technique → margins of perforation are freshened and the graft placed medial to
perforation or tympanic annulus, if large, and is supported by gel-foam in the middle ear
2) Overlay technique → the graft is placed lateral to fibrous layer of the TM after carefully
removing all squamous epi. from the lateral surface of TM remnant

It has the advantage of:

1. Restoring the hearing loss.
2. Checking re-infec. from EAM and ET
3. Checking aeroallergens reaching exposed middle ear mucosa, leading to persistent ear discharge

Contraindications
 Active discharge from the middle ear.
 Nasal allergy. It should be brought under control before surgery.
 Otitis externa.
 Ingrowth of squamous epithelium into the middle ear. In such cases, excision of squamous
epithelium from the middle ear or a tympanomastoidectomy may be required.
 When the other ear is dead or not suitable for hearing aid rehabilitation.
 Children < 3 years.

Tympanoplasty
It is an operation to eradicate disease in the middle ear and reconstruct hearing mechanism.
It may be combined with mastoidectomy if disease process so demands.
Type of middle ear reconstruction depends on the damage present in the ear.
The procedure may be limited only to repair of TM (myringoplasty), or to reconstruction of ossicular
chain (ossiculoplasty), or both (tympanoplasty).

Wullstein classified tympanoplasty into 5 types:

Type I → perforation of TM is repaired with a graft (myringoplasty).
Type II → perforation of TM with erosion of malleus. Graft is placed on incus or remnant of malleus.
Type III → Malleus and incus are absent. Graft is placed directly 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 ext. ear, and graft is placed b/w the oval and round windows.
 A narrow middle ear (cavum minor) is created, to have an air pocket around round window.
 A mucosa-lined space extends from the eustachian tube to the round window.
 Sound waves act directly on the footplate while the round window has been shielded.
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
It is required when there is destruction or fixation of ossicular chain.
Most common defect is necrosis of the long process of incus, the malleus and the stapes being normal.
Topic 15. Otosclerosis and its surgical treatment

Otosclerosis is a localized, progressive primary disease of the bony labyrinthine capsule.

 One or more foci of irregularly laid spongy bone replace part of normally dense enchondral
layer of bony otic capsule.
 Most often, otosclerotic focus involves the stapes region leading to stapes fixation and
conductive deafness. However, it may involve certain other areas of the bony labyrinth where it
may cause neurosensory loss, or no symptoms at all

Etiology
The exact cause is not known.
 Heredity→ AD inheritance (~50% of otosclerotics have (+) family history)
 Disorders of hormone and bone metabolism:
- Otosclerosis begins during pregnancy.
- Abnor. formation of lysosoms
- ↑ activity of histiocytes and osteocytes
- enzymatic collagenolysis

Types
1) Stapedial otosclerosis (most common)
2) Cochlear otosclerosis
3) Histologic otosclerosis

Stapedial otosclerosis
Result in stapes fixation and conductive deafness
Lesion may starts:
 In front of the oval window in area called "fissula ante fenestram" (ant. focus)
 Behind the oval window (post. focus)
 Margin of the stapes footplate (circumferential)
 In the footplate but annular ligament being free (biscuit type)
 May completely obliterate the oval window niche (obliterative type)

Cochlear otosclerosis → involves region of round window or other areas in the otic capsule; may
cause sensorineural hearing loss probably due to liberation of toxic materials into the inner ear fluid

Histologic otosclerosis → This type of otosclerosis remains asymptomatic and causes neither
conductive nor sensorineural hearing loss

Clinical presentation
Age of onset → deafness usually starts b/w 20-30 ys of age and rarely <10 and >40 years
Grossly, otosclerotic lesion appears chalky white, greyish or yellow. Sometimes, it is red in colour
due to ↑ vascularity, in which case, the otosclerotic focus is active and rapidly progressive

 Hearing loss → bilateral, painless, progressive with insidious onset.

- Conductive deafness in 80% of the patients.
- Mixed conductive and sensorineural deafness in 15% of the patients.
- Pure sensorineural deafness in 5% of the patients.
 Parac usis willisii → pts. hear better in noisy surroundings (normal person will raise his voice)
 Tinnitus → constant and progressive more common in cochlear otosclerosis
 Vertigo → uncommon symptom
The disease may be associated with osteogenesis imperfecta with history of multiple fractures.

Van der Hoeve sy. → triad of:

1. osteogenesis imperfect
2. otosclerosis
3. blue sclera

Lesions of otic capsule seen in osteogenesis imperfecta are histologically indistinguishable from
those of otosclerosis and both are due to genes encoding type I collagen

Diagnosis
 Family history, case history.
 Otoscopy → TM is quite normal and mobile +/- reddish hue (Schwartze sign) → indicative of
active focus
 ET function is normal.
 Tuning fork tests → show (-) Rinne (BC > AC)
 Pure tone audiometry
 Impedance audiometry → tympanogram with low peak,
Stapedial reflex is absent

Differential diagnosis
1. Tympanosclerosis
2. Posttraumatic dislocation or fracture of ossicles
3. Congenital anomalies of the middle ear
4. Osteogenesis imperfecta (blue eyes)

Treatment
1. Hearing aid
2. Stapedectomy → the fixed stapes is removed. The oval window is then closed by CT and the
stapes is replaced by a wire prosthesis
3. Stapedotomy → the head, neck and crura of the stapes are removed. An opening is made in the
central part of the footplate (small fenestra) – piston type prosthesis.
The wire is stainless steel or platinum.

Complications of stapedotomy
 Giddiness in few days
 Sensorineural hearing loss, total deafness 1–2%
 Perilymph fistula (a sudden fall in hearing – urgent revision)
Topic 16. Tumors in the external ear and middle ear

Of all the cases of ear carcinoma, 85% occur on pinna, 10% in the EAM and 5% in mid ear

Tumors of the external ear

Pinna External ear canal

Benign Benign
 Preauricular cyst or sinus  Osteoma
 Sebaceous cyst  Exostosis
 Dermoid cyst  Ceruminoma
 Keloid  Sebaceous adenoma
 Haemangioma  Papilloma
 Papilloma
 Cutaneous horn Malignant
 Keratoacanthoma  Squamous cell carcinoma
 Neurofibroma  Basal cell carcinoma
 Adenocarcinoma
Malignant  Malignant ceruminoma
 Squamous cell carcinoma  Melanoma
 Basal cell carcinoma
 Melanoma

Benign Tumors of pinna

Preauricular sinus or cyst
Results from faulty union of hillocks of the 1st and 2nd branchial arches during pinna development
Preauricular sinus presents as a small opening in front of the crus of helix. It has a branching tract
lined by squamous epi. which when blocked results in a retention cyst.
 Patient usually presents with a infected cyst.
 Surgery is indicated if there is unsightly swelling or infection.
 Cyst or sinus tract must be excised completely to avoid recurrence

Sebaceous cyst → Common site is postauricular sulcus or below and behind ear lobule.
Treatment is total surgical excision

Dermoid cyst → usually presents as rounded mass over the upper part of mastoid behind the pinna

Keloid → often follows trauma such as piercing the ear lobule for ornaments or a surgical incision

Haemangioma → congenital tumours often seen in childhood.

 Other parts of face and neck may also be involved
 Capillary (spider nevus)
 Cavernous (strawberry tumor)
 both are treated with cryosurgery

Papilloma (warts) → present as a tufted growth or flat grey plaque and is rough to feel. It is viral in
origin. Treatment is surgical excision or curettage with cauterisation of its base

Cutaneous horn → form of papilloma with heaping up of keratin and presents as horn-shaped
tumour. It is often seen at the rim of helix in elderly people. Treatment is surgical excision

Keratoacanthoma → benign tumour clinically resembling a malignant one. It presents as a raised

nodule with a central crater. Initially, it grows rapidly but slowly regresses leaving a scar. Treatment
is excision biopsy
Neurofibroma → presents as a non-tender, firm swelling and may be associated with von
Recklinghausen's disease. Treatment is surgical excision, if tumour occludes ear canal or presents a
cosmetic problem

Malignant tumors of pinna

Squamous cell carcinoma

The site of predilection is the helix.
 Exophytic, slowly growing, firm tumor
 May present as a painless nodule or an ulcer with raised edges and indurated base.
 Metastases to regional L.N occur very late.
 More common in males in their 50s who had prolonged exposure to direct sunlight.

Treatment
 Small lesions with no nodal metastases are excised locally with 1 cm of healthy area around it.
 Larger lesions of the pinna or those coming within 1 cm of EAM and lesions with nodal
metastases, may require total amputation of the pinna, often with en bloc removal of parotid
gland and cervical L.N

Basal cell carcinoma

 The common sites are the helix and the tragus.
 It is more common in men > 50 years of age.
 Non exophytic, ingrowing, smooth tumor.
 It presents as a nodule with central crust, removal of which results in bleeding.
 Ulcer has a raised or beaded edge.
 Lesion often extends circumferentially into the skin but may penetrate deeper → cartilage or
bone invasion.
 L.N metastases are rare

Treatment
 Supf. lesions, not involving cartilage, can be irradiated and cosmetic deformity avoided.
 Lesions involving cartilage may require surgical excision as in cases of squamous cell
carcinoma

Melanoma
 May occur anywhere over the auricle.
 It is more common in men
 Metastases are seen in 16-50% of the cases

Benign Tumors of EAM

Osteoma → arises from cancellous bone and presents as a single, smooth, bony, hard, pedunculated
tumour, often arising from the posterior wall of the osseous meatus, near its outer end.
Treatment is surgical removal by fracturing through its pedicle or removal with a drill

Exostosis
Multiple and bilat. often presenting as smooth, sessile, bony swellings in the deeper part of the
meatus near the TM (ant. and post. walls of the bony meatus)
 Often due to chr. irritation from infection, ekzema, trauma, cold water (swimmers)
 seen in persons exposed to entry of cold water in the meatus as in divers and swimmers.
 Males are affected more than females
 Asymptomatic
 Treatment: surgical excision when it is too large
Osteoma
 Localisation: post. wall of the bony meatus - mastoid.
 Treatment: surgical excision

Ceruminoma → tumor of modified sweat glands which secrete cerumen.

It presents as a smooth, firm, skin-covered polypoid swelling in outer part of the meatus, generally
attached to the posterior or inferior wall.
It obstructs the meatus leading to retention of wax and debris.

Sebaceous adenoma → arises from sebaceous glands of the meatus and presents as a smooth, skin-
covered swelling in the outer meatus. Treatment is surgical excision

Papilloma → Similar to the one seen on the pinna

Malignant tumors of EAM

Squamous cell carcinoma
 Most often seen in cases of long-standing ear discharge.
 May arise 10 from the meatus or be a 20 extension from the middle ear carcinoma
 Symptoms: blood staining of hitherto mucopurulent or purulent discharge and severe earache
 Examination may show an ulcerated area in the meatus or a bleeding polypoid mass or
granulations.
 Facial nerve may be paralysed because of local extension of disease through post. meatal wall
or its spread into the middle ear.
 Regional L.N (preauricular, postauricular, infra-auricular and upper deep cervical) may be
involved

Basal cell carcinoma → rarely arise from the meatus.

 Clinical picture is similar to that of squamous cell variety.
 Dg. is made only on biopsy.
 Treatment is wide surgical excision, Total petrosectomy, post-operative radiation

Tumors of the middle ear

Tumours of middle ear and mastoid can be divided into:
1) Primary Tumours
 Benign: Glomus tumour
 Malignant: Carcinoma, sarcoma
2) Secondary Tumours
 From adjacent areas → from nasopharynx, ext. meatus and parotid.
 Metastatic → from carcinoma of bronchus, breast, kidney, thyroid, prostate and GI

Glomus tumour
It is the most common benign neoplasm of middle ear and is so-named because of its origin from
the glomus bodies.
The glomus bodies resemble carotid body in structure and are found in the dome of jugular bulb or
on the promontory along the course of tympanic branch of CN IX (Jacobson's nerve).

The tumour consists of paraganglionic cells derived from the neural crest
benign, non-encapsulated but extremely vascular neoplasm, locally invasive
Often seen in the middle age (40-50 years), female predominance
Its rate of growth is very slow and several years may pass before there is any change from the initial
symptoms.
2 types:
1) Glomus jugulare → arise from the dome of jugular bulb, invade the hypotympanum and
jugular foramen, causing neurological signs of CN IX to XII involvement.
They may compress jugular vein or invade its lumen
2) Glomus tympanicum → arise from the promontory of the middle ear and cause aural
symptoms, sometimes with facial paralysis

Treatment involves:
 Surgical removal.
 Radiation.
 Embolisation.
 Combination of the above techniques
Topic 17. Toxic damages and circulatory disturbances in the inner ear (?)

Toxic Damage
Various drugs & chemicals can damage inner ear and cause sensorineural hearing loss and tinnitus
 Drugs → aminoglycosides, quinine, salicylates, diuretics, tobacco, alcohol
 Chemicals → arsenic, mercury, lead, sulfur, CO, benzol
 Endogenous → bacterial toxins, metabolites from DM & renal disease

Symptoms
 Tinnitus
 sensorineural bilateral hearing loss
 Positional vertigo with nausea, unsteady gait, and oscillopsia (visual sensation that stationary
objects are swaying back and forth)

Circulatory disturbances

Acute Vestibular paralysis

unknown cause, maybe due to disturbance in micro-circulation, making the blood sludgy.
 Symptoms: rotatory dizziness, vomiting, ataxia, spontaneous nystagmus
 hearing is normal!
 Treatment: anti-vertigo drugs, sedatives, IV rheomacrodex, corticosteroids, Antibiotics.

Sudden deafness
Unknown cause (same as above).
 Symptoms: unilateral feeling of pressure in ear, tinnitus→ severe hearing loss → deafness
 No dizziness or balance problems
 Treatment: IV LMW-dextran, corticosteroids, antibiotics.
 Recovery occurs within days if treated properly.
Topic 18. Acoustic injury

1) Conductive
2) Sensorineural
3) Mixed → elements of both conductive and sensorineural are present in the same ear
Conductive hearing loss
Any disease process which interferes with the conduction of sound to reach cochlea, from the
external ear to the stapediovestibular joint → thus the cause may lie in either
1. External ear (obstructions)
2. TM (perforation)
3. Middle ear (fluid)
4. Ossicles (fixation or disruption)
5. ET (obstruction)
Characteristics
 (-) Rinne test (BC > AC).
 Weber lateralised to poorer ear.
 Normal absolute bone conduction.
 Low frequencies affected more.
 Audiometry shows bone conduction better than air conduction with air-bone gap. Greater the
air-bone gap, more is the conductive loss.
 Loss is not > 60 dB.
 Speech discrimination is good.

Etiology
Congenital
1. Meatal atresia
2. Fixation of stapes footplate
3. Fixation of malleus head
4. Ossicular discontinuity
5. Congenital cholesteatoma

Acquired
1. External ear → any obstruction in the ear canal (wax, foreign body, furuncle, acute infla.
swelling, tumor or canal atresia)
2. Middle ear
 TM perforation → traumatic or infective
 Fluid in the middle ear → AOM, serous otitis media or haemotympanum
 Mass in middle ear → benign or malignant tumour
 Disruption of ossicles → trauma to ossicular chain, chr. suppurative OM, cholesteatoma
 Fixation of ossicles → otosclerosis, tympanosclerosis, adhesive otitis media
 ET blockage → retracted TM, serous otitis media.

Management
Most cases of conductive hearing loss can be managed by medical or surgical means. Treatment of
these conditions is discussed in respective sections, it consists of:
 Removal of canal obstructions → impacted wax, foreign body, osteoma or exostosis,
keratotic mass, benign or malignant tumours, meatal atresia.
 Removal of fluid → Myringotomy with or without grommet insertion.
 Removal of mass from middle ear → Tympanotomy and removal of small middle ear
tumours or cholesteatoma behind intact tympanic membrane.
 Stapedectomy → as in otosclerotic fixation of stapes footplate.
 Tympanoplasty → Repair of perforation, ossicular chain or both.
 Hearing aid → in cases, where surgery is not possible, refused or has failed
Sensorineural hearing loss
Results from lesions of cochlea (sensory type) or CN VIII and its central connections (neural type).
 The term retrocochlear is used when hearing loss is due to lesions of CN VIII
 central deafness, is used when it is due to lesions of central auditory connections
 In may be present at birth (congenital) or start later in life (acquired).
Characteristics
 (+) Rinne test (AC > BC).
 Weber lateralised to better ear.
 Bone conduction reduced on Schwabach and absolute bone conduction tests.
 More often involving high frequencies.
 No gap b/w air and bone conduction curve on audiometry
 Loss may > 60 dB.
 Speech discrimination is poor.
 There is difficulty in hearing in the presence of noise
Etiology
Congenital
It is present at birth and is the result of anomalies of the inner ear or damage to the hearing
apparatus by prenatal or perinatal factors

Acquired
It appears later in life. The cause may be genetic or non-genetic. The genetic cause may manifest
late (delayed onset) and affect only the hearing, or be a part of a larger syndrome affecting other
systems of the body as well. Common causes of acquired SNHL include:
1. Infec. of labyrinth → viral, bacterial or spirochaetal,
2. Trauma to labyrinth or CN VIII nerve → temporal fractures, labyrinth concussion, ear surgery
3. Noise-induced hearing loss
4. Ototoxic drugs
5. Presbycusis
6. Meniere's disease
7. Acoustic neuroma
8. Sudden hearing loss
9. Familial progressive SNHL
10. Sys. disorders→ DM, hypothyroidism, kidney disease, autoimm., MS, blood dyscrasias

Diagnosis of hearing loss

 History → congenital or acquired, stationary or progressive, associated with other sy.,
involvement of other members of the family and possible aetiologic factors

Every pt. should be questioned about the 3 most important symptoms of inner ear disorder:
1) Diminished hearing (hypoacusis)
2) Tinnitus
3) Vertigo

 Severity (by audiometry) → mild, moderate, moderately severe, severe, profound or total
 Type of audiogram → loss is high frequency, low frequency, mid-frequency or flat type
 Site of lesion → cochlear, retrocochlear or central
 Lab. tests → depend on suspected etiology
- X-rays or CT scan of temporal bone for evidence of bone destruction → congenital
cholesteatoma, glomus tumour, middle ear malignancy or acoustic neuroma
- blood counts (leukaemia), blood sugar (DM)
- serology for syphilis
- thyroid functions (hypothyroidism)…
Management of hearing loss
Early detection of SNHL is important as measures can be taken to stop its progress, reverse it or to
start an early rehabilitation programme
 Syphilis of the inner ear is treatable with high doses of penicillin and steroids with
improvement in hearing
 Serous labyrinthitis can be reversed by attention to middle ear infection.
 Early management of Meniere's disease can prevent further episodes of vertigo and hearing
loss. SNHL due to perilymph fistula can be corrected surgically by sealing the fistula in the
oval or round window with fat
 Ototoxic drugs should be used with care and discontinued if causing hearing loss. In many
such cases, it may be possible to regain hearing, total or partial, if the drug is stopped.
 Noise induced hearing loss can be prevented from further deterioration if the person is
removed from the noisy surroundings

Hearing aids
Conventional Hearing Aids
A hearing aid is a device to amplify sounds reaching the ear. Essentially, it consists of 3 parts:
1. Microphone → picks up sounds and converts them into electrical impulses
2. Amplifier → magnifies electrical impulses
3. Receiver→ converts electrical impulses back to sound. This amplified sound is then carried
through the earmould to the TM

There are many types → bone or air conduction hearing aid, Body-worn types (most commonly
used), behind-the-ear, in-the-ear and so on…

Implantable Hearing Aids

Are a new category of hearing devices that work on a direct drive principle → rather than delivering
acoustic energy into the EAM (as with traditional hearing aids), these implants use mechanical
vibrations delivered directly to the ossicular chain, bypassing the ear canal and TM, and leaving
the ear canal completely open
 This eliminates many of the inherent issues of conventional hearing aids such as occlusion,
feedback, discomfort and wax related problems.
 One major advantage is the ability to provide improved sound quality to the hearing-impaired
subjects particularly in noisy environments

Cochlear implant
A cochlear implant is an electronic device that can provide useful hearing for ppl. who have severe
to profound sensorineural hearing loss and who cannot benefit from hearing aids
It works by producing meaningful electrical stimulation of the auditory nerve where degeneration of
the hair cells in the cochlea has progressed to a point such that amplification provided by hearing
aids is no longer effective.

These implants usually consist of 2 main components:

1. External component → consists of an external speech processor and a transmitter. The
speech processor may be body worn or behind the ear type; the latter being preferred.
2. Internal component → surgically implanted and comprises the receiver/stimulator package
with an electrode array

Sound is picked up by the microphone in the speech processor → speech processor analyses and
codes sounds into electrical pulses. The processor uses a variety of coding strategies to deliver
meaningful speech parameters from the acoustic stimulus to the nerve.

The electrical impulses are sent from the processor to the transmitting coil which in turn sends the
signal to the surgically implanted receiver/stimulator via radiofrequency.
The receiver/stimulator decodes the signal and transmits it to the electrode array.
The electrode array which has been placed in the scala tympani of the cochlea stimulates the spiral
ganglion cells → auditory nerve is thus stimulated and sends these electrical pulses to the brain
which are finally interpreted as sound

The cochlear implant somewhat simulates natural hearing, where sound creates an electric current
that stimulates the auditory nerve. However, the result is not the same as normal hearing.
30% of patients can hear properly, while the rest just hear better.

Cochlear implants can help people who:

 have moderate to profound hearing loss in both ears
 receive little or no benefit from hearing aids
 score 50% or less on sentence recognition tests in the ear to be implanted
 score 60% or less in the non-implanted ear or in both ears with hearing aids
Topic 19. Meniere disease

Meniere's Disease (endolymphatic hydrops) is a disorder of inner ear in which the endolymphatic
sys. is distended with endolymph.
 Commonly seen in the age group of 35-60 years.
 Males are affected more than females.
 Usually the disease is unilateral but the other ear may be affected after a few years

It is characterised by aural fullness and a clinical triad of: 1) Vertigo

2) SNHL
3) Tinnitus
Pathological characteristics
The main pathology is distension of endolymphatic sys. due to ↑ vol. of endolymph, affecting mainly
the cochlear duct (scala media) & saccule, and to a lesser extent the utricle and semicircular canals.
 The dilatation of cochlear duct is such that, it may completely fill the scala vestibule
 There is marked bulging of Reissner's mem. which may even herniate through the helicotrema
into the apical part of scala tympani.
 The distended saccule may come to lie against the stapes footplate.
 The utricle and saccule may show out-pouchings into the semicircular canals

Etiology
MD can result either from ↑ production of endolymph or its faulty absorption or both.
Normally, endolymph is secreted by stria vascularis, fills the mem. labyrinth and is absorbed through
the endolymphatic sac

The exact cause of Meniere's disease is not known → various theories have been postulated:
1) Defective absorption by endolymphatic sac → thought cause the vertigo attack.
2) Vasomotor disturbance → sympathetic over-activity resulting in spasm of internal auditory
artery and/or its branches, thus interfering with the function of cochlear or vestibular sensory
neuroepithelium. This is responsible for deafness and vertigo
3) Allergy → an allergen may be a foodstuff or an inhalant. In these cases, inner ear acts as the
"shock organ" producing excess of endolymph.
4) Na and water retention
5) Hypothyroidism
6) Autoimmune and viral etiologies

Clinical presentation
Vertigo
At least 2 definitive episodes of vertigo of at least 20 min. must have occurred to make the diagnosis
 Duration is usually several hours long.
 Horizontal or rotatory nystagmus is always present during attacks of vertigo
 Symptoms are often accompanied with N&V and anxiety.
 Acute attacks may be accompanied with sudden falls without loss of consciousness → termed
crises of Tumarkin or drop attacks

Hearing loss
Sensorineural hearing loss must be documented audiometrically in the affected ear at least once
during the course of the disease.
 There may be fluctuation in the degree of hearing loss superimposed on gradual decrement in
function.
 Hearing loss affects low frequencies primarily.
Tinnitus and aural fullness
 Tinnitus is often non-pulsatile and may be described as whistling or roaring (high pitched)
 It may be continuous or intermittent.

Diagnosis
 Audiometry → sensorineural hearing loss: low tone  flat involving every frenquency.
 Recruitment phenomenon (pathologically ↑ loudness sensation, ↓ n. stapedial threshold)
 Vestibular investigation → spontaneous vestibular nystagmus to the healthy side, past-
pointing, falling (Romberg test) to the affected side, ↓ caloric response.
 X-ray, MRI, neurological-, ophthalmological investigations.
 There is no specific laboratory test → directed at diff. Ménière's disease from other causes

Glycerol test is useful → IV glycerol prompt eliminates the symptoms.

Differential Diagnoses
Ménière's disease must be distinguished from other causes of endolymphatic hydrops such as:
 post-traumatic
 post-infectious
 ototoxicity
 otosyphilis
 Cogan's sy. (autoimmune collagen disorder → interstitial keratitis)

Some other DD
1. Headache, Migraine
2. Subarachnoid Hemorrhage
3. Hypothyroidism
4. Temporal Lobe Epilepsy
5. Labyrinthitis
6. Acoustic neuroma
7. MS…

Treatment
Medical treatment is aimed at symptomatic relief → primary target is relief of vertiginous symptoms.
 Antiemetics may be used for N&V.
 Diuretics are often used, but their efficacy has not been established
 Vasodilators (betahistine) have been used for the treatment of vertigo but are not FDA
approved. They are thought to act by ↑ circulatory flow to the cochlear stria vascularis or
through inhibition of vestibular nuclei activity.

Other treatment options

 Bed rest
 IV fluids and electrolytes
 LMW-dextran infusion to improve the labyrinth circulation
 Psychological support
 In end stage cases → trans-tympanic labyrinthectomy
Topic 20. Acoustic neuroma and its early diagnosis

Acoustic neuroma (a.k.a vestibular schwannoma, neurilemmoma or 8th nerve tumor) is a benign,
encapsulated, extremely slow-growing tumor of the CN VIII
 Constitutes 80% of all cerebellopontine angle tumors and 10% of all the brain tumors
 Bilateral tumors are seen in patients with neurofibromatosis
 Mostly seen in age 40-60 years. Both sexes are equally affected

Origin of growth
The tumour almost always arises from the Schwann cells of the vestibular, but rarely from the
cochlear division of CN VIII within the internal auditory canal
As it expands, it causes widening and erosion of the canal and then appears in cerebellopontine
angle. Here, it may grow antero-superiorly to involve CN V OR inferiorly to involve the CN IX, X
and XI
In later stages, it causes displacement of brainstem, pressure on cerebellum and ↑ ICP
The growth of the tumour is extremely slow and the history may extend over several years.

Classification
Depending on the size, the tumour is classified as:
 Intracanalicular → when it is confined to internal auditory canal
 Small → up to 1.5 cm
 Medium → 1.5 - 4 cm
 Large → > 4 cm

Clinical presentation
Cochleovestibular symptoms
Are the earliest symptoms when tumor is still intra-canalicular and are caused by pressure on
cochlear or vestibular nerve fibres or on the internal auditory artery
 Progressive unilateral sensorineural hearing loss, often accompanied by tinnitus→ presenting
symptom in majority of cases.
 Characteristic of acoustic neuroma is a marked difficulty in understanding speech → out of
proportion to the pure tone hearing loss
 Some patients may get sudden hearing loss
 Vestibular symptoms are imbalance or unsteadiness. True vertigo is seldom seen

Cranial nerve involvement

V earliest nerve to be involved

reduced corneal sensitivity
numbness or paraesthesia of face
VII Sensory fibres are affected early
 hypoaesthesia of posterior meatal wall (Hitzelberger's sign)
 loss of taste
 ↓ lacrimation on Schirmer's test
Motor fibres are more resistant and are affected late → delayed blink reflex
IX and X dysphagia and hoarseness due to palatal, pharyngeal and laryngeal paralysis

 CN V Involvement indicates that the tumor is ~ 2.5 cm and occupies the cerebellopontine angle
 Other CN (XI and XII, III, IV and VI) are affected when tumor is very large

Brainstem involvement → ataxia, weakness and numbness of arms and legs with exaggerated
DTR
Cerebellar involvement → pressure symptoms are seen in large tumours.
 This is revealed by finger-nose test, knee-heel test
 Dysdiadochokinesia, ataxic gait, inability to walk along a straight line with tendency to fall to
the affected side
Raised ICP → late feature. headache, N&V, diplopia, papilloedema with blurring of vision

Investigation and diagnosis

Attempts should be made to dg. the tumor in its otological phase when it is still intra-canalicular.
This is possible when all cases of unilateral sensorineural hearing loss with tinnitus or imbalance
are carefully evaluated.

Audiological tests
 Pure tone audiometry → sensorineural hearing loss, more marked in high frequencies.
 Speech audiometry → poor speech discrimination, disproportionate to pure tone hearing loss.
Roll-over phenomenon (reduction of discrimination score when loudness is ↑ beyond a
particular limit) is most commonly observed
 Recruitment phenomenon is absent.
 Short Increment Sensitivity Index (SISI) test will show a score of 0-20% in 70-90% of cases.
 Threshold tone decay test shows retrocochlear type of lesion

Stapedial reflex decay test

High intensity stimulus is presented to the ear → stimulus is given in the form of a pure tone with a
frequency of at least 10dB above the range of the acoustic reflex
 This tone is played for 10 sec. (otherwise may damage the ear canal)
 If the reflex is functioning normally→ stapedial mm. stay contracted for the full 10 sec

Neurological tests
Complete examination of CN, cerebellar functions, brainstem signs of pyramidal and sensory tracts
should be done. Fundus is examined for blurring of disc margins or papilloedema

Imaging studies
1. Plain X-rays → give (+) findings in 80% of pts. (small intracanalicular tumors are not
detected!!)
2. CT → tumour that projects even 0.5 cm into the posterior fossa can be detected by a CT scan.
3. MRI (with gadolinium contrast) → superior to CT scan and is the gold standard for dg. of
acoustic neuroma. Intracanalicular tumour, of even a few millimetres, can be easily dg.
4. Vertebral angiography → differentiate AN from other tumors of cerebellopontine angle

Differential diagnosis
Acoustic neuroma should be differentiated from the cochlear pathology (Meniere's disease) and
other cerebellopontine angle tumours (meningioma, 10 cholesteatoma and arachnoidal cyst)

Treatment
Surgical removal of the tumour is the treatment of choice.
Surgical approach will depend upon the size of tumor →
 Middle cranial fossa approach. Conventional radioth. by external beam
 Translabyrinthine approach. has NO role in the treatment due to low
 Suboccipital (retrosigmoid) approach. tolerance of CNS to radiation
 Combined translabyrinthine-suboccipital approach
Topic 21. Hearing loss in childhood

Children with profound (>90 dB loss) or total deafness fail to develop speech and have often been
termed as deaf-mute or deaf and dumb
 These children have no defect in their speech producing apparatus → main defect is deafness
→ they have never heard speech and therefore do not develop it.
 In lesser degrees of hearing loss, speech does develop but is defective.
 The period from birth to 5 years of life is critical for the development of speech and language,
therefore, there is need for early identification and assessment of hearing loss and early
rehabilitation in infants and children.

Risk factors for hearing loss in children

1. Family history
2. Prenatal infec. (TORCHES).
3. Craniofacial anomalies including those of pinna and ear canal.
4. Birth weight < 1500 g
5. Hyperbilirubinaemia requiring exchange transfusion.
6. Ototoxic drugs → aminoglycosides, loop diuretics.
7. Bacterial meningitis
8. Apgar score of 0-4 at 1 min. or 0-6 at 5 min.
9. Mechanical ventilation for > 5 days

Etiology
Hearing loss in a child may develop from prenatal, perinatal or postnatal causes

Prenatal Causes
Infant factors
 An infant may be born with inner ear anomalies due to genetic or non-genetic causes.
 Anomalies may affect inner ear alone (non-syndromic) or may form part of a sy (syndromic).
 Anomalies affecting the inner ear may involve only the mem. labyrinth +/- bony labyrinths.

They include:
1) Sheibe's dysplasia → most common inner ear anomaly. dysplasia seen in cochlea & saccule
2) Alexander's dysplasia → affects basal turn of mem. cochlea → only high frequencies are affected.
3) Bing-Siebenmann dysplasia → complete absence of mem. labyrinth.
4) Michel aplasia → complete absence of bony and membranous labyrinth.
5) Enlarged vestibular aqueduct (>2 mm) → causes early onset SNHL which is progressive.
6) Semicircular canal malformations → lateral (+/- sup) semicircular canal malformation

Maternal factors TORCHES

1) Infections → TORCHES  Toxoplasmosis
2) Drugs → Streptomycin, gentamicin, Thalidomide…  Rubella
3) Radiation to mother in the 1st trimester  CMV
4) Other factors → DM, alcohol  HSV
 Syphilis
Perinatal Causes
1) Anoxia → damages the cochlear nuclei and causes haemorrhage into the ear (placenta praevia,
prolonged labour, prolapsed cord…)
2) Prematurity & LBW
3) Birth injuries → forceps delivery
4) Neonatal jaundice → kernicterus
5) Neonatal meningitis
6) Sepsis
7) Ototoxic drugs → used for neonatal meningitis or septicaemia
Postnatal Causes
1) Genetic → deafness may occur alone (familial progressive SNHL) or in association with
certain syndromes (Alport's, Klippel-Feil, Hurler, Down…)
2) Non-genetic → same as in adults and include
 Infections → measles, mumps, varicella, influenza, meningitis and encephalitis.
 Secretory otitis media
 Ototoxic drugs
 Trauma → fractures of temporal bone, middle ear surgery or perilymph leak.
 Noise-induced deafness.

Methods of hearing assessment in infants and children

 Neonatal screening procedures
- Arousal test
- Auditory response cradle
- ABR/OAE's
 Behaviour observation audiometry
- Moro's reflex
- Cochleopalpebral reflex
- Cessation reflex
 Distraction techniques
 Conditioning techniques
- Visual reinforcement audiometry
- Play audiometry
 Objective tests
- ABR
- Otoacoustic emissions
- Impedance audiometry

Management
It is essential to know the degree and type of hearing loss, and other associated handicaps such as
blindness or mental retardation and whether hearing loss is pre-lingual or post-lingual.
 Aims of habilitation of any hearing-impaired child are development of speech and language,
adjustment in society and useful employment in a vocation

Rehabilitation of the Hearing-Impaired

All hearing-impaired individuals need some sort of aural rehabilitation for communication.

The various means available to them are:

1) Instrumental devices
 Hearing aids → conventional, Bone anchored (BAHA)…
 Implants → cochlear implants, Auditory brainstem implants
 Assistive devices for the deaf
2) Training
 Speech (lip) reading
 Auditory training
 Speech conservation
Topic 22. Function of the facial nerve and facial palsy

Anatomy and function

Facial nerve is a mixed nerve having motor and a sensory root which carries secretomotor fibres to
the lacrimal and salivary glands, and brings fibres of taste and general sensation (overall → 2 efferent
and 2 afferent pathways).

1. Motor fibers
 Scalp, Face, and Auricula
 Buccinator m.
 Platysma m.
 Stapedius m.
 Stylohyoid m.
 Posterior Belly of Digastric m.
2. Autonomic motor fibers
 Vasodilatation and secretion
of salivary gl.
 Submaxillary gl.
 Sublingual gl.
3. Sensory fibers
 Taste for ant. 2/3 of Tongue
 Sensation to ear canal and behind ear

Nucleus of Facial Nerve

Motor nucleus of the nerve is situated in the pons, receives fibres from the precentral gyrus.
 Upper part of the nucleus which innervates forehead mm. receives fibres from both the cerebral
hemispheres
 Lower part of nucleus which supplies lower face gets only crossed fibres from one hemisphere.

Course of the facial n.

Motor fibres take origin from the nucleus of CN VII, hook round the nucleus of CN VI and are joined
by the sensory root (nerve of Wrisberg)

Facial nerve leaves the brainstem at pontomedullary junction → travels through post. cranial fossa →
enters the internal acoustic meatus.

At the meatus fundus (most lat. part of meatus), the nerve enters the bony facial canal → traverses
the temporal bone → comes out of the stylomastoid foramen → crosses the styloid process and
divides into terminal branches.

Therefore the course of the nerve can be divided into:

1) Intracranial part → from pons to internal acoustic meatus (15-17 mm)
2) Intratemporal part → from internal acoustic meatus to stylomastoid foramen, further divided:
 Meatal segment → within internal acoustic meatus (8-10 mm).
 Labyrinthine segment → from fundus of meatus to the geniculate ganglion where nerve
takes a turn posteriorly forming a "genu".
Here, the n. has the narrowest diameter and the bony canal in this segment is also the
narrowest → edema or infla. can easily compress the n. and cause paralysis.
 Tympanic (horizontal) segment → from geniculate ggl. to pyramidal eminence.
 Mastoid (vertical) segment → from the pyramid to stylomastoid foramen.
3) Extracranial part → from stylomastoid foramen to the termination of its peripheral branches
Branches of Facial Nerve

Innervations
Greater supf. petrosal n. carries secretomotor fibres to lacrimal gl. and the gl. of nasal mucosa
n. to stapedius supplies the stapedius m.
Chorda tympani carries secretomotor fibres to submandibular and sublingual gl.
taste sensation to ant. 2/3 of tongue
Communicating branch  conch
 retroauricular groove
 post. meatus
 outer surface of TM
Posterior auricular n. supplies muscles of pinna, occipital belly of occipitofrontalis
Muscular branches stylohyoid and post. belly of digastric

Peripheral branches → forms 2 divisions that together form the pes anserinus
They supply all the mm. of facial expression
1. Upper temporofacial
2. Lower cervicofacial → further divide into smaller branches: temporal, zygomatic, buccal,
mandibular and cervical branches

Classification of Nerve injury

Degree of nerve injury will determine the regeneration of nerve and its function.
Sunderland classified injuries into 5 degrees of severity based on anatomical structure of the n.

1° neurapraxia  Partial block to flow of axoplasm

 no morphological changes are seen.
 Recovery of function is complete
2° axonotmesis  Loss of axons, but endoneurial tubes remain intact.
 During recovery, axons will grow into their respective tubes
result is good
3° neurotmesis  Injury to endoneurium
 During recovery, axons of one tube can grow into another
 Synkinesis can occur
4° partial transection  Injury to perineurium in addition to above
 Scarring will impair regeneration of fibres
5° complete nerve Injury to epineurium in addition to above
transection

The first three degrees are seen in viral and infla. disorders while 4th and 5th are seen in surgical or
accidental trauma to the nerve or in neoplasms.
Facial nerve paresis
Cause may be central or peripheral.
 Peripheral lesion may involve the nerve in its intracranial, intratemporal or extratemporal parts.
 Peripheral lesions are more common and ~2/3 of them are of the idiopathic variety

1. Central → Brain abscess, Pontine gliomas, Poliomyelitis, MS

2. Intracranial part (cerebellopontine angle)
 Acoustic neuroma
 Meningioma
 Congenital cholesteatoma
 Metastatic carcinoma
 Meningitis
3. Intratemporal part
 Idiopathic → Bell's palsy, Melkersson's syndrome
 Infections → Acute/ chr. suppurative OM, Herpes zoster oticus, Malignant otitis externa
 Trauma → Surgical, Fractures of temporal bone
 Neoplasms → ext. and mid. ear tu., Glomus jugulare tumour, Facial n. neuroma
4. Extracranial part
 Malignancy of parotid
 Surgery of parotid
 Accidental injury in parotid region
 Neonatal facial injury (obstetrical forceps)
5. Systemic diseases → DM, Hypothyroidism, Uraemia, PAN, Wegener's granulomatosis…

Bell's Palsy
Defined as idiopathic, peripheral facial paralysis or paresis of acute onset.
 Accounts to 60-70% of facial n. paresis
 Can be causes by viral infe. (HSV, EBV), vascular ischemia, hereditary (family history) or due
to autoimm. Disorders
 Paralysis may be complete or incomplete

Clinical Features
 Onset is sudden.
 Pt. is unable to close his eye → when try, eyeball turns up and out (Bell's phenomenon).
 Saliva dribbles from the angle of mouth.
 Face are asymmetrical.
 Tears flow down from the eye (epiphora).
 Pain in the ear may precede or accompany the nerve paralysis.

Diagnosis
All other known causes of peripheral facial paralysis should be excluded.
 Nerve excitability tests are done daily or on alternate days and compared with the normal side to
monitor nerve degeneration
 Localising the site of lesion (topodiagnosis) helps in establishing the etiology and also the site
of surgical decompression of nerve, if that becomes necessary

Treatment
 Steroids, Analgesics
 Care of the eye → must be protected against exposure keratitis.
 Nerve decompression relieves pressure on the nerve fibres and thus improves the
microcirculation of the nerve.
Topic 23. Differential diagnosis of the tinnitus

Tinnitus is ringing sound or noise in the ear (sound originating within the patient..)
 Tinnitus is a symptom and not a disease.
 Usually, it is unilateral but may also affect both ears.
 It may vary in pitch and loudness and has been variously described by the patient as roaring,
hissing, swishing, rustling or clicking type of noise.
 Tinnitus is more annoying in quiet surroundings, particularly at night, when the masking effect
of ambient noise from the environment is lost

2 types of tinnitus are described:

1) Subjective → can only be heard by the patient.
2) Objective → less frequent, can even be heard by the examiner with the use of a stethoscope

Subjective tinnitus
 May have its origin in the external ear, middle ear, inner ear, CN VIII or CNS.
 In the presence of conductive deafness → pt. may hear abnor. noises in the head during eating,
speaking or even respiration

Objective tinnitus
Vascular lesions (glomus tumour or carotid a. aneurysm) cause swishing tinnitus synchronous with
pulse.
 It can be temporarily abolished by pressure on the common carotid artery.
 Venous hum can sometimes be stopped by pressure on the neck veins

Causes of Tinnitus

Subjective
Otologic  Impacted wax
 Fluid in the middle ear
 Acute and chronic otitis media
 Abnor. patent ET→ synchronous with resp.
 Meniere's disease
 Otosclerosis
 Presbyacusis
 Noise trauma
 Ototoxic drugs
 Acoustic neuroma
Non-otologic  Diseases of CNS
 Anaemia
 Arteriosclerosis
 HTN or Hypotension
 Hypoglycaemia
 Epilepsy
 Migraine
Objective  Vascular tumours of middle ear (glomus tumour)
 Aneurysm of carotid a.
 Palatal myoclonus

Sometimes, tinnitus is psychogenic and no cause can be found in the ear or CNS.
It should be diff. from auditory hallucinations in which a person hears voices or other organised
sounds like that of music (characteristic of psychogenic disorder)
Treatment
Where possible, the cause should be discovered and treated.
Sometimes, even the treatment of cause may not alleviate tinnitus.

When no cause is found, management of tinnitus includes

1) Reassurance and psychotherapy → many times pt. has to learn to live with tinnitus.
2) Techniques of relaxation.
3) Sedation and tranquillizers → may be needed in initial stages until patient has adjusted.
4) Masking of tinnitus → use of a fan, loudly clicking clock or a similar device may mask the
tinnitus and help the patient to go to sleep.
Hearing aids can be used in pt. who have no hearing loss (tinnitus masker)
Topic 24. Otalgy. Otalgy irradiata. Differential diagnosis. Task of the family doctor

Otalgy (earache) is a symptom. It is essential to find its cause before specific tr. can be instituted

Causes of otalgy
Can be due to causes occurring locally in the ear or referred to it from remote areas

Local causes
1) External ear → Furuncle, impacted wax, otitis externa, otomycosis, myringitis bullosa, herpes
zoster, and malignant neoplasms
2) Middle ear→ Acute otitis media, eustachian tube obstruction, mastoiditis, extradural abscess,
aero-otitis media, and carcinoma middle ear

Referred causes
As ear receives nerve supply from
1) CN V (auriculotemporal br.)
2) CN IX (tympanic br.)
3) CN X (auricular br.)
4) C2 and C3 spinal nn.

Via CN V
 Dental → Caries tooth, apical abscess, impacted molar, malocclusion
 Oral cavity → Benign or malignant ulcerative lesions of oral cavity or tongue
 TMJ disorders → Bruxism, osteoarthritis, recurrent dislocation, ill-fitting denture
 Sphenopalatine neuralgia

Via CN IX
 Oropharynx → Acute tonsillitis, peritonsillar abscess, tonsillectomy. Benign or malignant ulcers
of soft palate, tonsil and its pillars
 Base of tongue → TB, malignancy
 Elongated styloid process

Via CN X → tu. or ulcerative lesion of vallecula, epiglottis, larynx or laryngopharynx, esophagus

Via C2 and C3 → Cervical spondylosis, injuries of cervical spine, caries spine

Psychogenic Causes
When no cause has been discovered, pain may be functional in origin but the patient should be kept
under observation with periodic re-evaluation
Topic 25. Mastoiditis.

Refers to infla. of mucosal lining of antrum and mastoid air cell sys.
The term "mastoiditis" is used when infec. spreads from the mucosa, lining the mastoid air cells, to
involve bony walls of the mastoid air cell sys

There are 2 forms:

1) Acute mastoiditis →purulent liquefaction of the bony septa of the pneumatic sys. with
rupturing → forming abscess (rapid course).
2) Chronic Mastoiditis → productive infla. with obliteration of the space of the pneumatic sys.
by infla. granulation tissue and breakdown of bones

Acute Mastoiditis
Acute mastoiditis usually accompanies or follows acute suppurative otitis media, the determining
factors being high virulence of MO or lowered resistance of the pt. (measles, exanthematous fevers,
poor nutrition) or associated sys. disease (DM)
 Often seen in mastoids with well-developed air cell system.
 Children are affected more.
 β haemolytic strep. is the most common causative agent

Pathology
Main pathological processes are:
1. Production of pus under tension.
2. Hyperaemic decalcification and osteoclastic resorption of bony walls

Production of pus under tension

Extension of infla. process to muco-periosteal lining of air cell sys. ↑ the amount of pus produced
due to large surface area involved.
 Drainage of this pus, through a small perforation of TM and/or ET, cannot keep pace with the
amount being produced.
 Swollen mucosa of the antrum and attic also impede the drainage sys. resulting in accumulation
of pus under tension

Hyperaemic decalcification
Hyperaemia and engorgement of mucosa causes dissolution of Ca++ from the bony walls of the
mastoid air cells (hyperaemic decalcification)

Both these processes combine to cause destruction and coalescence of mastoid air cells, converting
them into a single irregular cavity filled with pus (Empyema of mastoid)
Pus may break through mastoid cortex leading to sub-periosteal abscess which may even burst on
surface leading to a discharging fistula

Clinical presentation
Symptoms
Are generally similar to that of acute suppurative OM, however, some changes in these
characteristic symptoms should point to the development of acute mastoiditis:
 Pain behind the ear → also seen in AOM but subsides with treatment. Here the pain is
persistent with ↑ intensity and may reoccur
 Fever → persistence or recurrence of fever in a case of acute otitis media, in spite of adequate
AB tr. points to the development of mastoiditis.
 Ear discharge → in mastoiditis, discharge becomes profuse and ↑ in purulence.
Any persistence of discharge > 3weeks points to mastoidits
Signs
 Mastoid tenderness
 Ear discharge → mucopurulent or purulent discharge, often pulsatile (light-house effect)
 Sagging of postero-superior meatal wall → due to periosteitis of bony party wall b/w antrum
and deeper posterosuperior part of bony canal.
 TM perforation → small, in pars tensa
 Swelling over the mastoid.
 Conductive hearing loss

Complications
1. Subperiosteal abscess
2. Labyrinthitis
3. Facial paralysis
4. Petrositis
5. Extradural abscess
6. Subdural abscess
7. Meningitis
8. Brain abscess Classical triad
9. Lateral sinus thrombophlebitis 1. Aural discharge
10. Otitic hydrocephalous 2. Tenderness of mastoid
3. retro-auricular swelling
Diagnosis
 Otoscopy → thick, opaque TM, Infla. in the postero-superior quadrant, and formation of a
nipple on the TM with fistulas.
 CBC → polymorphonuclear leucocytosis
 ↑ ESR
 X-ray mastoid

Differential diagnosis
1. Suppuration of mastoid lymph nodes
2. Furunculosis of meatus
3. Infected sebaceous cyst

Treatment
 Antibiotics → In the absence of culture and sensitivity, start with amoxicillin or ampicillin.
Specific antimicrobial is started on the receipt of sensitivity report. Since anaerobic organisms
are often present, chloramphenicol or metronidazole is added
 Myringotomy
 Cortical mastoidectomy

Masked (Latent) Mastoiditis

Is a condition of slow destruction of mastoid air cells W/O S&S of acute mastoiditis.
 No pain, no discharge, no fever and no mastoid swelling but mastoidectomy may show
extensive destruction of the air cells with granulation tissue
 The condition often results from inadequate AB th.
 Common in children presenting persistent hearing loss
 Cortical mastoidectomy with full doses of antibiotics is the treatment of choice.
Topic 1. Functional anatomy and physiology of the nose and paranasal sinuses
Functional anatomy of the nose
The external nose
pyramidal shaped structure with its root up and the base directed downwards.
Nasal pyramid consists of osteocartilaginous framework covered by mm. and skin.
Upper 1/3 of the external nose is bony while lower 2/3 are cartilaginous.
 It´s apex called the tip of the nose.
 The septum below the tip of the nose called "columella".
 The opening of the nose to air is called "nostrils" or "anterior nares"which are openings
through which air enters nasal cavities...
The bony nose
The bony part consists of 2 nasal bones which meet in the midline and rest on the upper part of the
nasal process of the frontal bones and are themselves held b/w the frontal processes of the maxillae
The external nose is pyramidal in shape , has anterior border called "dorsum" and two lateral sides.
The cartilaginous nose → consists of:
1) Upper lateral cartilages → extend from the undersurface of the nasal bones above, to the alar
cartilages below. They fuse with each other and with the upper border of the septal cartilage in
the midline anteriorly. The lower free edge of upper lateral cartilage is seen intranasally as limen
vestibuli or nasal valve on each side.
2) Lower lateral cartilages (alar cartilages) → each alar cartilage is U-shaped. It has a lateral crus
which forms the ala and a medial crus which runs in the columella. Lateral crus overlaps lower
edge of upper lateral cartilage on each side.
3) Lesser alar (sesamoid) cartilages → 2or more in number. They lie above and lateral to alar cart.
The various cartilages are connected with one another and with the adjoining bones by
perichondrium and periosteum.
Most of the free margin of nostril is formed of fibrofatty tissue and not the alar cartilage.
4) Septal cartilage → anterosuperior border runs from under the nasal bones to the nasal tip.
It supports the dorsum of the cartilaginous part of the nose.
In septal abscess or after excessive removal of septal cartilage as in SMR (submucosal resection)
operation, support of nasal dorsum is lost and a supratip depression results.

Nasal musculature
Osteocartilaginous framework of nose is covered by muscles which bring about movements of the
nasal tip, ala and the overlying skin:
 Procerus
 Nasalis (transverse and alar parts)
 Levator labii superioris alaeque nasi
 Ant. and post. dilator nares
 Depressor septi
The internal nose
Divided into R and L nasal cavities by nasal septum.
 Each nasal cavity opens to the exterior through naris and with the nasopharynx through the
choana (post. nasal aperture).
 Each nasal cavity consists of a skin-lined portion (vestibule), and a mucosa-lined portion (nasal
cavity proper).

Vestibule of Nose
Represent the ant. and inf. part of nasal cavity.
It is lined by skin and contains sebaceous glands, hair follicles and the hair (vibrissae).
Its upper limit on the lateral wall is marked by limen nasi (nasal valve)
Its med. wall is formed by the columella and lower part of the nasal septum up to its mucocutaneous
jun.

Nasal Cavity Proper

Each nasal cavity has a lateral wall, a medial wall, a roof and a floor

Lateral nasal wall

3 (occasionally 4) turbinates (or conchae) mark the lateral wall of nose.
 The turbinates are scroll-like bony projections covered by mucous mem.
 The spaces below the turbinates are called meatuses

Inferior turbinate
Is a separate bone and below it, into the inferior meatus, opens the nasolacrimal duct guarded at its
terminal end by a mucosal valve called Hasner's valve

Middle turbinate
Is a part of ethmoid bone (ethmoturbinal).
It is attached to the lateral wall by a bony lamella called basal lamella in an S-shaped manner.
 Anterior 1/3 → lies in sagittal plane and is attached to lateral edge of cribriform plate.
 Middle 1/3 → lies in frontal plane and is attached to lamina papyracea
 Posterior 1/3 → runs horizontally and forms roof of the middle meatus and is attached to lamina
papyracea and medial wall of maxillary sinus

The ostia of various sinuses draining anterior to basal lamella form anterior group of paranasal
sinuses while those which open posterior and superior to it form the posterior group
Middle meatus
Shows several important structures which are important in endoscopic surgery of the sinuses.
 Uncinate process is a hook-like structure. Its postero-superior border is sharp and runs parallel to
anterior border of bulla ethmoidalis → gap b/w the 2 is called hiatus semilunaris (inferior).
 Postero-inferior end of uncinate process is attached to inferior turbinate dividing the mem. part of
lower middle meatus into ant. & post. fontanelle.
 The fontanel area consists ONLY of mem. → leads into maxillary sinus when perforated.
 Upper attachment of uncinate process accounts for variations in drainage of frontal sinus

Bulla ethmoidalisi
Is an ethmoidal cell situated behind the uncinate process.
 Anterior surface of the bulla forms the posterior boundary of hiatus semilunaris (inf.)
 The bulla may be a pneumatised cell or a solid bony prominence.
 suprabullar or retrobullar recesses → space about or behind the bulla respectively, together they
form the lateral sinus (sinus lateralis of Grunwald)
 The cleft-like communication between the bulla and skull base and opening into middle meatus is
also called hiatus semilunaris superior

Agger nasi → an elevation just anterior to the attachment of middle turbinate.

When pneumatised it contains air cells, the agger nasi cells, which communicate with the frontal
recess. An enlarged agger nasi cell may encroach on frontal recess area, constricting it and causing
mechanical obstruction to frontal sinus drainage
Superior turbinate
Is also an ethmoturbinal and is situated post. and sup. to middle turbinate
 Sup. meatus → is a space below the superior turbinate. Posterior ethmoid cells open into it.
 Sphenoethmoidal recess → situated above the sup. turbinate. Sphenoid sinus opens into it
 Supreme turbinate → sometimes present above the superior turbinate and has a narrow meatus
below

Medial wall → formed by the nasal septum

Nasal septum consists of 3 parts:
1) Columellar septum → is formed of columella containing the medial crura of alar cartilages
united together by fibrous tissue and covered on either side by skin
2) Membranous septum → consists of double layer of skin with no bony or cartilaginous
support. It lies b/w the columella and the caudal border of septal cartilage.
Both columellar and membranous parts are freely movable from side to side
3) Septum proper → consists of osteocartilaginous framework, covered with nasal mucous
mem.
The septum proper principal constituents are:
 Perpendicular plate of ethmoid
 the vomer
 large septal (quadrilateral) cartilage
wedged b/w the above 2 bones anteriorly.

Other bones which make minor contributions at

the periphery are:
 crest of nasal bones
 nasal spine of frontal bone
 rostrum of sphenoid
 crest of palatine bones and crest maxilla
 anterior nasal spine of maxilla

Roof
 Anterior sloping part of the roof is formed by nasal bones
 Posterior sloping part is formed by the body of sphenoid bone
 the middle horizontal part is formed by the cribriform plate of ethmoid through which the
olfactory nerves enter the nasal cavity

Floor
Formed by palatine process of maxilla in its ant. 3/4 and horizontal part of palatine bone in its post.
1/4

Innervations of the nose

Olfactory nerves
carry sense of smell and supply olfactory region of nose
They are the central filaments of the olfactory cells and are arranged into 12-20 nerves which pass
through the cribriform plate and end in the olfactory bulb
These nerves can carry sheaths of dura, arachnoid and pia with them into the nose → injury to these
nerves can open CSF space leading to CSF rhinorrhoea or meningitis

Sensory innervation
1. Ant. ethmoidal n. → supplies anterior and superior part of the nasal cavity (lateral wall and
septum)
2. Branches of sphenopalatine ggl. → supply most of the post 2/3 of nasal cavity (both septum and
lateral wall)
3. Branches of infra-orbital n. → supply vestibule of nose both on its medial and lateral side

Motor innervation
1. mimetic muscles: facial n.
2. masticatory muscles : mandibular n. (trigeminal n.)

Autonomic nerves
Parasympathetic nerve fibres supply the nasal glands and control nasal secretion.
 They come from greater supf. petrosal nerve
 They also supply the blood vessels of nose and cause vasodilation

Sympathetic nerve fibres come from upper 2 thoracic segments of spinal cord. Their stimulation
causes vasoconstriction.
Blood Supply → see topic 6

The venous drainage

1. Facial vein
2. Retromandibular vein
3. Internal jugular vein.

Physiology of the nose

Functions of the nose are classified as:
1) Respiration
2) Air conditioning of inspired air
3) Protection of AW → Mucociliary mechanism, Enzymes and Ig (A, E) in nasal secretions
4) Vocal resonance
5) Nasal reflex functions → Sneezing
6) Olfaction

Olfaction
Intranasal olfactory mucosa -specialized olfactory epithelium.
The sensory cells consist of bipolar receptor cells whose proximal processes join to form the fila
olfactoria, which are relayed through additional neurons and are distributed to the primary, secondary,
and tertiary olfactory centers
Olfactory impression can be received only during inspiration, and only water-soluble and lipid-
soluble substances are perceived.

Functional anatomy of paranasal sinuses

Paranasal sinuses are air-containing cavities in certain bones of skull. They are 4 on each side
Clinically, paranasal sinuses have been divided into 2 groups:
1) Anterior group → maxillary, frontal and ant. ethmoidal.
They all open in the middle meatus and their ostia lie anterior to basal lamella of middle
turbinate
2) Posterior groups →
 Posterior ethmoidal sinuses which open in the superior meatus
 Sphenoid sinus which open in sphenoethmoidal recess

Maxillary Sinus (Antrum of Highmore)

Is the largest of paranasal sinuses and occupies the body of maxilla.
It is pyramidal in shape with base towards lateral wall of nose and apex directed laterally into the
zygomatic process of maxilla and sometimes in the zygomatic bone itself
On an average, maxillary sinus has a capacity of 15 ml in an adult
Frontal Sinus
Each frontal sinus is situated b/w the inner and outer tables of frontal bone, above and deep to the
supraorbital margin.
 It varies in shape and size and is often loculated.
 The 2 frontal sinuses are often asymmetric and the intervening bony septum is thin and often
obliquely placed or may even be deficient.
 Frontal sinus may be absent on one or both sides or it may be very large extending into orbital
plate in the roof of the orbit

Ethmoidal Sinuses (Ethmoid Air Cells)

Are thin-walled air cavities in the lateral masses of ethmoid bone.
Their number varies from 3-18.
They occupy the space b/w upper 1/3 of lateral nasal wall and the medial wall of orbit.
Clinically, ethmoidal cells are divided into:
1. Anterior ethmoid group → opens into the middle meatus
2. Posterior ethmoid group → opens into the superior meatus and sphenoethmoidal recess

Sphenoid Sinus
Occupies the body of sphenoid.
The 2 (R & L) sinuses, are rarely symmetrical and are separated by a thin bony septum which is often
obliquely placed and may even be deficient (compare frontal sinus).
Ostium of sinus is situated in the upper part of its ant. wall and drains into sphenoethmoidal recess

Physiology of paranasal sinuses

Ventilation of Sinuses
Ventilation takes place through their ostia v
it is paradoxical → they are emptied of air during inspiration and filled with air during expiration.
 During inspiration → air current causes (-) pressure in the nose.
 During expiration → (+) pressure is created in the nose.

Mucus Drainage of Sinuses

Mucus secreted in the sinuses travels to the ostium in a spiral manner.
Here the cilia are very active and propel mucus into the meatuses from where it is carried to the
pharynx.
In infections of the ant. gr. of sinuses get hypertrophied.

Functions of Paranasal Sinuses

It is not clear why nature provided paranasal sinuses. Probable functions are:
1. Air-conditioning of the inspired air by providing large surface area over which the air is
humidified and warmed.
2. To provide resonance to voice.
3. To act as thermal insulators to protect the delicate structures in the orbit and the cranium from
variations of intranasal temperature.
4. To lighten the skull bones.
Topic 2. Examination of the nose and paranasal sinuses

In order to examine the nose one needs:

1. Good source of light
 Semi-mobile (Bull's lamp) → Lamp is placed 6 inches above and behind the left shoulder
of the patient at the level of the ear of the patient.
 Mobile: Head light
2. Specialized instruments → such as:
 Nasal specula
 Indirect laryngoscopy mirrors
 Posterior Rhinoscopy mirrors
 Nasal and aural forceps

Head mirror → has 3 parts

1. Mirror → Hole in center. Concave. Focal length of 7-10 inches, therefore maximum
illumination is at the same distance
2. Lever with 2 ball and socket joints → The 2 joints should be at right angles to each other.
3. Plastic Head bands

Examination of the nose can be divided into 3 parts:

1) Examination of the external nose
2) Anterior Rhinoscopy
3) Posterior Rhinoscopy

Examination of the External Nose

Pay attention to:
1. Overlying skin → hardness, discoloration, swelling
2. Visible changes of cartilage or bony structures → flaring
3. Nasal vestibule and ant. border of the septum and the roof of the vestibule
4. any palpable masses, mobility of the nasal bony framework and sensitivty to pressure of the
forehead and cheeks

Inspection
 mouth breathing
 Congenital deformities: Clefts, sinuses.
 Acquired Deformities,
 Shape,
 Swelling → Inflammatory, cysts, tumors
 Ulceration → Trauma, neoplastic, infective

Palpation → is carried for

 Tenderness over the supraorbital, infraorbital, or mental
Tenderness over the tip is due to a boil
foramina → neuralgias
Over the dorsum is due to trauma
 Mobility or crepitus → fracture of the nasal pyramid
 Deformities

Anterior Rhinoscopy
Consists of the following steps:
1) Examination of the vestibule → Skin lined part of the nares
2) Examination of the nasal cavity using the Thudichum's speculum
3) Patency tests
4) Probe test
5) Examination after vasoconstriction
Examination of the vestibule
Tilte the pt. head back and check for:
 Boil → causes swelling in the roof and lateral wall.
 Ulceration → may be neoplastic, infective.
 Excoriation → because of discharge…

Examination of the nasal cavity using a speculum

Nasal speculum is an inverted 'U' shaped instrument. It has 2 blades at the lower end.
This exam. is carried out by:
1. Tilting the tip of the patient’s head in a vertical position to see the inf. turbinate and meatus,
2. Placing the head slightly backwards to visualize the middle meatus and middle turbinate
3. Placing the head totally backwards to see the olfactory cleft

Children→ Smaller instruments (pediatric specula), Aural specula can also be used, Decongestants
should always be properly diluted

Check for:
 Position of the nasal septum, deformities and narrowing or widening of the nasal meatus
 Nasal secretions → mucus, dryness, color
 Mucosa → color, moisture, pigmentation
 Abnor. masses

Indication
1. Nasal examination
2. Minor therapeutic procedures such as intranasal packing for epistaxis
3. Foreign body removal
4. Polypectomy

Probe test
Carried out by spraying the nose with 4% Lignocaine
The lesion or area is palpated to determine its character and mobility.

Patency test
Nasal patency can be assessed in 2 ways:
1. placing a cold tongue depressor → fogging (crude) Always compare the 2 sides
2. placing a wick of cotton below the nostril (subjective)

Posterior rhinoscopy
Carried out to examine the post nasal space (nasopharynx).
It is a difficult space to examine so the disease may be hidden for quite a long time.

Symptomatology of lesions of the nasopharynx:

 Nasal obstruction
 Post nasal drip
 Bleeding. Should be taken seriously as it may be due to a tumor.
 Pain
 Aural symptoms of deafness, discharge, and blockage.

Different methods of examining the area are:

1) Post nasal mirror.
2) Nasopharyngoscope.
3) Examination under anaesthesia after palatal retraction.
4) Digital palpation.
5) Radiological examination.
Post Nasal Mirror
Consists of a handle on which a small mirror is attached to shaft at an angle of 1100.
Used to examine the Choanna, posterior ends of turbinates, posterior septum, and the nasopharynx

Technique:
 Hold the mirror like a pen in the right hand. Warm it slightly on the flame of the spirit lamp to
avoid condensation from the expired air.
 Take the tongue depressor in the left hand and depress the anterior 2/3 of the tongue.
 Feel the warmth of the mirror on the back of the wrist. It should not be hot.
 Introduce the mirror from the angle of the mouth over the tongue depressor and slide it behind
the uvula. Avoid touching the posterior wall of the pharynx as it may trigger gagging.
 Instruct the patient to breath through the nose.
 Tilt the mirror in different direction tot see various structures of the nasopharynx.

Xylocain spray can be used to avoid gag reflex!

Check for:
1. Abnormal secretions in the chaonna
2. Mucosa (moist, dry, color, thick)
3. Abnormal masses (polyps)

Nasal Endoscopy
inspecting the nose, nasopharynx, all of the pharynx and larynx. Only close-up views
 Preparations: decongestion, topical anesthetic

Equipment
 Rigid endoscopes → 4-mm or 2.8-mm diameters and many viewing angles (0, 30,120)
 Flexible endoscopes → disadvantages compared with rigid scopes:
- Weaker light intensity and poorer image resolution
- Takes 2 hands to operate → a rigid scope leaves 1 hand free for manipulating instruments
 Diagnostic nasal endoscopy → 4-mm telescope. The 2.8-mm scope is used only in a very
narrow nasal cavity or in children.

Procedure
 First, advance endoscope into the nasopharynx and inspect the ET orifice, torus tubarius, post.
pharyngeal wall, and roof of the nasopharynx
 To inspect the middle meatus, the endoscope is first advanced toward the head of the middle
turbinate.

To advance farther into the ostiomeatal unit, the scope must negotiate the narrow passage b/w the
uncinate process and the middle turbinate → only with a narrow-gauge scope (2.8 mm).
The 4-mm is used only in pts who have had previous intranasal sinus surgery with resection of the
uncinate process.

Inspection of the paranasal sinuses is possible only to a limited degree:

sphenoid sinus can be examined with a thin telescope passed through the natural ostium in the
anterior sinus wall.
Maxillary sinus (for a suspected tumor), either through the inf. meatus after perforating the lat. nasal
wall or by a transfacial approach with incision of the maxillary sinus mucosa and perforation of its
anterior wall.
Topic 3. Value and indications of radiological examinations in paranasal sinus diseases
The use of radiology is very important in the diagnosis of diseases of the nasal sinuses.
Conventional Radiographs
Waters' view (Occipitomental view or nose-chin position)
It is taken in such a way that nose and chin of the patient touch the film while X-ray beam is
projected from behind. Waters' view with open mouth is preferred as it also shows sphenoid sinus.
In this view, petrous bones are projected below the maxillary antra
Structures seen are
 Maxillary sinuses (seen best).
 Frontal sinuses.
 Sphenoid sinus (if the film is taken with open mouth).
 Zygoma.
 Zygomatic arch.
 Nasal bone.
 Frontal process of maxilla.
 Superior orbital fissure.
 Intratemporal fossa
Caldwell view (Occipitofrontal view or nose-forehead position)
The view is taken with nose and forehead touching the film and X-ray beam is projected 15-20°
caudally. Structures seen are:
 Frontal sinuses (seen best).
 Ethmoid sinuses.
 Maxillary sinuses.
 Frontal process of zygoma and zygomatic process of frontal bone.
 Superior margin of orbit and lamina papyracea.
 Superior orbital fissure.
 Foramen rotundum (inferolateral to superior orbital fissure).
Lateral view
Lat. side of the skull lies against the film and X-ray beam is projected perpendicular from the other
side. Structures seen are
 Anterior and posterior extent of sphenoid, frontal and maxillary sinuses.
 Sella turcica.
 Ethmoid sinuses.
 Alveolar process.
 Condyle and neck of mandible.
Submentovertical (Basal) view
Structures seen are
 Sphenoid, posterior ethmoid and maxillary sinuses (seen best in that order).
 Zygoma & Zygomatic arch.
 Mandible along with coronoid and condyloid processes
Right and left oblique views → taken to see the posterior ethmoid sinuses and the optic foramen
of the corresponding side

Indications
1. Acute inflammation
2. Midfacial fractures
Diagnostic Value
Value of sinus radiographs is compromised by the presence of superimposed structures
 scar tissue from previous surgery on the paranasal sinuses which can mimic sinus opacity
 Difficult to evaluate the sphenoid sinus in the occipitomental projection (lateral sinus
projection should be added- craniocaudal extent of the frontal and maxillary sinuses can also
be evaluated with this technique.)

Computed Tomography (CT)

Indications
1. chronic sinusitis
2. trauma (especially frontobasal fractures)
3. tumors
4. malformation

Diagnostic Value
1. Compromised by metal-bearing denturesartifacts
2. provide nonsuperimposed primary images of the paranasal sinuses in coronal and axial planes
3. Sagittal images can be reconstructed secondarily from the axial or coronal scans, but they are
of poorer quality
Magnetic Resonance Imaging
Indications
1. diseases that involve the paranasal sinuses in addition to the cranial cavity or orbit ex:
(1) tumors
(2) congenital malformations such as encephaloceles, etc
2. Differentiating soft-tissue lesions within the paranasal sinuses:
(1) Mucocele
(2) Cyst
(3) polyp
3. distinguish between solid tumor tissue and inflammatory perifocal reaction
Contraindications
patients with electrically controlled devices such as
1. Cardiac pacemaker
2. insulin pump
3. cytostatic pump
4. cochlear implant

Diagnostic Value
1. markedly inferior to CT in defining the bony boundaries of the sinuses→ fewer indications
2. superior soft-tissue discrimination

Ultrasound (A and B mode)

Advantages
 follow-up of acute infla. processes, as it can eliminate the need for extra radiographic views
 Used in children and pregnant women for the same reason.

Disadvantages
 much less detailed images than CT and MRI
 cannot provide three dimensional rendering

Indications
1. frontal and maxillary sinuses → most easily accessible
2. anterior ethmoid cells → via the medial canthus the eye
3. middle and posterior ethmoid cells → by the transocular route: extremely challenging
4. sphenoid sinus is inaccessible
Topic 4. Diseases of the external nose and its complications

Cellulitis
The nasal skin may be invaded by strep. or staph. leading to a red, swollen and tender nose.
 Sometimes, it is an extension of infec. from the nasal vestibule.
 Treatment is systemic antibacterials, hot fomentation and analgesics

Nasal Deformities

Saddle nose
Depressed nasal dorsum may involve bony,
cartilaginous or both bony and cartilaginous
components of nasal dorsum

Etiology
 Nasal trauma → causing depressed
fractures is the most common etiology.
 Excessive removal of septum in submucous
resection
 Destruction of septal cartilage by
haematoma or abscess, leprosy, TB or
syphilis.

Treatment
The deformity can be corrected by augmentation rhinoplasty by filling the dorsum with cartilage,
bone or a synthetic (silicone or Teflon) implant.
 Autografts are preferred to allografts
 If depression is only cartilaginous → cartilage is taken from the nasal septum or auricle and
laid in a single or multiple layers.
 If deformity involves both cartilage & bone → cancellous bone from iliac crest is the best.

Hump nose
This may also involve the bone or cartilage or both.
It can be corrected by reduction rhinoplasty which consists of exposure of nasal framework by
careful raising of the nasal skin by a vestibular incision, removal of hump and narrowing of the
lateral walls by osteotomies to reduce the widening left by hump removal

Crooked or a Deviated Nose

Crooked → midline of dorsum from frontonasal angle to tip is curved in a C or S shaped manner.
Deviated → midline is straight but deviated to one side

Usually, these deformities are traumatic in origin.

Injuries sustained during birth, neonatal period or childhood, but not immediately recognised, will
also develop into these deformities with the growth of nose. The deviated or crooked nose can be
corrected by rhinoplasty or septorhinoplasty.
Aim of these operations is to correct not only the outer appearance of nose but also its function

Diseases of nasal vestibule

1) Inflammatory
 Pyodermas of the hair follicles → furuncle or boil
 Vestibulitis
 Erysipelas
2) Noninflammatory → Stenosis and Atresia of nares
Pyodermas of the hair follicles
Is a purulent Infla. of the hair follicles caused by staph. (mainly)
Trauma from nose picking or plucking the nasal vibrissae, is the usual predisposing factor
 If confined to the hair follicles → folliculitis.
 If infec. spreads to deeper tissues and forms a central core of purulent liquefaction → furuncle

Symptoms
 Small painful, tender, erythematous swellings about the nasal tip and nares
 May be concomitant edematous swelling of the upper lip.
 Confined to the outer skin and do not involve the mucosa.
 sometimes Fever

Treatment
Goal is to prevent potentially lethal complication of intracranial spread.
Consists of warm compresses, analgesics and topical and sys. antibiotics directed against staphy.
 high-dose parenteral flucloxacillin
 local chlortetracycline ointment

If a fluctuant area appears, incision and drainage can be done.

In NO case should the furuncle be squeezed or prematurely incised because of the danger of spread
of infec. to cavernous sinus through venous thrombophlebitis

Complications
1. hematogenous spread to intracranial structures
2. The furuncle may rupture spontaneously in the nasal vestibule
3. May complicate into cellulitis of the upper lip or septal abscess

Vestibulitis
Diffuse dermatitis of nasal vestibule.
Nasal discharge, due to any cause such as rhinitis, sinusitis or nasal allergy, coupled with trauma of
handkerchief, is the usual predisposing factor
The causative organism is S. aureus.

May be acute or chronic:

 Acute form → vestibular skin is red, swollen and tender, crusts and scales cover an area of skin
erosion or excoriation.
 Chr. form → induration of vestibular skin with painful fissures and crusting

Treatment
Consists of cleaning the nasal vestibule of all crusts and scales with cotton applicator soaked in
hydrogen peroxide and application of antibiotic-steroid ointment.
Chr. fissure can be cauterised with silver nitrate.

Erysipelas
Infla. spreads diffusely in the skin and subcutaneous tissue.
 Principal causative organisms are GAS (S. pyogen)
 May also caused by other strep., S. aureus, and G(-) rods (Klebsiella pneumoniae)

Symptoms
 High fever
 Broad areas of erythema and swelling with sharply demarcated margins
 Small blisters occasionally form.
 If spreads lateral to the nose and about the eyelids, there is a risk of intracranial involvement by
hematogenous spread.
Treatment: Parenteral penicillin and moist compresses soaked in an antiseptic solution

Differential diagnosis of facial soft-tissue swelling:

1. Lupus erythematosus (butterfly-shaped)
2. Allergic contact dermatitis
3. Angioedema

Stenosis and Atresia of the Nares

 Accidental or surgical trauma to the nasal tip or vestibule can lead to web formation and stenosis
of ant. nares. Destructive infla. lesions of nose also cause stenosis.
 Congenital atresia of ant. nares due to noncanalisation of epi. plug is a rare condition
 Stenosis of nares can be corrected by reconstructive plastic procedures
Topic 5. Nasal trauma and its treatment

Traumatic nasal fractures are classified as fractures of the mid. 1/3 of face (see topic 10!)

Nasal bones fractures

Fractures of nasal bones are the most common because of the projection of nose on the face.
 Traumatic forces may act from the front or side.
 Magnitude of force will determine the depth of injury
 The fractures are classified as open or closed on the basis of concomitant soft-tissue injuries.

Types of nasal fractures

1) Depressed → due to frontal blow. Lower thin part of nasal bones easily breaks.
A severe frontal blow will cause "open-book fracture" → nasal septum is collapsed and nasal
bones splayed out.
2) Angulated → a lateral blow may cause unilateral depression of nasal bone on the same side or
may fracture both the nasal bones and the septum with deviation of nasal bridge

Nasal fractures are often accompanied by injuries of nasal septum which may be simply buckled,
dislocated or fractured into several pieces. Septal haematoma may form

Clinical Features
 Swelling of nose → appear within few hours and may obscure details of examination.
 Periorbital ecchymosis
 Tenderness
 Nasal deformity → nose may be depressed from the front or side, or the whole of the nasal
pyramid deviated to one side.
 Crepitus and mobility of fractured fragments
 Epistaxis
 Nasal obstruction due to septal injury or haematoma.
 Lacerations of the nasal skin with exposure of nasal bones and cartilage may be seen in
compound fractures.

Diagnosis
Diagnosis is best made on physical examination.
 Inspection → deviation of the ext. nose, swelling (usually caused by a hematoma)
 Intranasal inspection → ant. rhinoscopy or endoscopy (check for mucosal injuries, septum)
 Palpation → Crepitus indicating fracture
 Radiographs → X-rays may or may NOT show fracture
X-rays should include Waters' view, R and L lateral views and occlusal view

Complications
When a septal fracture is covered by an intact soft-tissue envelope, there is a danger of
subperichondrial hemorrhage with hematoma formation → may become infected:
1) septal abscess → cartilage necrosis with loss of the nasal septum and dorsal saddling.
2) spread to the cranial cavity by the vascular route → meningitis

Treatment
Simple fractures w/o displacement need no treatment, others may require closed or open reduction.
 It is difficult to reduce a nasal fracture after 2 weeks because it heals by that time.
 Healing is faster in children and therefore earlier reduction is imperative
 Healed nasal deformities resulting from nasal trauma can be corrected by rhinoplasty or
septorhinoplasty
Closed reduction
Depressed fractures of nasal bones sustained by either frontal or lateral blow, can be reduced by a
straight blunt elevator guided by digital manipulation from outside.
 Laterally, displaced nasal bridge can be reduced by firm digital pressure in the opposite
direction. Impacted fragments sometimes require disimpaction with Walsham or Asche's
forceps before realignment.
 Septal haematoma, if present, must be drained.
 Simple fractures may not require intranasal packing. Unstable fractures require intranasal
packing and external splintage

Presence of edema interferes with accurate reduction by closed methods → the best time to reduce a
fracture is before the appearance of edema, or after it has subsided, which is usually in 5-7 days.

Open reduction
Early open reduction in nasal fractures is rarely required. It is indicated when closed methods fail.
Certain septal injuries can be better reduced by open methods

Fractures of nasal Septum

Trauma inflicted on the nose from the front, side or below can result in injuries to the nasal septum.
The septum may buckle on itself, fracture vertically, horizontally or be crushed to pieces as in a
smashed nose.
 The fractured pieces of septum may overlap each other or project into the nasal cavity through
mucosal tears.
 Fracture of the septal cartilage or its dislocation from the vomerine groove, can result from
trauma to the lower nose w/o associated fractures of nasal bones.

Types of fractures
1) "Jarjaway" fracture of nasal septum results from blows from the front
It starts just above the ant. nasal spine and runs horizontally backwards just above the junction
of septal cartilage with the vomer.
2) "Chevallet" fracture of septal cartilage results from blows from below
Runs vertically from the ant. nasal spine upwards to junction of bony and cartilaginous dorsum.

Complications
Septum is important in supporting the lower part of the external nose → if injuries are ignored, they
would result in deviation of cartilaginous nose or asymmetry of nasal tip, columella or the nostril

Septal injuries with mucosal tears cause profuse epistaxis while those with intact mucosa result in
septal haematoma which, if not drained early, will cause absorption of the septal cartilage and
saddle nose deformity.

Treatment
Early recognition and treatment of septal injuries is essential.
 Haematomas should be drained.
 Dislocated or fractured septal fragments should be repositioned and supported b/w
mucoperichondrial flaps with mattress sutures and nasal packing.
 Fractures of nasal pyramid are often complicated with fractures of the septum and both should be
treated concomitantly
Septal hematoma
It is collection of blood under the perichondrium or periosteum of the nasal septum.
Often results from nasal trauma or septal surgery. In bleeding disorders, it may occur spontaneously

Clinical Features and diagnosis

 Bilateral nasal obstruction is the commonest presenting symptom
 May be associated with frontal headache and a sense of pressure over the nasal bridge
 Examination reveals smooth rounded swelling of the septum in both the nasal fossae.
 Palpation may show the mass to be soft and fluctuant

Complications
Septal haematoma, if not drained, may organise into fibrous tissue → permanently thickened septum.
If 20 infec occurs → septal abscess with necrosis of cartilage and depression of nasal dorsum

Treatment
 Small haematomas can be aspirated with a wide bore sterile needle.
 Larger → are incised & drained by a small antero-posterior incision parallel to nasal floor.
Excision of a small piece of mucosa from the edge of incision gives better drainage.
Following drainage, nose is packed on both sides to prevent reaccumulation.
Systemic antibiotics should be given, to prevent septal abscess

Perforation of nasal septum

Etiology
1) Traumatic perforations → most common cause (surgiacal or accidental)
2) Pathological perforations → they can be caused by
 Septal abscess
 Nasal myiasis
 Rhinolith or neglected foreign body causing pressure necrosis.
 Chr. granulomatous conditions → lupus, TB and leprosy, syphilis…
 TB and leprosy → cause perforation in the cartilaginous part
 syphilis involves the bony part.
 Wegener's granuloma → midline destructive lesion, may cause total septal destruction.
3) Drugs and chemicals → steroid sprays, Cocaine, occupational (chromium plating…)
4) Idiopathic → In many cases, there is no history of trauma or previous disease

Clinical Features
 Small ant. perforations cause whistling sound during inspiration or expiration.
 Larger perforations develop crusts which obstruct the nose or cause severe epistaxis when removed

Treatment
An attempt should always be made to find out the cause before treatment of perforation → may
require biopsy from the granulation or the edge of the perforation.
 Inactive small perforations can be surgically closed by plastic flaps.
 Larger perforations are difficult to close → treatment is aimed to keep the nose crust-free by
alkaline nasal douches and application of a bland ointment.
 Sometimes, a thin silastic button can be worn to get relief from the symptoms
Naso-orbital Fractures
Direct force over the nasion fractures nasal bones and displaces them posteriorly.
 Perpendicular plate of ethmoid, ethmoidal air cells and medial orbital wall are fractured and
driven posteriorly.
 Injury may involve cribriform plate, frontal sinus, frontonasal duct, extraocular muscles, eyeball
and the lacrimal apparatus.
 Medial canthal ligament may be avulsed

Clinical Features
 Telecanthus → is an abnor. ↑ distance b/w the medial canthi of the eyelids due to lateral
displacement of medial orbital wall.
 Pug nose → bridge of nose is depressed and tip turned up.
 Periorbital ecchymosis
 Orbital haematoma → due to bleeding from anterior and posterior ethmoidal arteries.
 CSF leakage → due to fracture of cribriform plate and dura.
 Displacement of eyeball

Diagnosis
Various facial films will be required to assess the extent of fracture and injury to other facial bones.
CT scans are more useful

Treatment
Closed reduction
In uncomplicated cases, fracture is reduced with Asche's forceps and stabilised by a wire passed
through fractured bony fragments and septum and then tied over the lead plates.
Intranasal packing is given. Splinting is kept for 10 days or so

Open reduction
Required in cases with extensive comminution of nasal and orbital bones, and those complicated by
other injuries to lacrimal apparatus, medial canthal ligaments, frontal sinus…
 An H-type incision gives adequate exposure of the fractured area → can be extended to the
eyebrows if access to frontal sinuses is also required
 Nasal bones are reduced under vision and bridge height is achieved.
 Medial orbital walls can be reduced.
 Medial canthal ligaments, if avulsed, are restored with a through and through wire.
 Intranasal packing may be required to restore the contour.
 When bone comminution is severe, restoration of medial canthal ligaments and lacrimal
apparatus should receive preference over reconstruction of nasal contour
Topic 6. Epistaxis

Epistaxis is bleeding from inside the nose.

Epistaxis is a sign and NOT a disease per se and an attempt should always be made to find any local
or constitutional cause
 It is very common and seen in all age groups-children, adults and older people.
 It often presents as an emergency.

Blood supply of the nose

The Nose is richly supplied by both the ext.
and int. carotid sys, both on the septum and
the lateral walls

Nasal septum supply

Internal Carotid → ophthalmic artery → Ant.
& post. ethmoidal artery
External Carotid sys.:
1. maxillary a. → Sphenopalatine a. →
nasopalatine & post. med. nasal br.
2. maxillary a. → greater palatine a. →
Septal branch
3. facial a. → superior labial a. → septal
branch

Lateral wall
Internal carotid → same as to the septum
External carotid sys.:
Post. lateral nasal branches → From sphenopalatine artery
Greater palatine artery → From maxillary artery
Nasal branch of anterior superior dental → From infraorbital branch of maxillary a.
Branches of facial a. to nasal vestibule

Little's Area
Is situated in the anterior inferior part of nasal septum, just above the vestibule.
4 arteries anastomose here to form a vascular plexus called "Kiesselbach's plexus"→
1) ant. ethmoidal
2) septal branch of superior labial
3) septal branch of sphenopalatine
4) greater palatine

This area is exposed to the drying effect of inspiratory current and to finger nail trauma, and is the
usual site for epistaxis in children and young adults

Woodruff's Area
This vascular area is situated under the post. end of inf. turbinate where sphenopalatine a.
anastomoses with post. pharyngeal a.
Posterior epistaxis may occur in this area
Etiology of epitaxis
Can be divided into local (in the nose or nasopharynx), general & idiopathic

Local causes
Nose
1) Trauma → intranasal surgery, fractures of mid. 1/3 of face and base of skull, violent sneeze...
2) Infections → Viral rhinitis, nasal diphtheria, acute sinusitis, atrophic rhinitis, TB, syphilis…
3) Foreign bodies → rhinolith, maggots, leeches…
4) Neoplasms of nose and paranasal sinuses → Haemangioma, papilloma, cc. or sarcoma.
5) Atmospheric changes → High altitudes, sudden decompression (Caisson's disease)
6) Deviated nasal septum

Nasopharynx
1) Adenoiditis
2) Juvenile angiofibroma
3) Malignant tumors

General causes
1) C-V → HTN, arteriosclerosis, mitral stenosis, pregnancy…
2) Hematology → Aplastic anaemia, leukaemia, thrombocytopenic and vascular purpura,
haemophilia, hereditary haemorrhagic telangectasia…
3) Liver → cirrhosis (def. of factor II, VII, IX & X).
4) Kidney → chr. nephritis.
5) Drugs → Excessive use of salicylates and other analgesics, anticoagulants
6) Mediastinal compression → Tumours of mediastinum (↑ venous pressure in the nose).
7) Acute general infec. → influenza, measles, chickenpox, whooping cough, RF, mono…
8) Vicarious menstruation (epistaxis occurring at the time of menstruation).

Sites of epitaxis
1. Little's area → in 90% epistaxis cases
2. Above level of middle turbinate → from the ant. & post. ethmoidal vessels.
3. Below level of middle turbinate → from the br. of sphenopalatine a.
4. Post. part of nasal cavity → blood flows directly into the pharynx.
5. Diffuse → Both from septum and lateral nasal wall, often in sys. disorders and blood dyscrasias
6. Nasopharynx

Classification
1) Ant. Epistaxis → when blood flows out from the front of nose with pt. in sitting position
2) Post. Epistaxis → mainly the blood flows back into the throat.
Pt. may swallow it and later have a "coffee-coloured" vomitus.
This may incorrectly be dg. as haematemesis

The differences b/w the 2 types

Anterior Posterior
Incidence More common Less common
Site Mostly from Little's area or anterior Mostly from posterosuperior part of nasal cavity
part of lateral wall often difficult to localise the bleeding point
Age Mostly children or young adults > 40 years of age
Cause Mostly trauma Spontaneous
often due to HTN or arteriosclerosis
Bleeding Usually mild, can be easily Bleeding is severe, requires hospitalization
controlled by local pressure or Postnasal pack is often required
anterior pack
Management
Nosebleed is a self-limiting condition, rarely it may be quite dangerous and may prove a challenge
to even the most experienced rhinologist

General Measures in Epistaxis

1. Make the pts. sit up with a back rest and record any blood loss taking place through spitting or
vomiting.
2. Reassure the patient. Mild sedation should be given.
3. Keep check on HR, BP and RR.
4. Maintain haemodynamics → Blood transfusion may be required.
5. Antibiotics may be given to prevent sinusitis, if pack is to be kept beyond 24 hours.
6. O2 may be required in pts. with bilat. packs due to ↑ pul. resistance from nasopul. reflex.
7. Investigate and treat the patient for any underlying local or general cause.

First Aid
Most of the time, bleeding occurs from the Little's area and can be easily controlled by pinching the
nose with thumb and index finger for ~ 5 min.
 Trotter's method → pt is made to sit, leaning a little forward over a basin to spit any blood,
and breathe quietly from the mouth.
 Cold compresses should be applied to the nose to cause reflex vasoconstriction

Cauterisation
Useful in ant. epistaxis when bleeding point has been located.
The area is first anaesthetised and the bleeding point cauterised with a bead of silver nitrate or
coagulated with electrocautery

Anterior Nasal Packing

In cases of active ant. epistaxis, nose is cleared of blood clots by suction and attempt is made to
localise the bleeding site.
Ant. packing should be done if bleeding is profuse and/or the site of bleeding is difficult to localize

A ribbon gauze soaked with liquid paraffin is used. ~ 1 meter gauze is required for each cavity.
First, few cm of gauze are folded upon itself and inserted along the floor, and then the whole nasal
cavity is packed tightly by layering the gauze from floor to the roof.
Packing can also be done in vertical layers from back to the front

One or both cavities may need to be packed.

Pack can be removed after 24 hours if bleeding has stopped.
Sometimes, it has to be kept for 2-3 days → in that case, sys. AB should be given to prevent sinus
infec. and TSS

Posterior Nasal Packing

Required when bleeding is posteriorly into the throat.
Patients requiring postnasal pack should always be hospitalised.
This pack is first prepared by tying 3 silk ties to a piece of gauze rolled into the shape of a cone.
 A rubber catheter is passed through the nose and its end brought out from the mouth.
 Ends of the silk threads are tied to it and catheter withdrawn from nose.
 Pack, which follows the silk thread, is now guided into the nasopharynx with the index finger.
Anterior nasal cavity is now packed and silk threads tied over a dental roll.
 The 3rd silk thread is cut short and allowed to hang in the oropharynx → helps in easy removal
of the pack later.
Instead of postnasal pack, a Foley's catheter size 12-14 F can also be used.
After insertion balloon is inflated with 5-10 ml of saline.
The bulb is inflated with saline and pulled forward so that choana is blocked and then an anterior
nasal pack is kept in the usual manner.
These days nasal balloons are also available → it has 2 bulbs, one for the postnasal space and the
other for nasal cavity

Endoscopic Cautery
Post. bleeding point can sometimes be better located with an endoscope.
 It can be coagulated with suction cautery.
 Local anaesthesia with sedation may be required

Elevation of Mucoperichondrial Flap and SMR Operation

In case of persistent or recurrent bleeds from the septum, just elevation of mucoperichondrial flap
and then repositioning it back helps to cause fibrosis and constrict blood vessels.
SMR operation can be done to achieve the same result or remove any septal spur which is
sometimes the cause of epistaxis.

Ligation of Vessels
1) External carotid → when bleeding is from the ext. carotid sys. and the conservative measures
have failed, ligation of ext. carotid a. above the origin of sup. thyroid a. should be done.
It is avoided these days in favour of embolisation or ligation of more peripheral branches.
2) Maxillary artery → ligation of this a. is done in uncontrollable post. epistaxis.
Approach is via Caldwell-Luc operation.
Post. wall of maxillary sinus is removed and the maxillary a. or its br. are blocked by clips.
Endoscopic ligation of the maxillary artery can also be done through nose.
3) Ethmoidal arteries → in anterosuperior bleeding above the middle turbinate, not controlled
by packing, ant. & post. ethmoidal aa. can be ligated.
The vessels are exposed in the medial wall of the orbit by an external ethmoid incision
Topic 7. Differential diagnosis of nasal obstruction

DD in case of short duration of obstruction

1) Furuncle and eczema of the nostrils
2) Acute allergic rhinitis or sinusitis
3) Trauma → Nasal pyramid fracture, Sub-mucosal hematoma
4) Foreign bodies (especially in small children)
5) Edema

DD in case of long duration of obstruction

1) Collapsing nasal alae
2) Stenosis of the nostrils
3) Anterior Rhinitis sicca
4) Deviated septum (congenital, acquired)
5) Chronic rhinitis or sinusitis (allergic, atrophic)
6) Hypertophy of turbinates
7) Adenoids
8) Septal perforation
9) Foreign body, rhinolith
10) Nasal polyps
11) Cephalocele
12) Tumors of the nose, paranasal sinuses, and nasopharynx
13) Drugs → oral contraceptives, antiHTN, antidepressants…

Deviated nasal septum

This is an important cause of nasal obstruction

Etiology
Trauma and maldevelopment are the 2 important factors in the causation of deviated septum
Hereditary factors → Several members of the same family may have deviated nasal septum

Trauma
 Lat. blow on the nose may cause displacement of septal cart. from vomerine groove and
maxillary crest
 Crushing blow from the front may cause buckling, twisting, fractures and duplication of nasal
septum with telescoping of its fragments.

Injuries to the nose commonly occur in childhood but are often overlooked.
Trauma may also be inflicted at birth during difficult labour when nose is pressed during its passage
through the birth canal.

Developmental error
Nasal septum is formed by the tectoseptal process which descends to meet the 2 halves of the
developing palate in the midline.
During the 10 and 20 dentition → further development takes place in the palate, which descends and
widens to accommodate the teeth

Unequal growth b/w the palate and the base of skull may cause buckling of the nasal septum.
In mouth breathers (adenoid hypertrophy) the palate is often highly arched and septum is deviated.
Similarly, DNS may be seen in cases of cleft lip and palate and in those with dental abnor.
Types of DNS
Deviation may involve only the cartilage, bone or both the cartilage and bone
Anterior dislocation
Septal cartilage may be dislocated into one of the
nasal chambers.
This is better appreciated by looking at the base of
nose when patient's head is tilted backwards
C-shaped deformity
Septum is deviated in a simple curve to one side.
Nasal chamber on the concave side of the nasal
septum will be wider and may show compensatory
hypertrophy of turbinates
S-shaped deformity
S-shaped curve either in vertical or anteroposterior plane.
Such a deformity may cause bilateral nasal obstruction
Spurs
Is a shelf-like projection often found at the junction of bone and cartilage.
A spur may press on the lat. wall and cause headache. It may also predispose to repeated epistaxis
from the vessels stretched on its convex surface
Thickening → may be due to organised haematoma or over-riding of dislocated septal fragments
Clinical Features
 Nasal obstruction → may be unilateral or bilateral (depend on type)
 Headache → especially a spur
 Sinusitis → obstruct sinus ostia resulting in poor ventilation of the sinuses
 Epistaxis
 Anosmia → failure of the inspired air to reach the olfactory region may result in total or
partial loss of sense of smell
 External deformity → may be associated with deviation of the cartilaginous or both the bony
and cartilaginous dorsum of nose, deformities of the nasal tip or columella
 Middle ear infection
Treatment
Minor degrees of septal deviation with no symptoms are commonly seen in pts and dont tr.
Only when deviated septum produces mechanical nasal obstruction or sympt, operation is indicated
Submucous resection (SMR) operation
Generally done in adults under local anaesthesia.
It consists of elevating the mucoperichondrial and mucoperiosteal flaps on either side of the septal
framework by a single incision made on one side of the septum, removing the deflected parts of the
bony and cartilaginous septum, and then repositioning the flaps
Septoplasty
It is a conservative approach to septal surgery.
Here, much of the septal framework is retained and only the most deviated parts are removed.
Rest of the septal framework is corrected and repositioned by plastic means.
Mucoperichondrial/periosteal flap is generally raised only on one side of the septum, retaining the
attachment and blood supply on the other.
Septoplasty has now almost replaced SMR operation

Septal surgery is usually done after the age of 17 so as not to interfere with the growth of nasal
skeleton. However, if a child has severe DNS causing marked nasal obstruction, conservative septal
surgery (septoplasty) can be performed to provide a good AW
Topic 8. Acute and chronic rhinitis

Rhinitis is an infla. and swelling of the mucous mem. of the nose, characterized by a runny nose
and stuffiness, and is usually caused by common cold

Acute rhinitis → can be viral, bacterial or irritative type

Viral rhinitis
Common cold (coryza)
 Causative agents: adenovirus, picornavirus and its sub-gr. such as rhinovirus, coxsackie, ECHO
 Tramsmission: airborne droplets
 Incubation period:1-4 days
 Illness duration: 2-3 weeks

Clinical features
 Begins with burning sensation at the back of nose soon followed by nasal stuffiness,
rhinorrhoea and sneezing.
 Chills, low grade fever
 Initially, nasal discharge is watery & profuse but may become mucopurulent due to 20 bact. infec.
(S. haemolyticus, pneumococcus, staph., H. influenzae, Kleb. Pneumonia, M. catarrhalis)

Complications
The disease is usually self-limiting and resolves spontaneously after 2 to 3 weeks, but occasionally,
complications such as sinusitis, pharyngitis, tonsillitis, bronchitis, pneumonia and otitis media may
result

Treatment
 Bed rest, plenty of fluids…
 Symptoms can be controlled with antihistaminics and nasal decongestants.
 Analgesics → NOT aspirin (Reye sy.)
 Antibiotics are required when 20 infec. supervenes

Influenzal rhinitis
 Caused by influenza viruses A, B or C
 S&S are similar to those of common cold.
 Complications due to bacterial invasion are common

Rhinitis associated with exanthemas

Measles, rubella, chickenpox are often associated with rhinitis which precedes exanthemas by 2-3
days. 20 infec. and complications are more frequent and severe

Bacterial rhinitis
Non-specific infections
1) 10 infec. → seen in children, usually the result of infec. with pneumococcus, strep. or staph.
A greyish white tenacious mem. may form in nose.
2) 20 infec → is the result of bacterial infection supervening acute viral rhinitis.

Diphtheritic rhinitis
Diphtheria of nose is rare these days.
 It may be 10, or 20 to faucial diphtheria and may occur in acute or chronic form.
 A greyish mem. is seen covering the inf. turbinate and the floor of nose
 Mem. is tenacious and its removal causes bleeding.
 Excoriation of ant. nares and upper lip may be seen.
 Treatment is isolation of the patient, systemic penicillin and diphtheria antitoxin
Irritative rhinitis
This form of acute rhinitis is caused by:
1. Exposure to dust, smoke or irritating gases such as ammonia, formaline, acid fumes…
2. Trauma inflicted on the nasal mucosa during intranasal manipulation (foreign body removal)

There is an immediate catarrhal reaction with sneezing, rhinorrhoea and nasal congestion.
The symptoms may pass off rapidly with removal of the offending agent or may persist for some
days if nasal epithelium has been damaged.
Recovery will depend on the amount of epi. damage and the infection that supervenes

Chronic rhinitis
Chr. non-specific infla. of nose include:
1) Chronic simple rhinitis
2) Hypertrophic rhinitis
3) Atrophic rhinitis
4) Rhinitis sicca
5) Rhinitis caseosa

Chronic simple rhinitis

Recurrent attacks of acute rhinitis in the presence of predisposing factors leads to chronicity.
The predisposing factors are:
1. Persistence of nasal infec. due to sinusitis, tonsillitis, and adenoids.
2. Chr. irritation from dust, smoke, cigarette smoking, snuff…
3. Nasal obstruction due to DNS, synechia leading to persistence of discharge in the nose.
4. Vasomotor rhinitis.
5. Endocrinal or metabolic factors → hypothyroidism, excessive carbohydrates intake, Ø exercise…

Pathology
Simple chr. rhinitis is an early stage of hypertrophic rhinitis.
Hyperaemia & edema of mucous mem. with hypertrophy of seromucinous gl. and ↑ in goblet cells.
Blood sinusoids particularly those over the turbinates are distended.

Clinical Features
 Nasal obstruction → usually worse on lying and affects the dependent side of nose.
 Nasal discharge → may be mucoid or mucopurulent, thick and viscid and often trickles into
the throat as post-nasal drip.
 Headache → due to swollen turbinates impinging on the nasal septum.
 Swollen turbinates → nasal mucosa is dull red in colour. Turbinates are swollen
- They pit on pressure and shrink with application of vasoconstrictor drops (this
differentiates the condition from hypertrophic rhinitis)
- Middle turbinate may also be swollen and impinge on the septum.
 Post-nasal discharge → mucoid or mucopurulent discharge seen on post. pharyngeal wall.

Treatment
Treat the cause with particular attention to sinuses, tonsils, adenoids, allergy, personal habits
(smoking or alcohol indulgence), environment or work situation (smoky or dusty surroundings).
 Nasal irrigations with alkaline solution → help to keep the nose free from viscid secretions
and also remove supf. infec.
 Nasal decongestants → excessive use of nasal drops and sprays should be avoided because it
may lead to rhinitis medicamentosa.
 A short course of sys. steroids helps to wean the patients already addicted to excessive use of
decongestant drops or sprays.
 Antibiotics help to clear nasal infection and concomitant sinusitis
Hypertrophic rhinitis
Characterised by thickening of mucosa, submucosa, seromucinous glands, periosteum and bone.
Changes are more marked on the turbinates.

Common causes are:

1. Recurrent nasal infections
2. Chronic sinusitis
3. Chronic irritation of nasal mucosa due to smoking, industrial irritants, prolonged use of nasal
drops and vasomotor
4. Allergic rhinitis

Sign & Symptoms

 Nasal obstruction is the predominant symptom.
 Nasal discharge is thick and sticky.
 headache, heaviness of head or transient anosmia
 hypertrophy of turbinates. Turbinal mucosa is thick and does not pit on pressure. It shows little
shrinkage with vasoconstrictor drugs due to presence of underlying fibrosis

Maximum changes are seen in inf. turbinate → may be hypertrophied in its entirety or only at the
anterior end, posterior end or along the inferior border giving it a mulberry appearance

Treatment
Attempt should be made to discover the cause and remove it. Nasal obstruction can be relieved by
reduction in size of turbinates. The various methods are:
 Linear cauterisation.
 Submucosal diathermy.
 Cryosurgery of turbinates.
 Partial or total turbinectomy → hypertrophied inf. turbinate can be partially removed at its
anterior end, inferior border or posterior end.
- Middle turbinate, if hypertrophied, can also be removed partially or totally.
- Excessive removal of turbinates should be avoided as it leads to persistent crusting.
 Submucous resection of turbinate bone → remove bony obstruction but preserves turbinal
mucosa for its function.
 Lasers have also been used to reduce the size of turbinates

Compensatory Hypertrophic Rhinitis

Seen in cases of marked deviation of septum to one side.
 The roomier side of the nose shows hypertrophy of inferior and middle turbinates.
 This is an attempt on the part of nature to reduce the wide space to overcome the ill-effects of
drying and crusting that always attend wider nasal space.
 Hypertrophic changes in these cases are not reversible with the correction of nasal septum and
often require reduction of turbinates at the time of septal surgery

Atrophic rhinitis
It is a chr. infla. of nose characterised by atrophy of nasal mucosa and turbinate bones.
 The nasal cavities are roomy and full of foul-smelling crusts.
 Has 2 types: primary and secondary

Etiology
Primary form → idiopathic .
Secondary form → extensive tumor resection, excessive use of nose drops, drug abuse (cocaine),
radiotherapy for nasal and sinus tumors, Iatrogenic (improper septoplasty or an excessive turbinate
reduction (conchotomy))
Symptoms
 Pronounced dryness of the nasal mucosa.
 Severe cases, with secondary bacterial colonization, are marked by a fetid nasal odor that is not
perceived by the patient due to degeneration of the olfactory epithelium.
 Endoscopic examination: broad nasal cavity lined with dry, crusted mucosa.

Treatment
Begin with conservative, symptomatic measures → saline “nasal douche,” soothing mucosal ointments.
CI: decongestant-vasoconstriction exacerbates the symptoms.

If ineffective:
↓ the nasal cavity surgically by the submucous implantation of cartilage grafts → creates a relative
↑ in surface area in relation to the volume of the nasal cavity.

Rhinitis sicca
Is also a crust-forming disease seen in patients who work in hot, dry and dusty surroundings
(bakers, iron- and goldsmiths).
 Condition is confined to the ant. 1/3 of nose particularly of the nasal septum. Here, the ciliated
columnar epi. undergoes squamous metaplasia with atrophy of seromucinous glands.
 Crusts form on the ant. part of septum and their removal causes ulceration and epistaxis, and
may lead to septal perforation

Treatment consists of correction of the occupational surroundings and application of bland ointment
or one with an antibiotic and steroid, to the affected part.
 Nose pricking and forcible removal of crusts should be avoided.
 Nasal douche, like the one used in cases of atrophic rhinitis, is useful.

Rhinitis caseosa
Is an uncommon condition, usually unilateral and mostly affecting males
 Nose is filled with offensive purulent discharge and cheesy material.
 The disease possibly arises from chr. sinusitis with collection of inspissated cheesy material.
 Sinus mucosa becomes granulomatous.
 Bony walls of sinus may be destroyed, requiring differentiation from malignancy.
 Treatment is removal of debris and granulation tissue and free drainage of the affected sinus.
Topic 9. Clinical symptoms, diagnosis and treatment of allergic rhinitis

It is an IgE-mediated immunologic response of nasal mucosa to air-borne allergens(such as dust,

dander, or plant pollens) and is characterised by watery nasal discharge, nasal obstruction, sneezing
and itching in the nose
 Usually associated with symptoms of itching in eyes, palate and pharynx.
 When these symptoms are caused by pollen → allergic rhinitis is commonly called “hay fever”
 Onset is usually 12-16 yrs of age, but it may start in infants as young as 6 mo. or older ppl.

Etiology
 Inhalant allergens → are often the cause. Pollen from the trees and grasses, mould spores, house
dust, debris from insects or house mite are common offenders.
 Genetic predisposition

Types
2 clinical types have been recognised:
1) Seasonal → symptoms appear in or around a particular season when the pollens of particular
plant, to which the patient is sensitive, are present in the air.
2) Perennial → symptoms are present throughout the year.

Clinical presentation
Clinically, allergic response occurs in 2 phases:

Onset Cause Symptoms

Acute phase within 5-30 min after Release of vasoactive  Sneezing
(early) exposure to the specific amines (histamine)  rhinorrhoea
allergen  nasal blockage
 +/- bronchospasm
Late phase occurs 2-8 hours after infiltration of infla. cells  Swelling
(delayed) exposure to allergen w/o at the site of Ag  Congestion
additional exposure deposition  thick secretion

In the event of repeated or continuous exposure to allergen → acute phase S&S overlaps the late phase

Symptoms

Seasonal nasal allergy:

 paroxysmal sneezing
 10-20 sneezes at a time
 nasal obstruction
 watery nasal discharge and itching in nose (itching may also involve eyes, palate or pharynx).
 Some may get bronchospasm.
 The duration and severity of symptoms may vary with the season

Perennial allergy:
Symptoms are less severe, and include frequent colds, persistently stuffy nose, loss of sense of smell
due to mucosal edema, postnasal drip, chr. cough and hearing impairment due to ET blockage or fluid
in the mid. ear
Signs
Signs of allergy may be seen in the nose, eyes, ears, pharynx or larynx

Nasal signs
 transverse nasal crease → a black line across the middle of dorsum of nose due to constant upward
rubbing of nose
 pale and edematous nasal mucosa which may appear bluish
 Turbinates are swollen
 Thin, watery or mucoid discharge is usually present

Ocular signs
 edema of lids
 conjunctivitis → congestion and cobble-stone appearance of the conjunctiva
 dark circles under the eyes (allergic shiners)

Otologic signs → retracted TM or serous otitis media as a result of ET blockage

Pharyngeal signs
 granular pharyngitis due to hyperplasia of submucosal lymphoid tissue.
 A child with perennial allergic rhinitis may show all the features of prolonged mouth breathing as
seen in adenoid hyperplasia

Laryngeal signs → hoarseness of voice and edema of the vocal cords

Complications
1. Recurrent sinusitis because of obstruction to the sinus ostia
2. Nasal polypi
3. Serous otitis media
4. Orthodontic problems and other ill-effects of prolonged mouth breathing especially in children.
5. Bronchial asthma

Diagnosis
A detailed history and physical examination is helpful, and also gives clues to the possible allergen.
Other causes of nasal stuffiness should be excluded.
 Total and differential count → Peripheral eosinophilia may be seen
 Nasal smear → large number of eosinophils in allergic rhinitis.
Should be taken at the time of clinically active disease or after nasal challenge test.
 Skin tests → help to identify specific allergen.
 Nasal provocation test → crude method is to challenge the nasal mucosa with a small amount of
allergen placed at the end of a toothpick and asking the patient to sniff into each nostril and to
observe if allergic symptoms are reproduced.

Treatment → can be divided into

1) Avoidance of allergen
2) Treatment with drugs
3) Immunotherapy

Avoidance of allergen
Most successful if the antigen involved is single.
 Removal of a pet from the house, encasing the pillow or mattress with plastic sheet, change of
place of work or sometimes change of job may be required.
 A particular food article to which the patient is found allergic can be eliminated from the diet
Treatment with drugs
 Antihistaminics → control rhinorrhoea, sneezing and pruritis. (AE: drowsiness)
 Sympathomimetic drugs (oral or topical) → α adrenergic constrict blood vessels and reduce
nasal congestion and edema (for ex. Phenylephrine)
 Corticosteroids → Oral corticosteroids are very effective in controlling the symptoms of
allergic rhinitis but their use should be limited to acute episodes which have not been
controlled by other measures.
 Sodium cromoglycate → stabilises the mast cells and prevents them from degranulation
despite the formation of IgE-Ag complex. It is used as 2% solution for nasal drops or spray or
as an aerosol powder. It is useful both in seasonal and perennial allergic rhinitis

Immunotherapy
Immunotherapy or hyposensitisation is used when drug treatment fails to control symptoms or
produces intolerable AE.
 Allergen is given in gradually ↑ doses till the maintenance dose is reached.
 Immunotherapy suppresses the formation of IgE.
 It also raises the titre of specific IgG antibody.
 Has to be given for a year or so before significant improvement of symptoms can be noticed.
 It is discontinued if uninterrupted treatment for 3 years shows no clinical improvement
Topic 10. Traumatic lesion of facial cranium

Injuries of face may involve soft tissues, bones or both.

The majority of facial injuries are caused by automobile accidents. Others result from sports,
personal accidents, assaults and fights.

The face can be divided into 3 regions:

1. Upper 1/3 → above the level of supraorbital ridge
2. Middle 1/3 → b/w the supraorbital ridge and the upper teeth
3. Lower 1/3 → mandible and the lower teeth

According to these regions → Fractures of the face include:

Upper Middle Lower

 Frontal sinuses  Nasal bones and septum (topic 5)  Alveolar process
 Supraorbital ridge  Naso-orbital area  Symphysis
 Frontal bone  Zygoma  Body
 Zygomatic arch  Angle
 Orbital floor  Ascending ramus
 Maxilla  Condyle
- Le Fort I (transverse)  TMJ
- Le Fort II (pyramidal)
- Le Fort III (craniofacial dysjunction)

Fractures of upper 1/3

Frontal Sinus
Frontal sinus fractures may involve anterior wall, posterior wall or the nasofrontal duct

Anterior wall fractures

May be depressed or comminuted. Defect is mainly cosmetic.
 Sinus is approached through a wound in the skin if that is present, or through a brow incision.
 The bone fragments are elevated, taking care not to strip them from the periosteum.
 The interior of the sinus is always inspected to rule out fracture of the posterior wall.

Posterior wall fractures

 May be accompanied by dural tears, brain injury and CSF rhinorrhoea.
 They may require neurosurgical consultation.
 Dural tears can be covered by temporalis fascia. Small sinuses can be obliterated with fat.

Injury to nasofrontal duct

Cause obstruction to sinus drainage and may later be complicated by a mucocele (make a large
communication b/w the sinus and the nose).
Small sinuses can be obliterated with fat after removing the sinus mucosa completely.

Supraorbital Ridge
Ridge fractures often cause periorbital ecchymosis, flattening of the eyebrow, proptosis or downward
displacement of eye.
Fragment of bone may also be pushed into the orbit and get impacted.
Ridge fractures require open reduction through incision in brow or transverse skin line of forehead

Fractures of Frontal Bone

They may be depressed or linear, with or w/o separation. Often extend into the orbit.
Brain injury and cerebral edema are commonly associated and require neurosurgical consultation
Fractures of middle 1/3
Fractures of Zygoma (Tripod Fracture)
After nasal bones, zygoma is the 2nd most frequently
fractured bone.
Usually, the cause is direct trauma.
 Lower segment of zygoma is pushed medially and
posteriorly resulting in flattening of the malar prominence
and a step-deformity at the infraorbital margin.
 Zygoma is separated at its three processes.
 Orbital contents may herniate into maxillary sinus

Clinical Features
 Flattening of malar prominence
 Step-deformity of infraorbital margin
 Anaesthesia in the distribution of infraorbital n.
 Trismus → due to depression of zygoma on the underlying coronoid process
 Oblique palpebral fissure → due to the displacement of lat. palpebral lig.
 Restricted ocular movements → due to entrapment of inf. rectus muscle. may cause diplopia.
 Periorbital emphysema → due to escape of air from the maxillary sinus on nose-blowing

Diagnosis
 Waters' or exaggerated Waters' view shows the fracture and displacement the best.
 Maxillary sinus may show clouding due to the presence of blood.
 Comminution with depression of orbital floor and herniation of orbital contents cannot be seen
on plain X-rays.
 CT scan of the orbital will be more useful

Treatment
Only displaced fractures require treatment.
Open reduction and internal wire fixation gives best results.

Fracture is exposed at the frontozygomatic suture through lateral brow incision and reduced by
passing an elevator behind the zygoma.
 Wire fixation is done at frontozygomatic suture and infraorbital margin. The latter is exposed by
a separate incision in the lower lid.
 Fracture of orbital floor can also be repaired through this incision.

Transantral approach is less favourable.

Antrum is exposed as in Caldwell-Luc operation, blood is aspirated, fracture reduced and then
stabilised by a pack in the antrum (removed in ~10 days)

Fractures of Zygomatic Arch

Zygomatic arch generally breaks into 2 fragments which get depressed.
There are 3 fracture lines → one at each end and 3rd in the centre of the arch.

Clinical Features
Characteristic features are depression in the area of zygomatic arch, local pain aggravated by talking
and chewing, trismus or limitation of the movements of mandible due to impingement of fragments
on the condyle or coronoid process

Diagnosis
Arch fractures are best seen on submentovertical view of the skull. Waters' view is also taken
Treatment
A vertical incision is made in the hair-bearing area above or in front of the ear, cutting through
temporal fascia. An elevator is passed deep to temporal fascia and carried under the depressed bony
fragments which are then reduced.
Fixation is usually not required as the fragments remain stable

Fractures of Maxilla
They are classified into 3 types.
1) Le Fort I (transverse) runs above and parallel to the palate.
Crosses lower part of nasal septum, maxillary antra and the
pterygoid plates.
2) Le Fort II (pyramidal) → passes through the root of nose, lacrimal
bone, floor of orbit, upper part of maxillary sinus and pterygoid
plates. has some features common with zygomatic fractures.
3) Le Fort III (craniofacial dysjunction) → complete separation of
facial from cranial bones.
The fracture line passes through root of nose, ethmofrontal junction,
superior orbital fissure, lateral wall of orbit, frontozygomatic and
temporozygomatic sutures and the upper part of pterygoid plates.

Clinical Features
 Malocclusion of teeth with anterior open bite
 Elongation of midface
 Mobility in the maxilla
 CSF rhinorrhoea → cribriform plate is injured in Le Fort II and Le Fort III fractures
 Periorbital hematoma → unilateral or bilateral
 Dish face → is seen in combined fractures (Le Fort II–III, Escher III) where the midface has
been separated from the skull base and displaced inward.
 Vision loss caused by ocular destruction or injury to the optic nerve
 Diplopia due to oculomotor palsy from damage to the CN III, IV, VI
 Cerebral prolapse → brain tissue herniating externally or into the nasal cavity
 Anosmia → fracture of the cribriform plate with avulsion of the fila olfactoria, or central
damage due to cerebral concussion or contusion.

Diagnosis
 Palpation of the facial bones
 Inspection of the nasal cavity by rhinoscopy or endoscopy → confirm or exclude a CSF leak
 Inspect the oral cavity and oropharynx.
 Otoscopy or otomicroscopy → exclude petrous bone fracture.
 Intracranial complications (especially bleeding) should also be excluded
 Imaging → X-rays in Waters' view, posteroanterior view, lateral view and the CT scans.
 Testing of hearing and balance → possible only if the pt is conscious
 Olfactory testing → exclude anosmia

Treatment
Complex. Immediate attention is paid to restore the AW and stop severe haemorrhage from maxillary
a. or its branches. For good cosmetic and functional results, fractures should be treated as early as the
patient's condition permits. Associated intracranial and cervical spine injuries may delay specific tr.

Fixation of maxillary fractures can be achieved by:

 Interdental wiring.
 Intermaxillary wiring using arch bars.
 Open reduction and interosseous wiring as in zygomatic fractures.
 Wire slings from frontal bone, zygoma or infraorbital rim to the teeth or arch bars
Topic 11. Paranasal sinusitis in childhood and adults

Sinusitis is an infla. of sinus mucosa.

 Can be acute or chronic
 May be open or closed → depending on whether the infla. products of sinus cavity can drain
freely into the nasal cavity through the natural ostia or not.
A closed sinusitis causes more severe symptoms and is also likely to cause complications

Etiology in general
 Nasal infections → infec. from nose can travel directly by continuity or by way of submucosal
lymphatics.
 Swimming and diving → Infected water can enter the sinuses through their ostia. High content
of chlorine gas in swimming pools can also set up chemical infla.
 Trauma → compound fractures or penetrating injuries may permit direct infec. of sinus mucosa.
 Barotrauma may be followed by infection.
 Dental infe. → applies to maxillary sinus. Infec. from the molar or premolar teeth or their
extraction may be followed by acute sinusitis

Predisposing factors
Local
1. Obstruction to sinus ventilation and drainage → any factor which interfere with this function can
cause sinusitis due to stasis of secretions in the sinus. They are:
 Nasal packing
 Deviated septum
 Hypertrophic turbinates
 Edema of sinus ostia due to allergy or vasomotor rhinitis
 Nasal polypi
 Structural abno. of ethmoidal air cells
 Benign or malignant neoplasm.
2. Stasis of secretions in the nasal cavity → normal secretions may not drain into the nasopharynx
due to hyperviscosity (CF) or obstruction (enlarged adenoids, choanal atresia) and get infec.
3. Previous attacks of sinusitis → local defences of sinus mucosa are already damaged

Other
1. Environment → sinusitis is common in cold and wet climate. Atmospheric pollution, smoke, dust
and overcrowding also predispose to sinus infec.
2. Poor general health

Acute Sinusitis
 In adults the most commonly involved sinus is the maxillary > ethmoid > frontal > sphenoid.
 In children most affected is the ethmoid cells (incomplete pneumatization of the other sinuses)
 Often, more than one sinus is infected (multisinusitis).
 Sometimes, all the sinuses of are involved simultaneously (pansinusitis unilateral or bilateral).

Causative agents
Most cases of acute sinusitis start as viral infec. followed soon by bact. invasion.
The bacteria most often responsible for acute suppurative sinusitis are:
 S. Pneumonia
 S. pyogenes
 S. aureus
 H. influenza
 Moraxella catarrhalis
 K. pneumonia
  Anaerobic organisms and mixed infec. are seen in sinusitis of dental origin
Extent of the inflammation symptoms depend on various factors
1. Individual functional anatomy
2. Individual immune status
3. Specific virulence of the causative organism

Symptoms
Features of acute rhinitis combined with headache, which is exacerbated by bending over.
Tenderness & Pain is most intense over the affected sinuses → Ex:
 Ethmoid sinusitis → most painful over the bridge of the nose and the medial canthus of the eye,
 Frontal sinusitis → over the ant. wall and floor of the frontal sinus, with pain radiating toward the
medial canthus.
 Sphenoid sinusitis → pain is nonspecific, dull, aching pressure located at the center of the skull
and radiating to the occiput.

Other symptoms
 Fever, general malaise and body ache.
 Redness and edema of cheek → in maxillary sinusitis, commonly seen in children. The lower
eyelid may become puffy.
 Edema of upper eyelid with suffused conjunctiva and photophobia in cases of frontal sinusitis

Diagnosis
 Rhinoscopy or nasal endoscopy → pus along the middle meatus.
May not be seen if the mucosa is greatly swollen.
In isolated sphenoid sinusitis, pus may be found about the ostium in the ant. wall of the sphenoid
sinus or on the post. wall of the pharynx.
 Sinus radiographs → partial opacification of the affected sinus due to mucosal swelling or may
demonstrate a fluid level if the sinus contains free pus
 US (A or B-mode) → alternative to radiography, especially for follow-up and in children and
pregnant women

Chronic sinusitis
Is defined as a sinus infec. lasting for months or years.
 Mixed aerobic and anaerobic organisms are often present
 Chr. sinusitis frequently affects the maxillary sinus and ethmoid cells (frontal and sphenoid
sinuses are less commonly involved).

Causes include:
1. failure of acute infection to resolve (most important cause)
2. intranasal anatomic changes such as septal deviation and septal spurs
3. variety of other diseases of a chronic infla., allergic, traumatic or neoplastic nature

Pathophysiology
The common mechanism is impaired ventilation of the ostiomeatal unit due to stenosis or obstruction
of this region→ ↓drainage of the dependent sinus systems, particularly the adjacent maxillary sinus
and ant. ethmoid cells→ mucosa becomes swollen, especially in the narrow anatomical passages of
the ostiomeatal unit, a vicious cycle becomes established → recurrent bouts of acute infla. and
eventually persistent, chronic sinusitis.

 Acute infec. destroys normal ciliated epi. impairing drainage from the sinus.
 Pooling and stagnation of secretions in the sinus invites infection.
 Persistence of infec. causes mucosal changes → loss of cilia, edema and polyp formation →
continuing the vicious cycle
Clinical features
Are often vague and similar to those of acute sinusitis but of lesser severity.
 Purulent nasal discharge is the commonest complaint.
 Foul-smelling discharge suggests anaerobic infection.
 Local pain and headache are often not marked except in acute exacerbations.
 Some patients complain of nasal stuffiness and anosmia

Diagnosis
X ray
 X-ray of the involved sinus may show mucosal thickening or opacity.
 + contrast material may show soft tissue changes in the sinus mucosa.

CT scan
 Considered the only acceptable imaging modality for paranasal sinuses if chr. infec. is suspected.
 Particularly useful in ethmoid and sphenoid sinus infec. and has replaced studies with CM

Aspiration and irrigation → finding of pus in the sinus is confirmatory.

Rhinoscopy, endoscopy → check septum, the turbinates (turbinate hyperplasia, pneumatized middle
turbinate, concha bullosa), mucosal swelling, polyps, tumors…
Topic 12. Treatment of paranasal sinusitis

The primary objectives for sinusitis treatment are reduction of swelling, eradication of infec, draining
of the sinuses, and ensuring that the sinuses remain open.
 < 50% of patients reporting symptoms of sinusitis need aggressive treatment.
 Home remedies can be very useful.

Treatment of Acute Sinusitis

 Support tr. with only saline nasal irrigation, decongestants, antihistamines, and expectorants are
appropriate for a min. of 7-10 days for patients with mild-to-moderate symptoms
 Antibiotics are NOT helpful for patients with mild-to-moderate symptoms, so they should not be
prescribed for at least the first 7 days.

Medical treatment
Antimicrobial drugs
 Ampicillin and amoxicillin are quite effective and cover a wide range of organisms.
 Erythromycin or doxycycline or cotrimoxazole → in case of penicillin allergies.

Nasal decongestant
1% ephedrine or 0.1% xylo- or oxymetazoline nasal drops/sprays or inserting a cotton pack soaked
with nose drops into the middle meatus → improve ventilation and drainage of the paranasal sinuses

Steam inhalation
Steam alone or medicated with menthol provides symptomatic relief and encourages sinus drainage.
Inhalation should be given 15-20 minutes after nasal decongestion for better penetration.

Analgesics → Paracetamol or any other suitable analgesic

Hot fomentation → local heat to the affected sinus is often soothing and helps in resolution.

Surgical treatment

Maxillary sinusitis
Maxillary sinus puncture following decongestion and topical anesthesia of the nasal mucosa.
2 approaches:
(1) “Sharp puncture” through the inferior meatus, passing the needle below the inferior turbinate-
significant risk of complications due to air embolism if air is injected into the sinus after a
medication has been instilled. Or risk of perforation of the lateral sinus wall, resulting in a
buccal abscess or perforation of the sinus roof causing infection of th orbital contents
(2) “Blunt puncture” via the natural maxillary sinus ostium in the middle meatus.

Antral lavage
In acute sinusitis with throbbing headache, an antral wash out followed by medical treatment is still
the best option.
The purpose of an antral lavage is the removal of pus from the maxillary sinus.
 Under local anaesthesia, the partition wall b/w nose and maxillary sinus is pierced with needle
Then, the maxillary sinus is rinsed with a rinsing fluid.
 After rinsing, the needle is retracted into the nose and thereafter removed.
 The hole made in the partition wall by the needle heals within a day.
 Within several days, pus may be produced again and the whole procedure must be repeated.

The classical antral lavages are continued until the maxillary sinus stops producing pus.
Typically, average of 5 lavages are required.
Trephination of frontal sinus
If there is persistence or exacerbation of pain or pyrexia in spite of medical treatment for 48 hours, or
if the lid swelling is ↑ and threatening orbital cellulitis, frontal sinus is drained externally.
 2 cm long horizontal incision is made in the supero-medial aspect of the orbit below the eyebrow.
 Floor of frontal sinus is exposed and a hole drilled with a burr.
 Pus is taken for culture and sensitivity, and a plastic tube inserted and fixed.
 Sinus is irrigated with normal saline 2 or 3 times daily until frontonasal duct becomes patent.
 This can be determined by adding a few drops of methylene blue to the irrigating fluid and its
exit seen through the nose.
 Drainage tube is removed when frontonasal duct becomes patent.

Treatment of Chronic Sinusitis

It is essential to search for underlying etiology which obstruct sinus drainage and ventilation.
Initial treatment of chr. sinusitis is conservative, including antibiotics, decongestants, antihistaminics
and sinus irrigations.
More often, some form of surgery is required either to provide free drainage and ventilation or radical
surgery to remove all irreversible diseases so as to provide wide drainage or to obliterate the sinus

Medical treatment
Symptomatic benefit only. The only definitive treatment is sinus surgery
 A broad-spectrum antibiotic may be helpful.
 Decongestant nose drops (for no more than one week),
 A corticosteroid nasal spray → may be recommended for those patients who have nasal polyps
 Saline nasal irrigation is often needed on an ongoing basis.
 Heat therapy (electric light cabinet, microwaves, infrared)
 Mucolytics for supportive therapy
 antiallergic therapy if allergic etiology

Surgical treatment

Chronic Maxillary Sinusitis

1) Antral puncture and irrigation.
2) Intranasal antrostomy → indicated if sinus irrigations fail to resolve infection. A window is
created in the inferior meatus to provide aeration to the sinus and its free drainage.
3) Caldwell-Luc operation → antrum is entered through its ant. wall by a sublabial incision.
All irreversible diseases are removed and a window is created b/w the antrum and inf. meatus

Chronic Frontal Sinusitis

1) Intranasal drainage operations → correction of deviated septum, removal of a polyp or ant.
portion of middle turbinate, or intranasal ethmoidectomy, provide drainage through the
frontonasal duct. Tr. of associated maxillary sinusitis also helps to resolve chr. frontal sinusitis.
2) Trephination of frontal sinus
3) External frontoethmoidectomy (Howarth's or Lynch operation) → frontal sinus is entered
through its floor by a curvilinear incision round the inner margin of the orbit.
Diseased mucosa is removed, ethmoid cells exenterated and a new frontonasal duct created.
4) Osteoplastic flap operation → may be unilateral or bilateral.
 A coronal or a brow incision is used.
 The anterior wall of frontal sinus is reflected as an osteoplastic flap, based inferiorly.
 The diseased tissues are removed and the sinus drained through a new frontonasal duct.
 If it is desired to obliterate the sinus, all diseased as well as healthy mucosa are stripped off
and the sinus obliterated with fat.
Chronic Ethmoid Sinusitis
1) Intranasal ethmoidectomy → done for chronic ethmoiditis with polyp formation.
The ethmoid air cells and the diseased tissue are removed b/w the middle turbinate and the
medial wall of orbit by the intranasal route.
The frontal and sphenoid sinuses can also be drained by this operation.
2) External ethmoidectomy → ethmoid sinuses are approached through medial orbital incision.
Access can also be obtained to sphenoid and frontal sinuses and the operation is called
frontospheno-ethmoidectomy

Chronic Sphenoiditis
Sphenoidotomy → access to the sphenoid sinus can be obtained by removal of its anterior wall.
This is accomplished by external ethmoidectomy or transseptal approach, usually the former, because
of the co-existence of ethmoid disease with chronic sphenoiditis

Functional Endoscopic Sinus Surgery (FESS)

The principle is to enlarge the tight passages in the middle meatus and ostiomeatal unit including the
natural ostia of the maxillary sinus and, if necessary, the frontal sinus.
 A preliminary septoplasty may be necessary in pts with functionally significant septal deviation.
 The hazards \ are based mainly on the close proximity of the sinuses to the anterior cranial fossa,
optic nerve, and (in the case of the sphenoid sinus) to the int. carotid a.

Advantages
Superior visualization, better precision
Preserves function (recognizes normal mucociliary flow pattern at the osteomeatal complex)
Completeness
No external scar

Disadvantages: requires one-handed technique, monocular vision (difficulty with depth perception)

Indications
 Sinusitis (chronic, complicated, recurrent acute, fungal …)
 Obstructive nasal polyposis
 Sinus mucoceles
 Remove foreign bodies
 Tumor excision, transsphenoidal hypophysectomy
 Orbital decompression, Grave’s ophthalmopathy
 Choanal atresia repair
 CSF leak repair
 Control epistaxis
 Septoplasty, turbinectomy

Contraindications
Include osteomyelitis, no evidence of paranasal disease on CT, inaccessible lat. frontal sinus disease

Postoperative Care
sinus packing (2–6 days), oral antibiotics for a minimum of 2 weeks, aggressive nasal hygiene to
prevent adhesions (saline irrigations), nasal steroids, nasal debridement at 1, 3, and 6 weeks
Topic 13. Complications of paranasal sinusitis
Complications are said to arise when infec. spreads into or beyond the bony wall of the sinus
Local Mucocele/Mucopyocele

 Mucous retention cyst
 Osteomyelitis → Frontal bone (more common), Maxilla
Orbital  Preseptal infla. edema of lids
 Subperiosteal abscess
 Orbital cellulitis
 Orbital abscess
 Superior orbital fissure sy.
 Orbital apex syndrome
Intracranial  Meningitis
 Extradural abscess
 Subdural abscess
 Brain abscess
 Cavernous sinus thrombosis
Descending infections discharge constantly flows into the pharynx
 Otitis media
 Pharyngitis and tonsillitis
 Persistent laryngitis and tracheobronchitis

Local complications
Mucocele of Paranasal Sinuses and Mucous Retention Cysts
The sinuses commonly affected by mucocele in the order of frequency:
Frontal > ethmoidal > maxillary > sphenoidal.
 Mucocele can occur due to chronic obstruction to sinus ostium or cystic dilatation of mucous gl.
 Symptoms: depend on the affected sinus for ex.
- Frontal → cystic swelling of forehead, headache, diplopia, proptosis
- Ethmoid → expansion of the med. wall of the orbit, displacing the eyeball forward and lat.

Osteomyelitis
is infec. of BM and should be differentiated from osteitis (infec. of the compact bone).
Osteomyelitis, following sinus infec., involves either the maxilla or the frontal bone

Osteomyelitis of the maxilla

It is more often seen in infants and children than adults because of the presence of spongy bone in
the ant. wall of the maxilla.
 S&S: erythema, swelling of cheek, edema of lower lid, purulent nasal discharge, fever.
 Subperiosteal abscess & fistulae may form in infraorbital region, alveolus or palate, or in
zygoma. Sequestration of bone may occur
 Treatment: large doses of antibiotics, drainage of any abscess and removal of the sequestra.

Osteomyelitis of frontal bone

More often seen in adults as frontal sinus is not developed in infants and children.
 It results from acute infec. of frontal sinus either directly or through the venous spread.
 It can also follow trauma or surgery of frontal sinus in the presence of acute infection.
 Pus may form externally under the periosteum as soft doughy swelling (Pott's puffy
tumour), or internally as an extradural abscess.

Treatment: large doses of antibiotics, drainage of abscess and trephining of frontal sinus through its
floor +/- removal of sequestra and necrotic bone by raising a scalp flap through a coronal incision
Orbital complications
Orbit and its contents are closely related to the ethmoid, frontal, and maxillary sinuses, but most of
the complications, follow infec. of ethmoids as they are separated from the orbit only by a thin
lamina of bone-lamina papyracea.
Infec. travels from these sinuses either by osteitis or as thrombophlebitic process of ethmoidal veins

Infla. edema of lids.

This is only reactionary. Generally, upper lid is swollen in frontal, lower lid in maxillary, and both
upper and lower lids in ethmoid sinusitis.
 NO erythema or tenderness of the lids which characterises lid abscess.
 Involves only preseptal space → lies in front of orbital septum.
 Eyeball movements and vision are normal.

Subperiosteal abscess
Pus collects outside the bone under the periosteum.
 From ethmoids → forms on med. wall of orbit, displaces eyeball forward, downward and lat.
 From frontal sinus → abscess is situated just above and behind the medial canthus and
displaces the eyeball downwards and laterally
 From maxillary sinus → abscess forms in the floor of the orbit and displaces the eyeball
upwards and forwards.

Orbital cellulitis
When pus breaks through the periosteum and finds its way into the orbit, it spreads b/w the orbital
fat, extraocular muscles, vessels and nerves.
 lids edema, exophthalmos, chemosis of conjunctiva and restricted movements of the eye ball.
 Vision is affected causing partial or total loss which is sometimes permanent.
 +/- high fever.
 Potentially dangerous because of the risk of meningitis and cavernous sinus thrombosis.

Orbital abscess
Intraorbital abscess usually forms along lamina papyracea or the floor of frontal sinus.
 Clinical picture is similar to that of orbital cellulitis.
 Diagnosis can be easily made by CT or US of the orbit.
 Treatment: IV antibiotics and drainage of the abscess and that of the sinus (ethmoidectomy or
trephination of frontal sinus).

Superior orbital fissure syndrome

Infection of sphenoid sinus can rarely affect structures of superior orbital fissure.
Symptoms: deep orbital pain, frontal headache and progressive paralysis of CN VI, III and IV

Orbital apex syndrome

= superior orbital fissure sy. + additional involvement of the optic nerve and maxillary division of
the trigeminal (V2)
Topic 14. Tumors of the nose and paranasal sinuses

Tumors of external nose

1) Congenital → dermoid cysts, Encephalocele or meningoencephalocele, Glioma
2) Benign → Rhinophyma
3) Malignant → BBC, SCC, melanoma

Congenital Tumours
Dermoid cyst → Has 2 types:
1) Simple dermoid → occurs as a midline swelling under the skin but in front of the nasal
bones. It does not have any external opening
2) Cysts associated with a sinus → seen in infants and children and is represented by a pit or
a sinus in the midline of the dorsum of nose.

Encephalocele or meningoencephalocele
It is a herniation of brain tissue with meninges through a congenital bony defect.
An extranasal meningoencephalocele presents as a subcutaneous pulsatile swelling in the midline
at the root of nose (nasofrontal variety), side of nose (nasoethmoid variety) or on the
anteromedial aspect of the orbit (naso-orbital variety).

Treatment is neurosurgical → severing the tumour stalk from the brain and repairing the bony
defect through which herniation has taken place

Glioma
It is a nipped off portion of encephalocele during embryonic development.
 Most of them (60%) are extranasal and present as firm subcutaneous swellings on the bridge,
side of nose or near the inner canthus.
Extranasal gliomas are encapsulated and can be easily removed by external nasal approach
 Some are purely intranasal (30%)
 The rest (10%) are both intra and extranasal.

Benign tumors
They arise from the nasal skin and include papilloma (skin wart), haemangioma, pigmented
naevus, seborrhoeic keratosis, neurofibroma or tumour of sweat glands

Rhinophyma (potato tumor)

Is a slow-growing benign tumor due to hypertrophy of the sebaceous glands of the tip of nose
often seen in cases of long-standing acne rosacea.
 Mostly affects men past middle age
 It presents as a pink, lobulated mass over the nose with superficial vascular dilation
 Treatment: paring down the bulk of tumor with sharp knife or CO2 laser and the area allowed
to re-epithelialise. Sometimes, tumor is completely excised and the raw area skin-grafted.

Malignant tumors
Basal cell carcinoma (rodent ulcer)
Is the most common malignant tumor involving skin of nose (87%)
 Equally affecting males and females in the age group of 40-60.
 Common sites on the nose are the tip and the ala.
 It is very slow-growing and remains confined to the skin for a long time. Underlying cartilage
or bone may get invaded
 May present as a cyst or papulo-pearly nodule or an ulcer with rolled edges.
 Nodal metastases are extremely rare.
Treatment depends on the size, location and depth of the tumour.
 Early lesion → can be cured by cryosurgery, irradiation or surgical excision with 3-5 mm of
skin around the palpable borders of the tumour
 Lesions which are recurrent, extensive or with involvement of cartilage or bone are excised
and the surgical defect closed by local or distant flaps or a prosthesis

Squamous cell carcinoma (epithelioma)

This is the second most common malignant tumour (11%)
 Equally affecting both sexes in 40-60 age group.
 Infiltrating nodule or an ulcer with rolled out edges affecting side of nose or columella
 Nodal metastases are seen in 20% of cases

Treatment
 Early lesions respond to radiotherapy
 More advanced lesions or those with exposure of bone or cartilage require wide surgical
excision and plastic repair of the defect.
 Enlarged regional lymph nodes will require block dissection

Melanoma
This is the least common variety. Clinically, it is superficially-spreading type (slow-growing) or
nodular invasive type. Treatment is surgical excision

Tumors of the nasal vestibule

 Nasoalveolar cyst presents a smooth bulge in the lateral wall and floor of nasal vestibule.
The cyst can be excised by sublabial approach preserving the integrity of vestibular skin.
 Papilloma (wart) may be single or multiple, pedunculated or sessile. Treatment is surgical
excision under local anaesthesia.
 SCC arises from the lateral wall of the vestibule and may extend into nasal floor, columella
and upper lip.
- It can metastasise to the parotid and submandibular nodes.
- Treatment is surgical excision or irradiation.
Topic 15. Anatomy and physiology of the pharynx

The pharynx is a conical fibromuscular tube forming upper part of the air and food passages.
It is 12-14 cm long, extending from base of the skull (basiocciput and basisphenoid) to the lower
border of cricoid cartilage where it becomes continuous with the esophagus.

Musculature
External layer (constrictors):
1. sup. constrictor
2. mid. constrictor
3. inf. constrictor(oblique line and inf.cornu of thyroid cartilage)

Internal layer (elevators):

1. Stylopharyngeus mm. (bone)
2. Salpingopharyngeus mm. (auditory tube)
3. Palatopharyngeus (soft palate)

Innervation
 Pharyngeal plexus (IX, X, XI)
 Glossopharygeal n. & vagus n. & sup. Cervical ggl. → Pharyngeal br
 Vagal br. innervate all muscle (except stylopharyngeus - glossopharyngeal)
 Pharyngeal mucosa sensory by glossopharyngeal n.

Blood supply
1. Ascending pharyngeal a
2. Ascending palatine br. of facial a.
3. Descending palatine aa.
4. Pharyngeal br. Of maxilary a.
5. Br. of inf. And sup. Thyroid aa

Waldeyer's Ring
Scattered throughout the pharynx in its subepithelial layer is the lymphoid tissue which is
aggregated at places to form masses, collectively called Waldeyer's ring. The masses are
1. Nasopharyngeal tonsil or the adenoids
2. Palatine tonsils or simply the tonsils
3. Lingual tonsil
4. Tubal tonsils (in fossa of Rosenmuller)
5. Lateral pharyngeal bands
6. Nodules (in posterior pharyngeal wall)

Pharyngeal Spaces
There are 2 potential spaces in relation to the pharynx where abscesses can form
1) Retropharyngeal space → situated behind the pharynx and extending from the base of skull to
the bifurcation of trachea
2) Parapharyngeal space → situated on the side of pharynx. It contains carotid vessels, jugular
vein, last four cranial nerves and cervical sympathetic chain
Anatomically, pharynx is divided into 3 parts:
1) Nasopharynx (Epipharynx)
2) Oropharynx
3) Laryngopharynx (Hypopharynx)

Nasopharynx
Is the uppermost part of the pharynx, lies behind the nasal cavities and extends from the base of
skull to the soft palate or the level of the horizontal plane passing through the hard palate

Borders
 Roof → formed by basisphenoid and basiocciput.
 Posterior wall → formed by arch of the atlas vertebra covered by prevertebral mm. and fascia.
 Floor → formed by the soft palate anteriorly but is deficient posteriorly.
 Anterior wall → formed by post. nasal apertures or choanae, separated from each other by the
post. border of the nasal septum. Post. ends of nasal turbinates and meatuses are here.
 Lateral wall → each lateral wall presents the pharyngeal opening of ET
It is bounded above and behind by an elevation called torus tubarius raised by the cartilage of
the tube. Above and behind the tubal elevation is a recess called fossa of Rosenmuller which is
the commonest site for origin of carcinoma.

Nasopharyngeal Tonsil (Adenoids)

Is a subepi. collection of lymphoid tissue at the junction of roof and post. wall of nasopharynx and
causes the overlying mucous mem. to be thrown into radiating folds.
It ↑ in size up to the age of 6 years and then gradually atrophies

Nasopharyngeal Bursa
It is an epi.-lined median recess found within the adenoid mass and extends from pharyngeal
mucosa to the periosteum of the basiocciput.
When infected, it may be the cause of persistent postnasal discharge or crusting
Sometimes an abscess can form in the bursa (Thornwaldt's disease).

Rathke's Pouch
It is represented clinically by a dimple above the adenoids and is reminiscent of the buccal mucosal
invagination, to form the anterior lobe of pituitary. Craniopharyngioma may arise from it.

Tubal Tonsil
Collection of sub. lymphoid tissue situated at the tubal elevation.
It is continuous with adenoid tissue and forms a part of the Waldeyer's ring.
When enlarged due to infection, it causes ET occlusion
Sinus of Morgagni
Is a space b/w the base of the skull and upper free border of sup. constrictor mm.
Through it enters
 ET
 Levator veli palatini
 Tensor veli palatini
 Ascending palatine a. (br. of the facial a.)

Passavant's Ridge
It is a mucosal ridge raised by fibres of palatopharyngeus.
It encircles the post. and lat. walls of nasopharyngeal isthmus.
Soft palate, during its contraction, makes firm contact with this ridge to cut off nasopharynx from
the oropharynx during the deglutition or speech

Functions of Nasopharynx
1) conduit for air to larynx and trachea.
2) ventilates the middle ear and equalises air pressure on both sides of TM via ET
3) Elevation of the soft palate against post. pharyngeal wall and the Passavant's ridge helps to cut
off nasopharynx from oropharynx → important during swallowing, vomiting, gagging, speech.
4) Resonating chamber during voice production.
5) Drainage channel for the mucus secreted by nasal and nasopharyngeal glands.

Oropharynx
Extends from the plane of hard palate above to the plane of hyoid bone below.
It lies opposite the oral cavity with which it communicates through oropharyngeal isthmus.

Boundaries
Posterior wall → related to retropharyngeal space and lies opposite the second and upper part of
the third cervical vertebrae

Anterior wall → below it:

 Base of tongue → posterior to circumvallate papillae.
 Lingual tonsils → one on either side, situated in the base of tongue.
 Valleculae → cup-shaped depressions lying b/w the base of tongue and ant. surface of
epiglottis. Each is bounded medially by the median glossoepiglottic fold and laterally by
pharyngoepiglottic fold. They are the seat of retention cysts.

Lateral wall
 Palatine (faucial) tonsil
 Anterior pillar (palatoglossal arch) formed by the palatoglossus muscle.
 Posterior pillar (palatopharyngeal arch) formed by the palatopharyngeus muscle

Both anterior and posterior pillars diverge from the soft palate and enclose a triangular depression
called tonsillar fossa in which is situated the palatine tonsil

Functions of Oropharynx
1) Conduit for passage of air and food.
2) Helps in the pharyngeal phase of deglutition.
3) Forms part of vocal tract for certain speech sounds.
4) Helps taste sensation → taste buds are present in the base of tongue, soft palate, ant. pillars
and post. pharyngeal wall.
5) Provides local defence and immunity against harmful intruders into the air and food passages.
Hypopharynx
Is the lowest part of the pharynx and lies behind and partly on the sides of the larynx.
Hypopharynx lies opposite the 3rd, 4th, 5th, 6th cervical vertebrae.
 Sup. limit → is the plane passing from the body of hyoid bone to the posterior pharyngeal wall
 Inf. limit → is lower border of cricoid cart. where it becomes continuous with esophagus.

Clinically, it is subdivided into 3 regions

1. Pyriform sinus → lies on either side of the larynx and extends from pharyngoepiglottic fold to
the upper end of esophagus. Foreign bodies may lodge here.
2. Post-cricoid region → part of the ant. wall of laryngopharynx b/w the upper and lower borders
of cricoid lamina. It is a common site for carcinoma in females with Plummer-Vinson sy.
3. Post. pharyngeal wall → extends from level of hyoid bone to cricoarytenoid joint.

Functions of Hypopharynx
Laryngopharynx, like oropharynx, is a common pathway for air and food, provides a vocal tract for
resonance of certain speech sounds and helps in deglutition.
There is a coordination b/w contraction of pharyngeal mm. and relaxation of cricopharyngeal
sphincter at the upper end of esophagus.
Lack of this coordination (failure of cricopharyngeal sphincter to relax) when pharyngeal muscles
are contracting causes hypopharyngeal diverticulum
Topic 16. Diseases of the nasopharynx

Adenoids (hyperplasia, adenoiditis)

Adenoids are the common name of the nasopharyngeal tonsils located at the junction of the roof and
post. wall of the nasopharynx.
 Composed of vertical ridges of lymphoid tissue separated by deep clefts and covered by ciliated
columnar epi.
 Unlike palatine tonsils, adenoids have no crypts and no capsule.
 Adenoid tissue is present at birth, shows physiological enlargement up to the age of six years,
and then tends to atrophy at puberty and almost completely disappears by the age of 20.

Etiology
 Adenoids are subject to physiological enlargement in childhood.
 Recurrent attacks of rhinitis, sinusitis or chr. tonsillitis may cause chr. adenoid infection and
hyperplasia
 Allergy of the URT may also contribute to the enlargement of adenoids

Clinical Features
S&S depend not only on the absolute size of the adenoid mass but are relative to the available space
in the nasopharynx
Enlarged and infected adenoids may cause nasal, aural or general symptoms

Nasal Symptoms
 Nasal obstruction is the commonest symptom → leads to mouth breathing
 Nasal discharge → partly due to choanal obstruction and partly due to associated chr. rhinitis
 Sinusitis → chronic maxillary sinusitis is commonly associated with adenoids
 Epistaxis → when adenoids are acutely inflamed
 Voice change → toneless and loses nasal quality

Aural Symptoms
Tubal obstruction → Adenoid mass blocks the ET leading to retracted TM and CHL
Recurrent attacks of acute otitis media → infec. spread via the ET
Chronic suppurative otitis media → may fail to resolve in the presence of infected adenoids
Serous otitis media → imported cause in children

General Symptoms
 Adenoid facies → chronic nasal obstruction and mouth breathing lead to characteristic facial
appearance called adenoid facies.
- The child has an elongated face with dull expression, open mouth, prominent and crowded
upper teeth, and hitched up upper lip.
- Nose gives a pinched-in appearance due to disuse atrophy of alae nasi.
- Hard palate is highly arched as the moulding action of the tongue on palate is lost.
 Pul. HTN → due to long-standing nasal obstruction
 Aprosexia → lack of concentration

Diagnosis
 Examination of postnasal space → adenoid mass can be seen with a mirror.
 A rigid or a flexible nasopharyngoscope is also useful to see details of the nasopharynx.
 Soft tissue lateral radiograph of nasopharynx will reveal the size of adenoids and also the extent
to which nasopharyngeal air space has been compromised
 Detailed nasal exam. should always be conducted to exclude other causes of nasal obstruction
Treatment
When symptoms are not marked, breathing exercises, decongestant nasal drops and antihistaminics
for any co-existent nasal allergy can cure the condition without resort to surgery.
When symptoms are marked, adenoidectomy is done.

Acute nasopharyngitis
Acute infec. of the nasopharynx may be an isolated infec. confined to this part only or be a part of the
generalised upper AW infec.
It may be caused by viruses (common cold, influenza, para-influenza, rhino or adenovirus) or
bacteria (especially streptococcus, pneumococcus or Haemophilus influenzae).

Clinical features
 Dryness and burning of the throat above the soft palate is usually the first symptom
 Pain and discomfort localized to the back of nose with some difficulty on swallowing.
 In severe infec. → pyrexia and enlarged cervical L.N.

Diagnosis: exam. reveals congested and swollen mucosa often covered with whitish exudates

Treatment
 Analgesic for pain
 Mild cases clear up spontaneously.
 Severe cases with general symptoms → sys. antibiotic may be necessary.
 In children → there is associated adenoiditis which causes nasal obstruction, and requires nasal
decongestant drops

Chronic nasopharyngitis
Often associated with chr. infections of nose, paranasal sinuses and pharynx.
It is commonly seen in heavy smokers, drinkers and those exposed to dust and fumes
 Postnasal discharge and crusting with irritation at the back of nose is the most common
complaint. Examination of nasopharynx reveals congested mucosa and mucopus or dry crusts.
 In children, adenoids are often enlarged and infected (chr. adenoiditis).
 Alkaline nasal douche helps to remove crusts and mucopus. Steam inhalations are soothing.

Thornwaldt's disease (pharyngeal bursitis)

Infec. of the pharyngeal bursa which is a median recess representing attachment of notochord to
endoderm of the primitive pharynx.
Pharyngeal bursa is located in the midline of post. wall of the nasopharynx in the adenoid mass

Clinical Features
 Persistent postnasal discharge with crusting in the nasopharynx.
 Nasal obstruction due to swelling in the nasopharynx.
 Obstruction to eustachian tube and serous otitis media.
 Dull type of occipital headache.
 Recurrent sore throat.
 Low grade fever.

Diagnosis and treatment

 Examination would reveal a cystic and fluctuant swelling in the post. wall of nasopharynx.
 It may also show crusts in the nasopharynx due to dried up discharge
 Antibiotics are given to treat infec. and marsupialisation of the cystic swelling and adequate
removal of its lining mem.
Topic 17. Acute and chronic inflammation of the mesopharynx

Acute pharyngitis
Acute pharyngitis is very common and occurs due to varied etiological factors
 Viral causes are more common.
 Acute strep. pharyngitis (due to GAS) has received more importance because of its etiology in
rheumatic fever and post-streptococcal GN.

The causative agents include:

1) Viral → Rhinoviruses, Influenza, Parainfluenza, Measles, chickenpox, HSV, CMV, EBV…
2) Bacterial → GAS, Diphtheria, Gonococcus
3) Fungal → Candida albicans, Chlamydia trachomatis
4) Parasitic → Toxoplasmosis (rare)

Clinical features
Pharyngitis may occur in different grades of severity.

Milder  Malaise, low grade fever

 Discomfort in the throat
 Pharynx is congested but there is NO lymphadenopathy
Moderate & severe  Headache, malaise, high fever
 Throat pain, dysphagia
 Pharynx shows erythema, exudate and enlargement of tonsils
and lymphoid follicles on the post. pharyngeal wall.
Very severe Edema of soft palate and uvula with enlargement of cervical nodes

It is not possible, on clinical examination, to differentiate viral from bact. infec. but, viral infec. are
generally mild and are accompanied by rhinorrhoea and hoarseness while the bacterial ones are severe.

Diagnosis
 Culture of throat swab is helpful in the diagnosis of bacterial pharyngitis
 Failure to get any bacterial growth suggests a viral etiology

Treatment
Bed rest, plenty of fluids, warm saline gargles or pharyngeal irrigations and analgesics form the
mainstay of treatment
Local discomfort in the throat in severe cases can be relieved by lignocaine viscous before meals to
facilitate swallowing

Specific treatment
 Strep. pharyngitis → penicillin or erythromycin (in allergic individuals)
 Diphtheria → diphtheria antitoxin and penicillin or erythromycin
 Gonococcal pharyngitis → penicillin or tetracycline

Chronic pharyngitis
It is a chr. infla. condition of the pharynx. Pathologically, it is characterised by hypertrophy of mucosa,
seromucinous glands, subepithelial lymphoid follicles and even the muscular coat of the pharynx

Has 2 types
1. Chr. catarrhal pharyngitis
2. Chr. hypertrophic (granular) pharyngitis
Etiology
1. Persistent infection → chronic rhinitis and sinusitis, chronic tonsillitis
2. Mouth breathing → exposes the pharynx to air which has not been filtered, humidified and
adjusted to body temp. making it more susceptible to infec. can be due to:
 Obstruction in the nose → nasal polypi, allergic/vasomotor rhinitis, turbinal hypertrophy,
deviated septum, tumors
 Obstruction in the nasopharynx → adenoids and tumours,
 Protruding teeth → prevent apposition of lips
3. Chronic irritants → smoking, , alcohol, highly spiced food...
4. Environmental pollution→ Smoky or dusty environment or irritant industrial fumes
5. Faulty voice production → excessive use of voice

Clinical presentation
Severity of symptoms varies from person to person.
 Discomfort or pain in the throat → especially in mornings.
 Foreign body sensation in throat
 Tiredness of voice → pts cannot speak for long and has to make undue effort to speak as throat
starts aching. The voice may also lose its quality and may even crack.
 Cough

Signs and physical examination

Chronic catarrhal pharyngitis
 Congestion of posterior pharyngeal wall with engorgement of vessels
 faucial pillars may be thickened.
 ↑ mucus secretion which may cover pharyngeal mucosa

Chronic hypertrophic (granular) pharyngitis

 Pharyngeal wall appears thick and edematous with congested mucosa and dilated vessels.
 Post. pharyngeal wall may have reddish nodules (granular pharyngitis) → due to hypertrophy of
subepithelial lymphoid follicles normally seen in pharynx
 Lateral pharyngeal bands become hypertrophied.
 Uvula may be elongated and appear edematous

Treatment
 Voice rest and speech therapy is essential for those with faulty voice production.
 Warm saline gargles, especially in the morning
 Mandl's paint may be applied to pharyngeal mucosa.
 Cautery of lymphoid granules → throat is sprayed with local anaesthetic and granules are
touched with 10-25% silver nitrate.
 Electrocautery or diathermy of nodules may require general anaesthesia.

Atrophic pharyngitis
is a form of chr. pharyngitis often seen in patients of atrophic rhinitis.
Pharyngeal mucosa along with its mucous glands shows atrophy.
Scanty mucus production leads to formation of crusts which later get infected giving rise to foul smell.
Topic 18. Acute tonsillitis. Specific angina

Acute tonsillitis
The 2 palatine tonsils are an ovoid masses of lymphoid tissue situated in the lat. wall of oropharynx
b/w the ant. and post. pillars and they represent a part of the Waldeyer's ring
Acute tonsillitis often affects school-going children, but can also affects adults.
It is rare in infants and ppl. > 50 years of age

Classification
1) Acute catarrhal (supf) → tonsillitis is part of generalised pharyngitis, mostly in viral infec.
2) Acute follicular → infec. spreads into the crypts which become filled with purulent material,
presenting at the openings of crypts as yellowish spots
3) Acute parenchymatous → tonsil substance is affected. Tonsil is uniformly enlarged and red.
4) Acute membranous → stage ahead of acute follicular tonsillitis when exudation from the
crypts coalesces to form a mem. on the surface of tonsil.

Etiology
Haemolytic streptococcus is the most commonly infecting organism.
Other causes → staph, pneumococci or H. influenzae.
These bacteria may primarily infect the tonsil or may be secondary to a viral infection

Clinical presentation
The symptoms vary with severity of infection. The predominant symptoms are:
 headache, general body aches, malaise and constipation
 Fever +/- chills and rigors
 Sore throat, dysphagia
 Earache → either referred pain from the tonsil or the result of AOM as a complication.
 There may be abd. pain due to mesenteric lymphadenitis simulating a clinical picture of acute
appendicitis

Signs
 Often the breath is foetid and tongue is coasted.
 Hyperaemia of pillars, soft palate and uvula.
 The jugulodigastric lymph nodes are enlarged and tender

Acute follicular tonsillitis → tonsils are red and swollen with yellowish spots of purulent material
presenting at the opening of crypts
Acute mem. tonsillitis → whitish mem. on the medial surface of tonsil which can be easily wiped
away with a swab
Acute parenchymatous tonsillitis → tonsils may be enlarged and congested so much so that they
almost meet in the midline along with some edema of the uvula and soft palate

Diagnosis
 Clinical picture
 General investigations of the blood picture, ESR, urine and heart.
 Bacterial culture.

Differential diagnosis
 scarlet fever, mononucleosis, diphtheria, agranulocytosis, leukaemia
 In unilat. cases → TB, tonsillar tumour, peritonsillitis or abscess, ulceromembranous tonsillitis.
Treatment
Patient is put to bed and encouraged to take plenty of fluids.
 Analgesics (aspirin or paracetamol)
 antobiotic → most infec. are due to strep so penicillin is the drug of choice continued for 7-10d

Complications
1. Chr. tonsillitis with recurrent acute attacks → due to incomplete resolution of acute infec.
Chr. infec. may persist in lymphoid follicles of the tonsil in the form of microabscesses.
2. Peritonsillar abscess.
3. Parapharyngeal abscess.
4. Cervical abscess → due to suppuration of jugulodigastric L.N.
5. Acute otitis media → ecurrent attacks of AOM may coincide with recurrent tonsillitis.
6. Rheumatic fever & Acute GN
7. Subacute bacterial endocarditis → acute tonsillitis in pt. with valvular heart disease may be
complicated by endocarditis. It is usually due to S. viridans infec.

Vincent’s Angina (Angina ulceromembranacea)

Disease characterized by ulceration of the mucosa of the tonsils,pharynx, and mouth, caused by
spirochete (Vincent's spirillum ) in symbiosis with a fusiform bacillus.
 The course is short. The prognosis good.

Symptoms:
 unilateral pain on swallowing
 a feeling of a foreign body in the throat
 an ulcer on the upper pole of one tonsil
 oral fetor
 NO FEVER

Diagnosis: characteristic clinical picture & bacterial culture

Treatment: penicillin for 6 days.

Topic 19. Chronic tonsillitis and its secondary consequences

Chr. tonsillitis can occur as a complication of acute tonsillitis or be a subclinical tonsils infec. w/o an
acute attack
 Pathologically, microabscesses walled off by fibrous tissue have been seen in the lymphoid
follicles of the tonsils.
 Mostly affects children and young adults. Rarely occurs > 50 years.
 Chr. infection in sinuses or teeth may be a predisposing factor.

Types

Features Examination
Chr. follicular Tonsillar crypts are full of infected cheesy Yellowish spots (beads) of pus on
material the medial surface of tonsil
Chr. hyperplasia of lymphoid tissue. Tonsils may show varying degree
parenchymatous Tonsils are very much enlarged and may of enlargement.
interfere with speech, deglutition and resp. Sometimes they meet in the
 Attacks of sleep apnoea may occur. midline
 Long-standing cases develop features
of cor pulmonale.

Chr. fibroid tonsils are small but infected, with history Tonsils are small but pressure on
of repeated sore throats the anterior pillar expresses frank
pus or cheesy material

Clinical Features
 Recurrent attacks of sore throat or acute tonsillitis.
 Chr. irritation in throat with cough.
 Bad taste in mouth and foul breath (halitosis) due to pus in crypts.
 Thick speech, difficulty in swallowing and choking spells at night (when tonsils are large and
obstructive)

Examination
 Flushing of anterior pillars compared to the rest of the pharyngeal mucosa is an important sign of
chronic tonsillar infection.
 Enlargement of jugulodigastric lymph nodes is a reliable sign of chronic tonsillitis.
During acute attacks, the nodes enlarge further and become tender

Treatment
 Conservative treatment consists of attention to general health, diet, treatment of co-existent
infection of teeth, nose and sinuses.
 Tonsillectomy is indicated when tonsils interfere with speech, deglutition and respiration or
cause recurrent attacks

Complications
1) Peritonsillar abscess
2) Parapharyngeal abscess
3) Intratonsillar abscess
4) Tonsilloliths
5) Tonsillar cyst
6) Focus of infection in rheumatic fever, acute glomerulonephritis, eye and skin disorders.
Peritonsillar Abscess (Quinsy)
Infla. spreads from the tonsillar parenchyma to the parapharyngeal spaces.
From here it may extend as a descending internal cervical phlegmone → mediastinitis!!

Symptoms:
Rapidly ↑ difficulty in swallowing after a symptom free interval of a few days following tonsillitis.
 high fever
 Severe pain → pts. refuses to eat, to drink, the pain irradiates to the ear
 Trismus
 Sialorrhoe
 Indistinct speech
 the head is held over the diseased side

Local findings include swelling, redness and protrusion of the tonsil, the faucal pillar, the soft palate
and the uvula.
Diagnosis: clinical picture, chest X-ray, Blood test (CBC, ESR)
Treatment: involves drainage and tonsillectomy

Tonsilloliths (calculus of the tonsil)

It is seen in chr. tonsillitis when its crypt is blocked with retention of debris → deposition of
inorganic salts of Ca and Mg → formation of a stone.
It may gradually enlarge and then ulcerate through the tonsil.

Tonsilloliths are more often seen in adults and give rise to local discomfort or foreign body sensation.
They are easily dg. by palpation or gritty feeling on probing.
Treatment is simple removal of the stone or tonsillectomy, if that be indicated for associated sepsis or
for the deeply set stone which cannot be removed

Intratonsillar abscess
It is accumulation of pus within the substance of tonsil. It usually follows blocking of the crypt
opening in acute follicular tonsillitis.
 There is marked local pain and dysphagia.
 Tonsil appears swollen and red.
 Treatment: antibiotics and drainage of the abscess, later tonsillectomy should be performed

Tonsillar cyst
It is due to blockage of a tonsillar crypt and appears as a yellowish swelling over the tonsil.
 Very often it is asymptomatic
 Can be easily drained
Topic 20. Indication for adenectomy and tonsilectomy

Adenoidectomy
May be indicated alone or in combination with tonsillectomy.
In the latter event, adenoids are 1st removed and the nasopharynx packed before starting tonsillectomy

Indications
1) Adenoid hypertrophy causing snoring, mouth breathing, sleep apnoea syndrome or speech abnor.
(for ex. rhinolalia clausa).
2) Recurrent rhinosinusitis
3) Chr. secretory otitis media associated with adenoid hyperplasia.
4) Recurrent ear discharge in benign CSOM associated with adenoiditis/adenoid hyperplasia
5) Dental malocclusion → adenoidectomy does not correct dental abnor. but will prevent its
recurrence after orthodontic treatment

Contraindications
 Cleft palate or submucous palate → adenoids removal causes velopharyngeal insuff. in such cases.
 Haemorrhagic diathesis
 Acute infec. of URT

Tonsillectomy
Indications are divided into absolute, relative and part of another operation.

Absolute
1) Recurrent throat infec. → most common indication. Are further defined as EITHER:
 ≥ 7 episodes in one year
 5 episodes per year for 2 years
 3 episodes per year for 3 years
 ≥ 2 weeks of lost school or work in one year.
2) Peritonsillar abscess → in children, tonsillectomy is done 4-6w after abscess has been treated.
In adults, second attack of peritonsillar abscess forms the absolute indication.
3) Tonsillitis causing febrile seizures
4) Hypertrophy of tonsils causing
 AW obstruction (sleep apnoea)
 Difficulty in deglutition
 Interference with speech.
5) Suspicion of malignancy → unilaterally enlarged tonsil may be a lymphoma in children and an
epidermoid carcinoma in adults. An excisional biopsy is done

Relative
1) Diphtheria carriers, who do not respond to antibiotics
2) Strep. carriers, who may be the source of infec. to others.
3) Chr. tonsillitis with bad taste or halitosis which is unresponsive to medical treatment.
4) Recurrent strep. tonsillitis in a pts. with valvular heart disease.

As a Part of Another Operation

1) Palatopharyngoplasty which is done for sleep apnoea sy.
2) Glossopharyngeal neurectomy → tonsil is removed first, then CN IX is severed in the tonsil bed
3) Removal of styloid process
Topic 21. Tumors of the mesopharynx and hypopharynx.

Tumors of the oropharynx

Benign tumors
Are far less common compared to malignant tumors.
Lipoma, fibroma and neuroma are rare benign tumors

Papilloma
It is usually pedunculated, arises from the tonsil, soft palate or faucial pillars.
 Often asymptomatic, it may be discovered accidentally by the patient or the physician.
 When large, it causes local irritation in the throat.
 Treatment is surgical excision

Haemangioma
Can occur on the palate, tonsil, posterior and lateral pharyngeal wall.
 It may be of capillary or cavernous type.
 Capillary haemangioma or asymptomatic cavernous haemangioma may be left alone.
 It is treated only if it is ↑ in size or giving symptoms of bleeding and dysphagia.
 Treatment is diathermy coagulation or injection of sclerosing agents. Cryotherapy or laser
coagulation is very effective

Pleomorphic Adenoma
Mostly seen submucosally on the hard or soft palate. It is potentially malignant and should be
excised totally

Mucous Cyst
It is usually seen in the vallecula.
 It is yellow in appearance and may be pedunculated or sessile.
 When large, it causes foreign body sensation in the throat.
 Treatment is surgical excision, if pedunculated, or incision + drainage with removal of cyst wall

Malignant tumors
The common sites of malignancy in the oropharynx are:
1. Post. 1/3 (or base) of tongue.
2. Tonsil and tonsillar fossa.
3. Faucial palatine arch → soft palate and anterior pillar.
4. Posterior and lateral pharyngeal wall.

Gross appearances of the tumour can be divided into 4 types:

 Superficially spreading
 Exophytic
 Ulcerative
 Infiltrative

The first 2 types are seen in the palatine arch, they are rarely associated with metastasis.
Ulcerative and infiltrative types often involve the base of tongue and tonsil. They have poor
prognosis and deeply invade the adjoining structures and have marked tendency for regional
metastasis.
Histologically, the tumours may be
1) Squamous cell carcinoma → Shows various grades of differentiation (well, moderately or
poorly diff.) and is the most common variety.
2) Lymphoepithelioma → A poorly differentiated variant of the above, with admixture of
lymphocytes, which do not show any features of malignancy. This is often seen in tonsil, base
of tongue and vallecula.
3) Adenocarcinoma → It arises from minor salivary glands. It is mostly seen on the palate and
fauces.
4) Lymphomas → Both Hodgkin and non-Hodgkin lymphomas arise from the tonsil and base of
tongue. They are seen in the young adults and sometimes in the children.
Enlarged cervical nodes may co-exist.

Treatment
Depend upon the site and extent of disease, patient's general condition, philosophy and experience of
the treating surgeon and facilities available at a particular centre. The various options are:
 Surgery alone
 Radiation alone
 Combination of surgery and radiotherapy
 Chemotherapy alone or as an adjunct to surgery or radiotherapy
 Palliative therapy.
Topic 22. Dysphagia and its management by the family doctor

Dysphagia is difficulty in swallowing.

The term odynophagia is used when swallowing causes pain, it is more marked in ulcerative and
infla. lesions of food passages (oral cavity, oropharynx and esophagus)

Etiology
The cause of dysphagia may be divided into:
1. pre-esophageal → due to disturbance in the oral or pharyngeal phase of deglutition
2. esophageal → when disturbance is in oesophageal phase.

This classification is clinically useful as most of the pre-esophageal causes can be easily excluded
by physical exam. while esophageal ones require investigation

Pre-esophageal Causes
Oral phase
Normally, food must be masticated, lubricated with saliva, converted into a bolus by movements of
tongue and then pushed into the pharynx by elevation of the tongue against the hard palate.
Any disturbance in these events will cause dysphagia → cause may be:
 Disturbance in mastication → trismus, mandible fractures, tumors of the upper or lower jaw,
disorders of TMJ.
 Disturbance in lubrication → xerostomia, Mikulicz disease.
 Disturbance in mobility of tongue → paralysis of tongue, painful ulcers, tongue tumors,
lingual abscess, total glossectomy.
 Defects of palate → cleft palate, oronasal fistula.
 Lesions of buccal cavity and floor of mouth → stomatitis, ulcerative lesions, Ludwig's angina.

Pharyngeal phase
For a normal swallow, food should enter the pharynx and be directed towards esophageal opening.
All unwanted communications into the nasopharynx, larynx, oral cavity should be closed.
Disturbances in this phase can arise from:
 Obstructive lesions of pharynx → tumours of tonsil, soft palate, pharynx, base of tongue,
supraglottic larynx, or even obstructive hypertrophic tonsils.
 Inflammatory conditions → acute tonsillitis, peritonsillar abscess, retro or para-pharyngeal
abscess, acute epiglottitis, edema larynx.
 Spasmodic conditions → tetanus, rabies.
 Paralytic conditions → for ex. paralysis of soft palate due to diphtheria, bulbar palsy, CVA.

Esophageal Causes
The lesions may lie in the lumen, in the wall or outside the wall of esophagus
1) Lumen Obstruction → atresia, foreign body, strictures, benign or malignant tumours.
2) Wall → acute or chr. esophagitis, or motility disorders which are:
 Hypomotility → achalasia, scleroderma, amyotrophic lateral sclerosis.
 Hypermotility → cricopharyngeal spasm, diffuse oesophageal spasm.
3) Outside the wall → lesions cause obstruction by pressing on the esophagus from outside:
 Hypopharyngeal diverticulum
 Hiatus hernia
 Cervical osteophytes
 Thyroid lesions→ enlargement, tumors, Hashimoto's thyroiditis
 Mediastinal lesions → tumors, lymphadenomegaly, aortic aneurysm, cardiomegaly
 Vascular rings (dysphagia lusoria)
Investigations
History → detailed history is of paramount importance. Ascertain, if dysphagia is of
 Sudden onset → foreign body or impaction of food on a preexisting stricture or malignancy,
neurological disorders
 Progressive → malignancy
 Intermittent → spasms or spasmodic episodes over an organic lesion
 More to liquids → paralytic lesions
 More to solids and progressing even to liquids → malignancy or stricture
 Intolerance to acid food or fruit juices → ulcerative lesions

Note any associated symptoms such as:

 Regurgitation and heart burn (hiatus hernia)
 Regurgitation of undigested food while lying down, with cough at night (hypopharyngeal
diverticulum)
 Aspiration into lungs (laryngeal paralysis)
 Aspiration into the nose (palatal paralysis)

Clinical examination
Examination of oral cavity, oropharynx, and larynx and hypopharynx can exclude most of the
pre-esophageal causes of dysphagia.
Exam. of the neck, chest and nervous system, including CN should also be undertaken

Blood examination
Haemogram is important in the dg. and tr. of Plummer-Vinson sy. and to know pt. nutritional status

Radiography
 X-ray chest → exclude cardiovascular, pul. and mediastinal diseases.
 Lateral view neck → exclude cervical osteophytes and any soft tissue lesions of post-cricoid
or retropharyngeal space.
 Barium swallow → useful in the dg. of malignancy, cardiac achalasia, strictures, diverticula,
hiatus hernia or esophageal spasms. Combined with fluoroscopic control or cineradiography, it
can help in the diagnosis of motility disorders of esophageal wall or sphincters.

Manometric and pH studies

A pressure transducer along with a pH electrode and an open-tipped catheter is introduced into the
esophagus to measure the pressures in the esophagus and at its sphincters. A
cid reflux into the esophagus is measured by pH electrode. It also measures the effectiveness of
oesophagus to clear the acid load after acid solution is put in the oesophagus.
These studies help in motility disorders, GERD and to find whether esophageal spasms are
spontaneous or acid-induced

Esophagoscopy
Gives direct exam. of esophageal mucosa and permits biopsy specimens.
Flexible fibre-optic or rigid scopes can be used

Other investigations
 Bronchoscopy (for bronchial carcinoma)
 Cardiac catheterisation (for vascular anomalies)
 Thyroid scan (for malignant thyroid)
Topic 1. Functional anatomy of the larynx

The larynx lies in front of the hypopharynx opposite the 3rd – 6th cervical vertebrae.
 It moves vertically and in anteroposterior direction during swallowing and phonation.
 It can also be passively moved from side to side producing a characteristic grating sensation
called laryngeal crepitus.
 In an adult, the larynx ends at the lower border of C6 vertebra.

Laryngeal Cartilages
Larynx has 3 unpaired and 3 paired cartilages
 Unpaired: Thyroid, cricoid, epiglottis
 Paired: Arytenoid, corniculate, cuneiform

Thyroid
the largest. Its 2 alae meet anteriorly forming an angle
of 90° in males and 120° in females.
 Vocal cords are attached to mid. of thyroid angle.
 Most of laryngeal foreign bodies are arrested
above the vocal cords, above the middle of
thyroid cartilage and an effective AW can be
provided by cricothyrotomy.

Cricoid
is the only cartilage forming a complete ring.
Its posterior part is expanded to form a lamina while anteriorly it is narrow forming an arch.

Epiglottis
Is a leaf-like, yellow, elastic cartilage forming anterior wall of laryngeal inlet.
It is attached to the hyoid bone body by hyoepiglottic lig. which divides it into suprahyoid and
infrahyoid epiglottis.
 A stalk-like process of epiglottis (petiole) attaches the epiglottis to the thyroid angle.
 The ant. surface is separated from thyrohyoid mem. and upper part of thyroid cartilage by a
potential space filled with fat-the pre-epiglottic space → may be invaded in cc. of supraglottic
larynx or base of tongue.

Arytenoid cartilages
Each arytenoid cartilage is pyramidal in shape, and has:
1. base → articulates with cricoid cartilage
2. muscular process → directed laterally to give attachment to intrinsic laryngeal muscles
3. vocal process → directed anteriorly, giving attachment to vocal cord
4. apex → supports the corniculate cartilage.

Corniculate cartilages (of Santorini) → each articulates with the apex of arytenoid cartilage.

Cuneiform cartilages (of Wrisberg) → rod shaped, each is situated in aryepiglottic fold in front of
corniculate cartilage and provides passive supports to the fold.

Thyroid, cricoid and most of the arytenoid cartilages are hyaline cartilages
Epiglottis, corniculate, cuneiform and tip of arytenoid near the corniculate are fibroelastic cartilage.
Hyaline cartilages can undergo ossification → begins at 25 years in thyroid, a little later in cricoid
and arytenoids, and is complete by 65 years of age
Laryngeal Joints
Cricoarytenoid joint → synovial joint surrounded by capsular lig. which is formed b/w the base of
arytenoid and a facet, on the upper border of cricoid lamina.
2 types of movements occur in this joint:
1. rotator → arytenoid cartilage moves around a vertical axis, abducting or adducting the vocal cord
2. gliding → one arytenoid glides towards the other cartilage or away from it, closing or opening
the post. part of glottis

Cricothyroid joint → also synovial, each is formed by the inf. cornua of thyroid cartilage with a
facet on the cricoid cartilage

Laryngeal Membranes

Extrinsic Membranes
 Thyrohyoid mem. → connects thyroid cartilage to hyoid bone. It is pierced by sup. laryngeal
vessels and int. laryngeal n.
 Cricothyroid mem. → connects thyroid cartilage to cricoid cartilage.
 Cricotracheal mem. → connects cricoid cartilage to the first tracheal ring.

Intrinsic mem.
 Cricovocal mem. → triangular fibroelastic mem.
- Upper border is free and stretches b/w middle of thyroid angle to the vocal process of
arytenoid and forms the vocal ligament.
- Lower border attaches to the arch of cricoid cartilage. From its lower attachment the mem.
proceeds upwards and medially and thus, with its fellow on the opposite side, forms conus
elasticus where subglottic foreign bodies sometimes get impacted.
 Quadrangular mem. → lies deep to mucosa of aryepiglottic folds and is not well defined.
It stretches b/w the epiglottic and arytenoid cartilages.
Its lower border forms the vestibular ligament which lies in the false cord.

Muscles of Larynx
They are of 2 types → intrinsic, which attach laryngeal cartilages to each other, and extrinsic, which
attach larynx to the surrounding structures

Intrinsic muscles may act on vocal cords or laryngeal inlet

Acting on vocal cords

Abductors Posterior cricoarytenoid
Adductors Lateral cricoarytenoid
Interarytenoid (transverse arytenoid)
Thyroarytenoid (external part)
Tensors Cricothyroid
Vocalis (internal part of thyroarytenoid)
Acting on laryngeal inlet
Openers of laryngeal inlet Thyroepiglottic (part of thyroarytenoid)
Closers of laryngeal inlet Interarytenoid (oblique part)
Aryepiglottic (posterior oblique part of interarytenoids)
Extrinsic muscles → connect the larynx to the neighbouring structures and are divided into elevators
or depressors of larynx.
Depressors
 Sternohyoid
 sterno-thyroid
 omohyoid
Elevators
Primary elevators act directly as they are attached to the thyroid cartilage and include
 stylopharyngeus
 Salpingopharyngeus
 palatopharyngeus
 thyrohyoid.

Secondary elevators act indirectly as they are attached to the hyoid bone and include
 mylohyoid (main)
 digastrics
 stylohyoid
 geniohyoid.

Cavity of the Larynx

Laryngeal cavity starts at the laryngeal inlet where it communicates with the pharynx and ends at the
lower border of cricoid cartilage where it is continuous with the lumen of trachea.
2 pairs of folds (vestibular and vocal), divide the cavity into 3 parts: vestibule, ventricle and
subglottic space

Inlet of larynx
Is an oblique opening bounded anteriorly by free margin of epiglottis, on the sides, by aryepiglottic
folds and posteriorly by interarytenoid fold

Vestibule
It extends from laryngeal inlet to vestibular folds.
 Ant. wall is formed by posterior surface of epiglottis
 Sides by the aryepiglottic folds
 Post. wall by mucous membrane over the anterior surface of arytenoids

Ventricle (sinus of larynx)

Is a deep elliptical space b/w vestibular and vocal folds, also extending a short distance above and
lateral to vestibular fold.
The saccule is a diverticulum of mucous mem. which starts from the anterior part of ventricular
cavity and extends upwards b/w vestibular folds and lamina of thyroid cartilage.
When abnormally enlarged and distended, it may form a laryngocele → an air containing sac which
may present in the neck.

Subglottic space (infraglottic larynx) → extends from vocal cords to lower border of cricoid cart.

Vestibular folds (false vocal cords)

There are 2, each is a fold of mucous mem. extending anteroposteriorly across the laryngeal cavity.
It contains vestibular lig., a few fibres of thyroarytenoideus mm. and mucous glands

Vocal folds (true vocal cords)

2 pearly-white sharp bands extending from mid. of thyroid angle to the vocal processes of arytenoids.
Each vocal cord consists of a vocal lig. which is the true upper edge of cricovocal mem. covered by
closely bound mucous mem. with scanty subepithelial CT
Glottis (rima glottidis)
Elongated space b/w vocal cords anteriorly, and vocal processes and base of arytenoids posteriorly
Anteroposteriorly. It is the narrowest part of laryngeal cavity.
Ant. 2/3 of glottis are formed by mem. cords while post. 1/3 by vocal processes of arytenoids.
Size and shape of glottis varies with the movements of vocal cords.

Blood supply
 Laryngeal branch of sup. thyroid a.
 Cricothyroid branches of the sup. thyroid a.
 Laryngeal branch of inf. thyroid a.

Nerve supply of larynx

Recurrent laryngeal nerve
 Right RLN arises from the vagus at the level of subclavian artery, hooks around it and then
ascends b/w the trachea and esophagus.
 Left RLN arises from the vagus in the mediastinum at the level of arch of aorta, loops around it
and then ascends into the neck in the tracheo-esophageal groove → left recurrent laryngeal n. has
a much longer course which makes it more prone to paralysis compared to R one

Superior laryngeal nerve

Arises from inf. ganglion of the vagus, descends behind int. carotid a. and, at the level of greater
cornua of hyoid bone, divides into ext. & int. branches.
 External br. → supplies cricothyroid muscle
 Internal br. → pierces thyrohyoid mem. and supplies sensory innervation to larynx and
hypopharynx

Motor
All the muscles which move the vocal cord (abductors, adductors or tensors) are supplied by the RLN
except the cricothyroid muscle which receives its innervation from the ext. laryngeal n.

Sensory
 Above vocal cords → internal laryngeal n.
 Below vocal cords → recurrent laryngeal n.

Functions of the larynx

Respiration
 Glottis is the narrowest part of resp. tract (the space b/w the 2 vocal folds)
 The glottis are controlled by abductors and adductors.
 The glottis become large as inspiration and become small as expiration

Sound: Larynx produces sound vibration, modified by mouth, pharynx, nose, chest. Including:

Protection of the lower airway passage (“three defence line”)

1. protective to prevent during swallowing
2. laryngeal closure (resembles as sphincter with the true & false cords)
3. arytenoid &the aryepiglottis fold all coming together,

Closure of the larynx also allows the buildup of intrathoracic pressure, important in defecation,
lifting, deliver or straining for any reason
Topic 2. Malformations of the larynx

1) Laryngomalacia (congenital laryngeal stridor)

2) Congenital vocal cord paralysis
3) Congenital subglottic stenosis → see topic 20
4) Laryngeal web
5) Subglottic haemangioma
6) Laryngo-esophageal cleft
7) Laryngocele
8) Laryngeal cyst

Laryngomalacia (congenital laryngeal stridor)

It is the most common congenital abnor. of the larynx, characterised by excessive flaccidity of
supraglottic larynx which is sucked in during inspiration producing stridor and sometimes cyanosis.
 Pathophysiology: immature cartilage, abnormal calcium metabolism
 Manifests at birth or soon after, usually disappears by 2 years of age (self limiting)

Clinical presentation
 Stridor is ↑ on crying but subsides on placing the child in prone position
 The voice and cry are normal.

Diagnosis
Direct laryngoscopy shows elongated epiglottis, curled upon itself (omega-shaped Ω), floppy
aryepiglottic folds and prominent arytenoids.
Flexible laryngoscope is very useful to make the dg.

Treatment → Is mostly conservative

 epiglottoplasty (removes excess tissue),
 Tracheostomy may be required for some cases of severe resp. obstruction

Congenital vocal cord paralysis

Results from birth trauma when recurrent laryngeal n. is stretched during breech or forceps delivery
or can result from anomalies of the CNS

Laryngeal web
It is due to incomplete recanalisation of larynx. Mostly, the web is seen between the vocal cords and
has a concave posterior margin.
Presenting features are airway obstruction, weak cry or aphonia dating from birth.

Treatment depends on the thickness of the web.

 Thin webs can be cut with a knife or CO2 laser.
 Thick ones may require excision via laryngofissure and placement of a silicon keel and
subsequent dilatations

Subglottic haemangioma
Occurs due to incomplete recanalization at 8th week of embryological development
Types: supraglottic (2%), glottic (75%), subglottic (7%)

Clinical presentation
Patient is asymptomatic till 3-6 months of age when haemangioma begins to ↑ in size.
 Patient may present with inspiratory stridor but has a normal cry.
 Agitation of the patient or crying may ↑ AW obstruction due to venous filling.
 ~ 50% of the children have associated cutaneous haemangiomas.
 Some patients have associated mediastinal haemangioma
Diagnosis
 Direct laryngoscopy shows reddish-blue mass below the vocal cords.
 Biopsy may be (not always) associated with haemorrhage.

Treatment
 Tracheostomy and observation → many haemangiomas involute spontaneously.
 Steroid (Dexamethasone)
 CO2 laser excision if lesion is small

Laryngo-esophageal cleft
Due to failure of the fusion of cricoid lamina
 Patient presents with repeated aspiration and pneumonitis.
 Coughing, choking and cyanosis are present at the time of feeding
 Associated with TE fistulas, laryngomalacia, congenital heart defects, cleft lip/palate, Down
syndrome, others

Classifications
I. Supraglottic arytenoid only
II. extends past true vocal fold
III. extends past cervical trachea
IV. extends past thoracic trachea

Treatment
 Consider tracheotomy
 Endoscopic repair for Type I & II, anterior vs. lateral
external approaches

Laryngocele
It is dilatation of laryngeal saccule and extends b/w thyroid cartilage and the ventricle.
 It may be internal, external or combined.
 Treatment is endoscopic or external excision

Laryngeal cyst
Arises in aryepiglottic fold and appears as bluish, fluid-filled smooth swelling in supraglottic larynx.
 Resp. obstruction may necessitate tracheostomy.
 Needle aspiration or incision and drainage of cyst provides an emergency AW.
 Treatment is deroofing the cyst or excision with CO2 laser
Topic 3. Traumas of the larynx. Treatment of laryngeal trauma

Etiology
1. Most common cause is MVA when neck strikes against the steering wheel or the instrument panel.
2. Blow or kick on the neck
3. Neck striking against a stretched wire or cable
4. Strangulation
5. Penetrating injuries with sharp instruments or GSW

Pathology
The degree and severity of damage will vary from slight bruises externally or the tear and laceration of
mucosa internally to a comminuted fracture of the laryngeal framework. The wound may be
compounded externally, due to break in the skin, or internally by mucosal tears. Laryngeal fractures
are common after 40 years of age because of calcification of the laryngeal framework. In children,
cartilages are more resilient and escape injury

Pathological changes that may be seen in laryngeal trauma are:

 Haematoma and edema of supraglottic or subglottic region.
 Tears in laryngeal or pharyngeal mucosa leading to subcutaneous emphysema.
 Dislocation of cricoarytenoid joints → arytenoid cart. may be displaced ant. or be dislocated
 Dislocation of cricothyroid joint → may cause recurrent laryngeal n. paralysis
 Fractures of the hyoid bone
 Fractures of thyroid cart. → may be vertical or transverse.
- Fracture of upper part may result in avulsion of epiglottis and one or both false cords.
- Fractures of lower part may displace or disrupt the true vocal cords.
 Fractures of cricoid cartilage
 Fractures of upper tracheal rings
 Trachea may separate from the cricoid and retract into upper mediastinum

Clinical Features
Symptoms of laryngotracheal injury would vary, greatly depending on the structures damaged and the
severity of damage. They include:
1. Resp. distress
2. Hoarseness of voice or aphonia
3. Painful and difficult swallowing accompanied by aspiration of food
4. Local pain in the larynx → marked on speaking or swallowing.
5. Haemoptysis → usually the result of tears in laryngeal or tracheal mucosa.

External signs include

1. Bruises or abrasions over the skin.
2. Palpation of the laryngeal area is painful.
3. SQ emphysema due to mucosal tears → may ↑ on coughing.
4. Flattening of thyroid prominence → thyroid notch may not be palpable.
5. Fracture displacements of thyroid or cricoid cartilage or hyoid bone → dap may be felt b/w the
fractured fragments.
6. Bony crepitus b/w fragments of hyoid bone, thyroid or cricoid cart.
7. Separation of cricoid cartilage from larynx or trachea
Diagnosis
 Indirect laryngoscopy
 Direct laryngoscopy → rarely informative in early period following injury.
 X-rays Soft tissue lateral film of the neck → very useful and may reveal SQ emphysema, swelling
of laryngeal mucosa, displacement of epiglottis, fracture displacements of hyoid bone, thyroid and
cricoid cartilages or change in the configuration of air column.
 CT → valuable in assessing moderately severe or severe injuries of larynx.
 CXR for pneumothorax and gastrograffin swallow for oesophageal tears may be required.

Treatment

Conservative
 Patient should be hospitalised and observed for respiratory distress.
 Voice rest is essential.
 Humidification of inspired air is essential.
 Steroid therapy should be started immediately and in full dose. It helps to resolve oedema and
haematoma and prevent scarring and stenosis.
 Antibiotics are given to prevent perichondritis and cartilage necrosis.

Surgical
 Tracheostomy → ET intubation may be difficult and hazardous.
 Open reduction → ideally done 3-5 days after injury and if possible should not be delayed >10d
Topic 4. Functional disorders of the larynx

Functional disorders can be classified according to:

1) Nervous (nerve paralysis)
2) Myogenic (fibrosis)
3) Articular (ankylosis of the arytenoids joint)
They are all characterized by voice disorders → dysphonia, aphonia, dyspnea (audible stridor)

Laryngeal Paralysis
Classification
Laryngeal paralysis may be unilateral or bilateral, and may involve:
1) Recurrent laryngeal n.
2) Superior laryngeal n.
3) Both (combined or complete paralysis)

Etiology
1. Supranuclear (Rare)
2. Nuclear → involvement of nucleus ambiguus in the medulla due to vascular, neoplastic, motor
neurone disease, polio, and syringobulbia.
In nuclear lesions, there would be associated paralysis of other CN and neural pathways.
3. High vagal lesions → Vagus may be involved in the skull, at the exit from jugular foramen or
in parapharyngeal space (intracranial tumor, skull base fracture…)
4. Low vagal or RLN
5. Systemic disease → DM, syphilis, diphtheria, typhoid, strep. or viral infec., lead poisoning.
6. Idiopathic → in ~ 30% of cases

Recurrent laryngeal n. paralysis

Unilateral injury to RLN results in ipsilateral paralysis of all the int. mm. except the cricothyroid
 Causes include neck trauma, thyroid disease or surgery, Cervical lymphadenopathy,
 1/3 of pts. are asymptomatic
 Symptoms include some change in voice but no problems of aspiration or airways obstruction
 Generally no treatment is required

Bilatreral injury to RLN

 Neuritis or surgical trauma (thyroidectomy) are the most common causes
 All the intrinsic muscles of larynx are paralysed
 Dyspnoea and stridor but the voice is good
 Treatment include Tracheostomy and/or surgical repair of the vocal cords

Superior laryngeal n. paralysis

Isolated lesions of this nerve are rare, it is usually a part of combined paralysis
Paralysis of superior laryngeal n. causes paralysis of cricothyroid mm. and ipsilateral anaesthesia of
the larynx above the vocal cord.
Paralysis of cricothyroid can also occur when ext. laryngeal n. is involved in thyroid surgery, tumors,
neuritis or diphtheria.
 Symptoms: aspiration, loss of power over the voice, inability to sing
 Diagnosis: laryngoscope shows flaccidity of the affected vocal fold., the glottis doesn’t close
completely on phonation
 Management: steroid and speech therapy.

Combined lesion of the laryngeal nerves

Central or peripheral damage to the vagus causing flaccid paralysis with immobility of the affected
 Vocal cord in the intermediate position.
 Dysphonia, aphonia, aspiration pneumonia, dyspnea in exertion, inability to cough
 Speech therapy, Tracheostomy, Epiglottopexy, Total laryngectomy
Topic 5. Acute and chronic inflammation of the larynx

Acute laryngitis
Acute laryngitis may be infectious or non-infectious
1) The infec. type is more common and usually follows URTI → begins as viral infec. soon
followd by bact. infec. by S. pneumoniae, H. influenzae or S. aureus.
Exanthematous fevers (measles, chickenpox whooping cough) are also associated with laryngitis
2) The non-infec. type is due to:
 Vocal abuse
 Allergy
 Thermal or chemical burns to larynx due to inhalation or ingestion of various substances
 Laryngeal trauma such as endotracheal intubation

Clinical presentation
Symptoms are usually abrupt in onset and consist of:
 Hoarseness → may lead to complete loss of voice.
 Discomfort or pain in throat, Dry, irritating cough
 General symptoms of head, cold, rawness or dryness of throat, malaise and fever if laryngitis
has followed viral URTI.

Diagnosis and Laryngeal appearances

Vary with severity of disease.

Early stages  Erythema and edema of epiglottis, aryepiglottic folds, arytenoids and
ventricular bands
 Vocal cords appear white and near normal and stand out in contrast to
surrounding mucosa
Later  hyperaemia and swelling ↑
 Vocal cords also become red and swollen
 Subglottic region also gets involved
 Sticky secretions are seen b/w the cords and interarytenoid region

Treatment
 Vocal rest → most important single factor (use of voice during acute laryngitis may lead to
incomplete or delayed recovery)
 Avoidance of smoking and alcohol
 Steam inhalations
 Cough sedative → to suppress troublesome irritating cough.
 Antibiotics → in 20 infection with fever and toxaemia or purulent expectoration.
 Analgesics, Steroids (useful in laryngitis following thermal or chemical burns).

Chronic Laryngitis without Hyperplasia (Chronic Hyperaemic Laryngitis)

Diffuse infla. condition symmetrically involving the whole larynx → true cords, ventricular bands,
interarytenoid region and root of the epiglottis

Etiology
1. It may follow incompletely resolved acute simple laryngitis or its recurrent attacks.
2. Presence of chr. infec. in paranasal sinuses, teeth and tonsils and the chest are important
contributory causes.
3. Occupational factors → exposure to dust and fumes such as in miners…
4. Smoking and alcohol.
5. Persistent trauma of cough as in chr. lung diseases.
6. Vocal abuse.
Clinical Features
 Hoarseness → commonest complaint
 Constant hawking → dryness and intermittent tickling in the throat
 Discomfort in the throat and dry, irritating cough

Diagnosis
Laryngeal examination revels hyperaemia of laryngeal structures.
Vocal cords appear dull red and rounded. Flecks of viscid mucus are seen on the vocal cords and
interarytenoid region

Treatment
 Elimination of URTI or LRTI
 Avoidance of irritating factors (smoking, alcohol or polluted environment..)
 Voice rest and speech therapy
 Steam inhalations
 Expectorants

Chronic Hypertrophic Laryngitis (Chronic Hyperplastic Laryngitis)

It may be either a diffuse and symmetrical process or a localised one, appearing like a tumor
 Localised form can presents as dysphonia plica ventricularis, vocal nodules, vocal polyp,
Reinke's edema and contact ulcer
 Etiology is same as discussed under chronic laryngitis without hyperplasia
 This disease mostly affects males 30-50 years of age.

Pathology
Pathological changes start in the glottic region and later may extend to ventricular bands, base of
epiglottis and even subglottis.
Mucosa, submucosa, mucous gl. and in later stages intrinsic laryngeal mm. & j. may be affected.

Clinical Features
 Hoarseness, tiredness of voice
 Discomfort in throat when voice has been used for long period of time
 Constant desire to clear the throat
 Dry cough

Examination → changes are often diffuse and symmetrical

Symptoms
 Laryngeal mucosa, in general, is dusky red and thickened.
 Vocal cords appear red and swollen. Their edges lose sharp demarcation and appear rounded.
In late stages, cords become bulky and irregular giving nodular appearance.
 Ventricular bands appear red and swollen and may be mistaken for prolapse or eversion of the
ventricle.

Treatment
 Conservative → same as for chronic laryngitis without hyperplasia
 Surgical → stripping of vocal cords, removing the hyperplastic and edematous mucosa, may be
done in selected cases. One cord is operated at a time.
Topic 6. Acute laryngitis in childhood

Acute epiglotitis (Supraglottic Laryngitis)

Acute infla. confined to supraglottic structures → epiglottis, aryepiglottic folds and arytenoids.
 There is marked edema of these structures which may obstruct the AW
 Serious condition and affects children of 2-7 years of age but can also affect adults.
 H. influenzae B is the most common organism responsible for this condition in children

Clinical Features
Onset of symptoms is abrupt with rapid progression. Patient's condition may rapidly deteriorate
 Fever (due to septicaemia)
 Sore throat and dysphagia → common presenting symptoms in adults.
 Dyspnoea and stridor → common presenting symptoms in children. Rapidly progressive and
may prove fatal unless relieved.

Diagnosis
 Depressing the tongue with a tongue depressor may show red and swollen epiglottis.
 Indirect laryngoscopy may show edema and congestion of supraglottic structure → should be
avoided for fear of precipitating complete obstruction.
 Lateral soft tissue X-ray of neck may show swollen epiglottis (thumb sign)

Treatment
Hospitalisation is essential because of the danger of resp. obstruction.
 Adequate hydration
 Antibiotics → Ampicillin or 3rd gen. cephalosporin
 Steroids (Hydrocortisone or dexamethasone)
 Intubation or tracheostomy may be required for resp. obstruction.

Acute laryngo-tracheo-bronchitis
It is an infla. condition of the larynx, trachea and bronchi; more common than acute epiglottitis.
Mostly, it is viral infection (parainfluenza type I and II) affecting children between 6 months to 3
years of age
Male children are more often affected. Secondary bacterial infection by Gram positive cocci soon
supervenes

Pathology
The loose areolar tissue in the subglottic region swells up and causes respiratory obstruction and
stridor. This, coupled with thick tenacious secretions and crusts, may completely occlude the airway

Clinical presentation
Disease starts as upper respiratory infection with hoarseness and croupy cough. There is fever of 39-
40°C. This may be followed by difficulty in breathing and inspiratory type of stridor. Respiratory
difficulty may gradually increase with signs of upper airway obstruction, i.e. suprasternal and
intercostal recession.

Treatment
Hospitalisation is often essential because of the increasing difficulty in breathing.
 Antibiotics → ampicillin is effective against 20 infec. due to G(+) cocci and H. influenzae.
 Humidification helps to soften crusts and tenacious secretions
 Steroids
 Adrenaline administered via a respirator (bronchodilator and relieve dyspnoea)
 Intubation/tracheostomy → Tracheostomy is done if intubation is required > 72 hours.
 Assisted ventilation may be required.
Topic 7. Benign tumors and precancerous diseases of the larynx. papillomas

Neoplastic Neoplastic
Solid  Squamous papilloma → Juvenile or Adult-onset type
 Vocal nodules  Chondroma
 Vocal polyp  Haemangioma
 Reinke's edema  Granular cell tumor
 Contact ulcer  Glandular tumors
 Intubation granuloma  Rhabdomyoma
 Leukoplakia  Lipoma
 Amyloid tumors  Fibroma

Cystic
 Ductal cysts
 Saccular cysts
 Laryngocele

Non-neoplastic lesions
They are not true neoplasms but are tumor-like masses which form as a result of infection, trauma or
degeneration. They are seen more frequently than true benign neoplasms

Vocal Nodules (Singer's or Screamer's Nodes)

They appear symmetrically on the free edge of vocal cord, at the junction of ant. 1/3, with the post. 2/3
 Their size varies from that of pin-head to half a pea
 Result of vocal trauma when person speaks in unnatural low tones for prolonged periods or at
high intensities
 Hoarseness, vocal fatigue and pain in the neck on prolonged phonation
 Early cases of vocal nodules can be treated conservatively by educating the patient in proper use
of voice. Surgery is required for large nodules or nodules of long-standing in adults

Vocal Polyp
Also the result of vocal abuse or misuse. Other contributing factors are allergy and smoking.
 Mostly, it affects men in the age group of 30-50.
 Typically, a vocal polyp is unilateral arising from the same position as vocal nodule.
 soft, smooth and often pedunculated.
 Hoarseness is a common symptom.
 Large polyp may cause dyspnoea, stridor or intermittent choking +/- diplophonia (double voice)
due to diff. vibratory frequencies of the 2 vocal cords
 Treatment is surgical excision under operating microscope followed by speech therapy

Reinke's edema (Bilateral Diffuse Polyposis)

Due to collection of edema fluid in the subepithelial space of Reinke.
 Usual cause is vocal abuse and smoking.
 Both vocal cords show diffuse symmetrical swellings.
 Treatment is vocal cord stripping, preserving enough mucosa for epithelialisation. Only one cord
is operated at a time. Re-education in voice production and cessation of smoking are essential to
prevent recurrence
Neoplastic lesions
Except for laryngeal papillomas which constitute ~ 80% of the total occurrence of neoplasms of the
larynx, others are uncommon.

Squamous Papillomas
Juvenile papillomas
They are viral in origin (HPV 16, 18, 6, 11) and multiple, often involving infants and young children
who present with hoarseness and stridor.
 They are mostly seen on the true and false cords and the epiglottis, but they may involve other
sites in the larynx and trachea.
 Appear as glistening white irregular growths, pedunculated or sessile, friable and bleeding easily
 Known for recurrence after removal and therefore multiple laryngoscopies may be required.
 They tend to disappear spontaneously after puberty.

Treatment
 They have been treated by endoscopic removal with cup forceps, cryotherapy and
microelectrocautery.
 These days, CO2 laser is preferred because of the precision in removal and less bleeding.
 Interferon th. is being tried to prevent recurrence and has been found successful.
 Avoid tracheotomy, may seed lower airway or stoma

Adult-onset papilloma
Usually, it is single, smaller in size, less aggressive and does not recur after surgical removal.
It is common in males in age of 30-50 and usually arises from the ant. 1/2 of vocal cord or ant.
commissure.
Treatment is the same as for juvenile type

Chondroma
Most of them arise from cricoid cartilage and may present in the subglottic area causing dyspnoea or
may grow outward from the posterior plate of cricoid and cause sense of lump in throat and dysphagia.
 Mostly affect men, 40-60 years of age.
 Lesion is smooth, firm, fixed tumor, normal mucosa
 Symptoms: insidious hoarseness, dyspnea for subglottic lesions, dysphagia, globus sensation
 Diagnosis: endoscopic wedge biopsy, CT of neck (calcification)
 Treatment: complete excision via endoscopic or ext. approach (depending on the lesion size)

Haemangioma
Infantile haemangioma involves subglottic area and presents with stridor in the first 6 months of life.
 ~50% of children have haemangiomas elsewhere in the body particularly in the head and neck.
 They tend to involute spontaneously but a tracheostomy may be needed to relieve resp.
obstruction if AW is compromised.
 Most of them are of capillary type and can be vaporised with CO2 laser

Adult haemangiomas involve vocal cord or supraglottic larynx.

They are cavernous type and cannot be treated with laser.
They are left alone if asymptomatic. For larger (causing symptoms), steroid or radiation therapy may
be employed

Symptoms
polypoid or sessile lesions (left > right), biphasic stridor, worse with crying (hemangiomas become
engorged with blood), dysphonia, dysphagia, seldom causes bleeding in the larynx
Granular Cell Tumour
arises from Schwann cells in the posterior aspect of true vocal fold or arytenoids and is often
submucosal.
 Overlying epi. shows pseudo-epitheliomatous hyperplasia → on histology, resemble well diff. cc.
 small, sessile, gray mass lesion
 3% risk of malignant degeneration
 insidious hoarseness
 treated by complete excision via an endoscopic or external approach (depending on lesion size)

Glandular Tumour → pleomorphic adenoma or oncocytoma are rare glandular tumors.

Other rare benign tu. include rhabdomyoma, neurofibroma, neurilemmoma, lipoma or fibroma
Topic 8. Malignant tumors of the larynx

Tumor arising in the larynx have been divided into 3 sites (or regions) with several subsites under
each site (they are further classified according to the TNM sys.)

Site Subsite
Supraglottis  Suprahyoid epiglottis (both lingual and laryngeal surfaces)
 Infrahyoid epiglottis
 Aryepiglottic folds (laryngeal aspect only)
 Arytenoids
 Ventricular bands (or false cords)
Glottis  True vocal cords including anterior and posterior commissure
Subglottis  Subglottis up to lower border of cricoid cartilage

Risk factors
 Genetic factors
 Smoking and alcohol are well established risk factors in laryngeal cancer.
 Previous radiation to neck for benign lesions or laryngeal papilloma may induce laryngeal cc.
 Occupational → asbestos, mustard gas and other chemical...

Histopathology
~ 90-95% of laryngeal malignancies are SCC with various grades of differentiation.
Cordal lesions are often well-differentiated while supraglottic ones are anaplastic
The rest 5-10% include verrucous cc., spindle cell cc., malignant salivary gl. tu. and sarcomas.

Supraglottic Cancer
 Supraglottic cancer is less frequent than glottic cancer.
 Frequency: epiglottis > false cords > aryepiglottic folds

Spread

Supraglottic region Spread locally and invade the adjoining areas

(vallecula, base of tongue and pyriform fossa)
Infrahyoid epiglottis and anterior Extend into pre-epiglottic space and penetrate thyroid cart.
ventricular band

 Nodal metastases occur early.

 Upper and middle jugular nodes are often involved.
 Bilateral metastases may be seen in cases of epiglottic cancer

Symptoms
Supraglottic growths are often silent.
Throat pain, dysphagia and referred pain in the ear or mass of L.N in the neck
Hoarseness, weight loss, resp. obstruction, halitosis are late features

Glottic Cancer
In vast majority of cases, laryngeal cancer originates in the glottic region.
Free edge and upper surface of vocal cord in its ant. and mid. 1/3 is the most frequent site

Spread
Locally → may spread to ant. commissure and then to the opposite cord, vocal process and
arytenoid region, ventricle and false cord, subglottic region.
There are few lymphatics in vocal cords → nodal metastasis are NEVER seen in cordal lesions
unless the disease spreads beyond the region of membranous cord
Symptoms
 Vocal cord mobility is unaffected in early stages
 Hoarseness of voice is an early sign because lesions of cord affect its vibratory capacity →
because of this glottic cancer is detected early
 Fixation of vocal cord indicates spread of disease to thyroarytenoid mm. and is a bad
prognostic sign

Subglottic Cancer (1-2%)

Subglottic region extends from glottic area to lower border of cricoid cartilage. Lesions of this
region are rare

Spread
 Growth starts on one side of subglottis and may spread around the anterior wall to the opposite
side or downwards to the trachea.
 Subglottic growths can invade cricothyroid mem, thyroid gl. and ribbon muscles of neck.
 Lymphatic metastases go to prelaryngeal, pretracheal, paratracheal and lower jugular nodes

Symptoms
 The earliest presentation of subglottic cancer may be stridor or laryngeal obstruction
 Hoarseness of voice → is a late feature that indicates spread of disease to the undersurface of
vocal cords, infiltration of thyroarytenoid mm. or involvement of RLN at the cricoarytenoid j.

Diagnosis

Examination of neck
done to find extralaryngeal spread of disease and/ or nodal metastasis
 Growths of anterior commissure and subglottic region spread through cricothyroid mem. and
may produce a midline swelling.
 They may also invade the thyroid cartilage and cause perichondritis when cartilage will be
tender on palpation.
 Search should be made for metastatic L.N, their size and number, if they are mobile or fixed,
unilateral, bilateral or contralateral.

Radiography
 CXR → is essential for co-existent lung disease, pul. metastasis or mediastinal nodes
 Soft tissue lateral view neck → extent of lesions of epiglottis, aryepiglottic folds, arytenoids
and involvement of pre-epiglottic space
 Contrast laryngograms → radio-opaque dye (dionosil) is instilled into the larynx and checl for
extent of tumors. This investigation has now been replaced by CT scan
 CT → very useful investigation to find the extent of tumour, invasion of pre-epiglottic or
paraepiglottic space, destruction of cartilage and L.N involvement
 MRI

Direct laryngoscopy
It is done to see the hidden areas of larynx and extent of disease.
Hidden areas of the larynx include infrahyoid epiglottis, anterior commissure, subglottis and
ventricle, which may not be clearly seen by mirror examination making direct laryngoscopy
essential.

Microlaryngoscopy → for small lesions of vocal cords

Supravital staining and biopsy → cc.-in-situ and supf cc. take up dye while leukoplakia does not
Topic 9. Treatment of the laryngeal cancer. Surgical procedures for laryngeal carcinoma

Treatment depends upon the site of lesion, extent of lesion, presence or absence of nodal and distant
metastases. Treatment consists of:
1) Radiotherapy
2) Surgery → conservation laryngeal surgery OR total laryngectomy
3) Combined therapy

Radiotherapy
Curative radiotherapy is reserved for early lesions which neither impair cord mobility nor invade
cartilage or cervical nodes.
 Cancer of the vocal cord w/o impairment of its mobility gives 90% cure rate after irradiation and
has the advantage of preservation of voice.
 Supf. exophytic lesions, especially of tip of epiglottis, and aryepiglottic folds give 70-90% cure.
 Radiotherapy does NOT give good results in lesions with fixed cords, subglottic extension,
cartilage invasion, and nodal metastases. These lesions require surgery

Surgery

Conservation surgery
Earlier total laryngectomy was done for most of the laryngeal cancers and the patient was left with no
voice and a permanent tracheostome.
Lately, there has been a trend for conservation laryngeal surgery which can preserve voice and also
avoid a permanent tracheal opening. However, few cases would be suitable for this type of surgery and
they should be carefully selected.

Conservation surgery includes

1) Excision of vocal cord after splitting the larynx (cordectomy via laryngofissure),
2) Excision of vocal cord and anterior commissure region (partial frontolateral laryngectomy)
3) Excision of supraglottis → epiglottis, aryepiglottic folds, false cords and ventricle-a sort of
transverse section of larynx above the vocal cords (partial horizontal laryngectomy).

Total laryngectomy
The entire larynx including the hyoid bone, pre-epiglottic space, strap mm., and one or more rings of
trachea are removed.
 Pharyngeal wall is repaired and lower tracheal stump sutured to the skin for breathing.
 Laryngectomy may be combined with block dissection for nodal metastasis

Total laryngectomy is indicated in:

 T3 lesions (i.e. with cord fixed)
 All T4 lesions
 Invasion of thyroid or cricoid cartilage
 Bilateral arytenoid cartilage involvement
 Lesions of posterior commissure
 Failure after radiotherapy or conservation surgery

It is contraindicated in patients with distant metastasis

Combined therapy
Surgical ablation may be combined with pre- or post-operative radiation to decrease the incidence of
recurrence. Pre-operative radiation may also render fixed nodes resectable
Topic 10. Dyspnea caused by disorders of the upper respiratory tract

Is a clinical term for the symptom of shortness of breath experienced by both healthy subjects and
patients with resp. diseases.
 Dyspnea is a term used to characterize a subjective experience of breathing discomfort
 Other approaches to describe dyspnea → Breathlessness, Air hunger, Labored breathing

URT disorders that involves dyspnea as a symptoms include:

Infectious origin → URTI caused by bact. or virus

 Rhinitis
 Rhinosinusitis or sinusitis
 Nasopharyngitis (rhinopharyngitis or the common cold)
 Pharyngitis
 Epiglottitis (supraglottitis)
 Laryngitis
 Laryngotracheitis
 Tracheitis

Non-infectious origin
1) Malformations
2) Trauma of the larynx
3) Functional disorders of the larynx
4) Laryngeal edema
5) Polyps, papilloma and malignant tumor of the larynx
6) Foreign body
7) Stenosis in the larynx and URT.
Topic 11. Edema in the larynx

Often termed "edema glottidis" → in the past, it involves the supraglottic and subglottic region
where laryngeal mucosa is loose.
Edema of the vocal cords occurs rarely because of the sparse subepithelial CT.

Etiology
1) Infections
 Acute epiglottitis, laryngo-tracheo-bronchitis, TB or syphilis of larynx.
 Peritonsillar abscess, retropharyngeal abscess and Ludwig's angina.
2) Trauma
 Surgery of tongue, floor of mouth
 laryngeal trauma
 foreign body
 endoscopy (especially in children)
 intubation
 thermal or caustic burns or inhalation or irritant gases or fumes.
3) Neoplasms → cancer of larynx or laryngopharynx often associated with deep ulceration.
4) Allergy → angioneurotic edema, anaphylaxis
5) Radiation → for larynx or pharynx cancer
6) Systemic diseases → nephritis, HF, or myxoedema.

Symptoms
 AWO → degree of resp. distress varies. Tracheostomy may become essential.
 Inspiratory stridor

Diagnosis
Indirect laryngoscopy shows edema of supraglottic or subglottic region.
Children may require direct laryngoscopy.

Treatment
 If there is AWO → intubation of larynx or tracheostomy will be immediately required.
 Less severe cases are treated conservatively and treatment will depend on the cause.
 IM adrenaline injection → useful in allergic or angioneurotic edema.
 Steroids are useful in epiglottitis, laryngo-tracheo-bronchitis or edema due to traumatic allergic
or post-radiation causes.
Topic 12. Indication for conicotomy, tracheotomy and its techniques

Indication for conicotomy

Also called cricothyrotomy, laryngotomy or mini (emergency) tracheostomy
This is a procedure for opening the AW through the cricothyroid mem.
 Mini tracheostomy is an emergency procedure to buy time to allow patient to be carried to O.R
 Commercial emergency kits are also available for this.
 As an elective procedure → done to clear the bronchial secretions following thoracic surgery

Procedure
Patient's head and neck is extended, lower border of thyroid cartilage and cricoid ring are identified.
Skin in this area is incised vertically and then cricothyroid mem. cut with a transverse incision.
This space can be kept open with a small tracheostomy tube or by inserting the handle of knife and
turning it at right angles if tube is not available.

It is essential to perform an orderly tracheostomy as soon as possible because perichondritis,

subglottic edema and laryngeal stenosis can follow prolonged laryngotomy

Indications
 Can't intubate or ventilate
 Severe facial or nasal injuries (that do not allow oral or nasal tracheal intubation)
 Massive midfacial trauma
 Possible cervical spine trauma preventing adequate ventilation
 Anaphylaxis
 Chemical inhalation injuries

Tracheotomy
Tracheostomy is an operative procedure that creates a surgical AW in the cervical trachea
 It is performed in emergency situations, in the O.R, or at bedside of critically ill patients.
 The term tracheostomy is sometimes used interchangeably with tracheotomy → but
tracheostomy usually refers to the opening itself while a tracheotomy is the actual operation.

Types
Emergency tracheotomy → done only in emergency situations and can be performed quite rapidly.

Surgical tracheotomy
Takes more time and is usually done in an O.R. under general anaesthesia
The surgeon first makes an incision in the skin over the trachea, b/w the thyroid cart. and top of the
sternum (2-3cm from the second tracheal ring down)
Neck mm. are separated and the thyroid gland is usually cut down the middle.
Than a hole is done through the 3rd and 4th tracheal rings and a tracheotomy tube, is inserted through
the opening. Dressing is placed around the opening.
 If a cannula is in place, an unsutured opening heals into a patent stoma within a week.
 If decannulation is performed → the hole usually closes in a similar amount of time.
 The cut edges of the tracheal opening can be sutured to the skin with a few absorbable sutures to
facilitate cannulation and, if necessary, recannulation
 a permanent stoma can be created with circumferential sutures.
Indications
A tracheostomy is most commonly performed in patients who have had difficulty weaning off
a ventilator, followed by those who have suffered trauma or some catastrophic neurologic insult.
Infectious and neoplastic processes are less common in diseases that require a surgical AW
1) Bypass obstruction
 Congenital anomaly → laryngeal hypoplasia, vascular web…
 Foreign body that cannot be dislodged with Heimlich and BCLS maneuvers
 Supraglottic or glottic pathologic condition → infection, tu., bilateral vocal cord paralysis
2) Neck trauma that results in severe injury to thyroid or cricoid cart., hyoid bone, or great vessels.
3) SQ emphysema → appears in face, neck, or chest
4) Facial fractures that may lead to upper AWO → comminuted fractures of the midface
and mandible
5) Edema → due to Trauma, Burns, Infection, Anaphylaxis
6) To provide a long-term route for mechanical ventilation in cases of resp. failure
7) To provide pulmonary toilet → assist with tracheal-bronchial suctioning
 Inadequate cough due to chronic pain or weakness
 Aspiration and the inability to handle secretions
8) Prophylaxis → preparation for extensive head & neck procedures and the convalescent period
9) Severe sleep apnea not amendable to CPAP devices or other, less invasive surgery

Management
Tracheotomy Care
 Maintain AW → especially for first 48 hrs to prevent accidental loss of AW
- suture tracheotomy to neck skin
- tight tracheotomy ties
- clean inner cannula
- first tracheotomy change may be considered after 3–5 days to allow the tract to form
 Humidity → prevents tracheal crusting and mucous plugs, initially saline should also be
dropped into tube every 3-4 hours
 Pulmonary Toilet (Aseptic Technique Suctioning) → tracheotomy tubes disrupt ciliary function,
↓ subglottal pressure required for an adequate cough, and ↑ risk of microaspiration
It requires regular suctioning of the tracheal AW, especially for the first few days
 Skin Care → cuff dressings may be considered to prevent skin breakdown
 Check Cuff Pressure → cuff pressure should be less than capillary pressure (<25 cm H2O) to
prevent pressure necrosis (subglottic stenosis, tracheal-innominate a. erosion, tracheomalacia)
 Feeding → no solid food ingestion when cuff is inflated, capping tracheotomy tube facilitates
swallowing

Decannulation
tracheotomy tubes should be removed ASAP (especially in children) to prevent long-term sequelae
(tracheal ulceration, subglottic stenosis, tracheomalacia…)
 prior to decannulation patient should undergo tracheotomy tube downsizing and a trial of
capping (24 hours for 7 consecutive days w/o respiratory difficulties)
 original indication for tracheotomy must be resolved
 consider flexible nasopharyngoscopy to evaluate AW patency (evaluate subglottis with
retroflexed look through the stoma)
 place airtight dressing to seal stoma after removal of tracheotomy tube
Complications

Immediate  Haemorrhage, e.g. from the thyroid isthmus

 Hypoxia
 Trauma to the recurrent laryngeal nerve
 Damage to the esophagus
 Pneumothorax
 Infection
 Subcutaneous emphysema
Early  Tube obstruction or displacement
 Aspiration
 Bleeding from tracheostomy site
 Infection
Late  Airway obstruction with aspiration
 Damage to the larynx, e.g. stenosis
 Tracheal stenosis
 Tracheo-malacia
 Aspiration & pneumonia
 Fistula formation, e.g. tracheo-cutaneous or tracheo-
esophageal

Care of a patient with a short-term tracheostomy

 Meticulous care towards hygiene & asepsis
 Speaking → once the cuff can be deflated, the patient can begin to speak if the opening is
occluded. Usually this takes time and patients need lots of support.
 Removal → as the patient improves the tracheostomy can be plugged for longer durations each
day, provided the patient can tolerate it.
 Swallowing → oral intake can occur but swallowing may be difficult. Patients must be watched
for aspiration risk.

Care of a patient with a long-term tracheostomy

 Educate patient and carers
 Meticulous care towards hygiene & asepsis
 Carers will need to be taught how to suction and replace outer tubes
 Providing humidification
 Management regarding speaking and eating as above
Topic 13. Intubation or tracheotomy
Intubation
Refers to the placement of a tube into an external or internal orifice of the body.
Although the term can refer to endoscopic procedures, it is most often used to denote ET intubation.
Tracheal intubation is the placement of a flexible plastic tube into the trachea to protect the patient's
airway and provide a means of mechanical ventilation.
The most common tracheal intubation is oro-tracheal intubation, where (with the assistance of a
laryngoscope) an ET tube is passed through the mouth, larynx, and vocal cords, into the trachea.
A bulb is then inflated near the distal tip of the tube to help secure it in place and protect the airway
from blood, vomit, and secretions.
Another possibility is naso-tracheal intubation, where a tube is passed through the nose, larynx,
vocal cords, and trachea.

Indications
1) Comatose or intoxicated patients who are unable to protect their airways.
2) General anesthesia → spontaneous resp. is ↓ or absent due to the effect of anesthetics, opioids, or
muscle relaxants.
3) Diagnostic manipulations of the airways → bronchoscopy.
4) Endoscopic procedures to the AW → laser therapy or stenting of the bronchi.
5) Patients who require resp. support, including CPR.

Endotracheal tube
Can be introduced by laryngoscopes, blindly or by brocho- fiberoscope

The tube is inserted with the aid of a laryngoscope → 2 types:

1) Curved blade (Macintosh) → inserted into the vallecula, and pressure on the hyoepiglottic
ligament with elevation of the base of the tongue moves the epiglottis upwards to expose the
glottis.
2) Straight blade (Miller) → Passes posteriorly to epiglottis and lift it anteriorly.

The head of the patient is slighly elevated and the neck extended ("sniffing" or Jackson position)
For direct laryngoscopy the instrument is held in the L hand and introduced from the R side deflecting
the tongue. After blade positioning, an upwards lift will provid visualisation of glottis.

Advantages
 Reliable maintenance of airway patency
 Prevention of aspiration
 Easy to aspirate bronchial secrets
 (+) pressure ventillation (even with higher pressures) possible

Disadvantages
 The introduction of the tube requires skill and knowledge.
 Circulatory reactions to the intubation/extubation (pressor reaction)
 general anesthesia or sedation + local anesthesia is necessary
 Tube cuff may cause lesion of the tracheal wall and soft tissue trauma
 Complications of long term intubation → decubitus, mucociliar lesion, sinusitis, infec,
bronchopneumonia
Alternatives to intubation
1) Tracheotomy → typically for patients who require long-term respiratory support.
2) Cricothyrotomy → when intubation is unsuccessful and tracheotomy is not an option.
Difficult AW
3 unsuccessful visualization attempts of cords = criteria for difficult AW (?)

Common causes of intubation difficulties

 Serious mouth opening limitation
 Difficulties of laryngosopic visualisation
 Diffiulties of tube insertion

Can be predicted from

 Face abnor.
 Short neck
 Mouth opening limitation → Mallampati classification
 Thyreomental distance → If < 65 mm, difficulties are possible!

Mallampati classification of oral opening

class I uvula and pharyngeal pillars well visible

class II Only soft palate and part of the uvula are visible
class III Only soft palate is visible (palatal arches are not)
class IV only part of hard palate is visible (Soft palate is not)

Cormak classification of laryngeal view

Grade I Easy to visualise, well visible glottis

Grade II Only the post. part of glottis is visible
(visualisation is good, but slightly difficult for the beginner)
Grade III Only epiglottis is visible
Grade IV Not even the epiglottis can be seen
Extrem difficult intubation, use of several intubation tools
and the procedure may last >10 min.
Topic 14. Diagnosis and management of foreign bodies in the upper and lower respiratory tract

A foreign body aspirated into air passage can lodge in the larynx, trachea, or bronchi.
Site of lodgment would depend on the size and nature of the foreign body
 A large foreign body, unable to pass through the glottis, will lodge in the supraglottic area while
the smaller one will pass down through the larynx into the trachea or bronchi.
 Foreign bodies with sharp points (pins, needles, fish bones) can stick anywhere in the larynx, or
tracheobronchial tree

Children are more often affected → >50% are below 4 years

In children, peanut is the most common vegetable foreign body while nonvegetable matters include
plastic whistle, plastic toys, safety pins..

In adults, foreign bodies are aspirated during coma, deep sleep or alcoholic intoxication.
Loose teeth or denture may be aspirated during anaesthesia

Symptomatology of foreign body is divided into 3 stages

1) Initial period of choking, gagging and wheezing → lasts for a short time, may be coughed out
2) Symptomless interval → resp. mucosa adapts to the presence of foreign body and initial
symptoms disappear
3) Later symptoms → caused by obstruction to the AW, infla. or trauma induced by the foreign
body and depend on the site
 Laryngeal → may totally obstruct the airway leading to sudden death
 Tracheal (carina) → only produce cough and haemoptysis, "audible slap"
 Bronchial (most commonly R) → may totally obstruct a lobar or segmental bronchus
causing atelectasis

Diagnosis
Made by detailed history of the foreign body "ingestion", physical examination of the neck and chest.
A history of sudden onset of coughing, wheezing and diminished entry of air into the lungs on
auscultations forms a classical triad.

Radiology
 Soft tissue posteroanterior and lateral view of the neck in its extended position → can show
radio-opaque and sometimes the radiolucent foreign bodies in the larynx and trachea
 Plain X-ray chest in PA and lat. views → may show:
- Radio-opaque foreign body-its size, shape and location.
- Lobar or segmental atelectasis (complete obstruction by foreign body).
- Unilateral hyperinflation of lobe or segment or entire lung (if ball valve obstruction).
- Mediastinal shift to opposite side is seen in hyperinflation.
- Penumomediastinum or PTx.
- Pneumonitis/bronchiectasis
 X-ray chest at the end of inspiration and expiration → atelectasis and obstructive emphysema
can be seen. also give indirect evidence of radiolucent foreign bodies
 Fluoroscopy/videofluoroscopy → evaluation during inspiration and expiration
 Chest CT

Management
 Laryngeal foreign body → Heimlich's manoeuvre, if fails – crico. or emergency tracheostomy
 Tracheal and bronchial foreign bodies → removed by bronchoscopy with full preparation and
under general anaesthesia
Topic 15. Differential diagnosis of cervical enlargements and inflammations

Clinically neck masses can be divided into:

1. Those in the midline
2. Those in the lateral aspect of neck → can be grouped according to triangles of neck.

Differential diagnosis of common neck masses

Neoplastic Congenital/developmental Inflammatory

 10 neck tumor  Sebaceous cysts  Lymphadenopathy (bact., viral,
 Metastatstasis  Branchial cleft cysts granulomatous)
 Thyroglossal duct cysts  Tuberculous
 Lymphangioma/hemangioma - Cat-scratch
 Ectopic thyroid tissue - Sarcoidosis
 Laryngocele - Fungal
 Pharyngeal diverticulum  Staladenitis (parotid, submaxillary)
 Thymic cysts  Congenital cycts
 Throtrast granulomas

10 neck tumor include adenocc., thyroid, lymphoma, salivary, lipoma, angioma, carotid body tu.,
rhabdomyosarcoma…

Diagnostic steps
History
 Developmental time course
 Associated symptoms (dysphagia, otalgia, voice)
 Personal habits (tobacco, alcohol)
 Previous irradiation or surgery

Physical Examination
 Complete head and neck exam (visualize & palpate)
 Emphasis on location, mobility and consistency

Tests
 Fine needle aspiration biopsy (FNAB)
 CT, MRI, US
 Radionucleotide scanning
Topic 16. Ludovic's angina, parapharyngeal and retropharyngeal abscess. Cervical phlegmone

Ludovic's angina
Ludwig's angina is infec. of submandibular space

Submandibular space lies b/w mucous mem. of the floor of mouth and tongue on one side and supf.
layer of deep cervical fascia extending b/w the hyoid bone and mandible on the other .
It is divided into 2 compartments by the mylohyoid mm.:
1. Sublingual compartment (above the mylohyoid)
2. Submaxillary and submental compartment (below the mylohyoid).

Etiology
1. Dental infections → account for 80% of the cases. Roots of premolars often lie above the
attachment of mylohyoid and cause sublingual space infec. while roots of the molar teeth extend
up to or below the mylohyoid line and primarily cause submaxillary space infection.
2. Submandibular sialadenitis
3. injuries of oral mucosa
4. fractures of the mandible account

Causative agents
 Mixed infections involving both aerobes and anaerobes are common.
 α haemolytic Strep., Staph., and bacteroides groups are common.
 Rarely H. influenzae, E. coli and Pseudomonas are seen.

Clinical presentation
 There is marked odynophagia with varying degrees of trismus.
 When infection is localised to the sublingual space → structures in the floor of mouth are
swollen and tongue seems to be pushed up and back
 When infection spreads to submaxillary space → submental and submandibular regions become
swollen and tender, and impart woody-hard feel.
 Usually, there is cellulitis of the tissues rather than frank abscess.
 Tongue is progressively pushed upwards and backwards threatening the airway.
 Laryngeal edema may appear.

Treatment
 Systemic antibiotics
 Incision and drainage of abscess.
- Intraoral → if infec. is still localised to sublingual space.
- External → if infec. involves submaxillary space. A transverse incision extending from
one angle of mandible to the other is made with vertical opening of midline musculature
of tongue with a blunt haemostat.
 Tracheostomy, if AW is endangered.

Complication
1. Spread of infec. to parapharyngeal and retropharyngeal spaces and thence to the mediastinum
2. AWO due to laryngeal edema, or swelling and pushing back of the tongue
3. Septicaemia
4. Aspiration pneumonia
Parapharyngeal abscess
Abscess of pharyngomaxillary or lateral pharyngeal space
Parapharyngeal space is pyramidal in shape with its base at the base of skull and its apex at the hyoid

Infection of parapharyngeal space can occur from:

1. Pharynx → acute and chr. infec. of tonsil and adenoid, bursting of peritonsillar abscess.
2. Teeth → dental infec. usually comes from the lower last molar tooth.
3. Ear → Bezold's abscess, petrositis.
4. Other spaces → Infec. of parotid, retropharyngeal and submaxillary spaces.
5. External trauma → penetrating injuries of neck, injection of local anaesthetic for
tonsillectomy or mandibular nerve block.

Clinical features → depend on the compartment involved

Anterior compartment infections produce a triad of symptoms:
1) prolapse of tonsil and tonsillar fossa
2) trismus (due to spasm of medial pterygoid muscle)
3) external swelling behind the angle of jaw. There is marked odynophagia associated with it.

Posterior compartment involvement produces

 bulge of pharynx behind the posterior pillar
 paralysis of CN IX, X, XI, and XII and sympathetic chain
 swelling of parotid region.
 minimal trismus or tonsillar prolapse

Fever, odynophagia, sore throat, torticollis (due to spasm of prevertebral muscles) and signs of
toxaemia are common to both compartments

Complications
1. Acute oedema of larynx with respiratory obstruction.
2. Thrombophlebitis of jugular vein with septicaemia.
3. Spread of infection to retropharyngeal space.
4. Spread of infection to mediastinum along the carotid space.
5. Mycotic aneurysm of carotid artery from weakening of its wall by purulent material. It may
involve common carotid or internal carotid artery.
6. Carotid blow out with massive haemorrhage.

Treatment
Systemic antibiotics
Drainage of abscess → usually done under general anaesthesia.
 If the trismus is marked, pre-operative tracheostomy becomes mandatory.
 Abscess is drained by a horizontal incision, made 2-3 cm below the angle of mandible.
 Blunt dissection along the inner surface of medial pterygoid muscle towards styloid process is
carried out and abscess evacuated.
 A drain is inserted. Transoral drainage should never be done due to danger of injury to great
vessels which pass through this space

Retropharyngeal abscess
The retropharyngeal space lies behind the pharynx b/w the buccopharyngeal fascia covering
pharyngeal constrictor mm. and the prevertebral fascia.
 It extends from the base of skull to the bifurcation of trachea.
 The space is divided into 2 lateral compartments (spaces of Gillette) by a fibrous raphe.
 Each lateral space contains retropharyngeal nodes which usually disappear at 3-4 years of age.
Parapharyngeal space communicates with the retropharyngeal space → infec. of retropharyngeal
space can pass down behind the esophagus into the mediastinum

Retropharyngeal abscess is commonly seen in children < 3 years.

 It is the result of suppuration of retropharyngeal L.N 20 to infec. in the adenoids, nasopharynx,
post. nasal sinuses or nasal cavity.
 In adults, it may result from penetrating injury of post. pharyngeal wall or cervical esophagus.
 Rarely, pus from acute mastoiditis tracks along the undersurface of petrous bone to present as
retropharyngeal abscess.

Clinical Features
1. Dysphagia and difficulty in breathing are prominent symptoms as the abscess obstructs the air
and food passages.
2. Stridor and croupy cough may be present.
3. Torticollis → neck becomes stiff and the head is kept extended.
4. Bulge in posterior pharyngeal wall. Usually seen on one side of the midline.

Diagnosis
Radiograph of soft tissue lateral view of the neck shows widening of prevertebral shadow and
possibly even the presence of gas

Treatment
 Incision and drainage of abscess → usually done without anaesthesia as there is risk of rupture
of abscess during intubation. Child is kept supine with head low. Mouth is opened with a gag. A
vertical incision is given in the most fluctuant area of the abscess. Suction should always be
available to prevent aspiration of pus.
 Systemic antibiotics
 Tracheostomy → large abscess may cause mechanical AWO or lead to laryngeal edema.
Tracheostomy becomes mandatory in these cases.

Cervical phlegmone
Phlegmon is a spreading diffuse infla. process with formation of suppurative/purulent exudate or pus.
It is caused by bact. → staph, strep, pneumococci, spore and non-spore forming anaerobes…

Treatment
The main goal is to remove the cause of the phlegmonous process in order to achieve effective
treatment and prevention of residual disease.
If the patient’s condition is mild and the signs of infla. process is present w/o signs of infiltrates →
conservative treatment with antibiotics is sufficient.

In severe condition → immediate operation is necessary with application of drainage system.

 All of these are done under general anesthesia.
 During operation, the cavity or place of the phlegmonous process are washed with antiseptic &
antibiotic solutions, and with proteolyic ferments.
 In post-operative period → IV drips of detoxification, antibiotics, and vitamin therapy.

During operation of phlegmon dissection at any location, it is important:

 To avoid spreading the pus during the operation
 To take into account the cosmetic value of operating site, especially in phlegmonous process
of the face.
 During the dissection, to avoid damaging nerves, especially facial nerves. Use the correct
incision line.
Topic 17. Corrosive injury and stenosis of the esophagus. Task of the family doctor

Corrosive injury
Acids, alkalies or other chemicals may be swallowed accidentally in children or taken with the purpose
of suicide in adults

Pathology
Severity of esophageal burns depends on the nature of corrosive substance, its quantity and cc. and the
duration of its contact with the esophageal wall.
Alkalies are more destructive and penetrate deep into the layers of the esophagus.
With lye burns, entire esophagus and stomach may slough off causing fatal mediastinitis and peritonitis

Esophageal burns run through 3 stages:

1) Stages of acute necrosis.
2) Stage of granulations: Slough separates leaving granulating ulcer.
3) Stage of stricture: Stricture formation begins at 2 weeks and continues for 2 months or longer.

Symptoms
 Severe pain in the mouth / sub-sternal pain / epigastric pain
 vomiting, reflux
 difficult swallowing
 sialorhea
 redness, vesicle formation on the mucosa, white membranes, and mucosal edema.
 It may also cause shock, renal damage, hematuria, hemolysis, and CNS problems.

Evaluation of the patient

Evaluate the patient and determine the type of caustic ingested, signs and symptoms of shock, upper
airway obstruction, mediastinitis, peritonitis, acid-base imbalance, and associated burns of face, lips
and oral cavity. Take X-ray of the chest and soft tissue lateral view of neck

Management
 Hospitalise the patient.
 Treat shock and acid-base imbalance by IV fluids and electrolytes. Monitor urine output for RF
 Relieve pain.
 Relieve AWO → tracheostomy may be required.
 Neutralisation of the corrosive by appropriate weak acid or alkali, given by mouth, can be done
but is effective only if done within first 6 hours.
 Parenteral antibiotics should be started immediately and continued for 3-6 weeks depending on
the degree of burns.
 Nasogastric tube → useful to feed the patient and to maintain oesophageal lumen.
 Esophagoscopy→ some advocate an early esophagoscopy within 2 days to know if burns in the
oesophagus have occurred and if so, their degree and extent so as to plan further treatment.
esophagoscope is not passed beyond the first severe circumferential burn.
 Steroids should be started within 48-96 hours and continued for 4-6 weeks to prevent stricture.
 Follow the patient with esophagogram and esophagoscopy every two weeks, till healing is
complete, for the development of any stricture.
 If stricture develops it can be treated by:
- esophagoscopy and prograde dilatations, if permeable,
- Gastrostomy and retrograde dilatation, if impermeable,
- esophageal reconstruction or by-pass, if dilatations are impossible.

Patients of corrosive injuries of esophagus may require life-long follow-up.

Stenosis of the esophagus
Strictures usually occur when muscular coat of the oesophagus is damaged. The common causes are:
1. Burns due to corrosive substances or hot fluids.
2. Trauma to esophageal wall due to impacted foreign bodies or instrumentation or external injuries.
3. Ulcerations due to reflux esophagitis.
4. Ulcerations due to diphtheria, typhoid.
5. Sites of surgical anastomosis.
6. Congenital, usually in the lower 1/3.

Clinical Features and Diagnosis

Dysphagia, first to solids and then to liquids, is the common complaint. When obstruction is complete,
regurgitation and cough may occur. Patient is malnourished
Barium swallow establishes the diagnosis. Oesophagoscopy is required to exclude malignancy

Treatment
 Prograde dilatation with bougies → should be done under direct vision through esophagoscope.
Dilatations may be required frequently
 Gastrostomy → helps to feed the patients and give rest to the inflamed area above the strictures
After a few days, when inflammation subsides, lumen may become visible and prograde dilatation
can be restored. Patient can be given a thread to swallow, which is recovered from the stomach,
and prograde or retrograde bouginage can be done
 Surgery → excision of strictured segment and reconstruction of food passage using stomach,
colon or jejunum
Topic 18. Foreign bodies in the pharynx and esophagus. What to do?
An ingested foreign body may lodge in:
1. Tonsil → sharp fish bone or a needle, easily observed and removed
2. Base of tongue/vallecula → can be observed by mirror examination
3. Pyriform fossa
4. Esophagus → coin, piece of meat, chicken bone, denture, marble…
By far the commonest site is at or just below the cricopharyngeal sphincter.
 Flat objects like coins are held up at the sphincter while others are held in the upper esophagus just
below the sphincter due to poor peristalsis.
 Foreign bodies which pass the sphincter can be held up at the next narrowing at broncho-aortic
constriction or at the cardiac end.
 Sharp or pointed objects lodge anywhere in the oesophagus
Etiology
1. Age → children are more often affected.
2. Loss of protective mechanism → LOC, seizures, deep sleep or alcoholic intoxicatio…
3. Carelessness. Poorly prepared food, improper mastication, hasty eating and drinking.
4. Narrowed esophageal lumen. → stricture or carcinoma.
5. Psychotics
Symptoms
 History of initial choking or gagging.
 Discomfort or pain just above the clavicle on the R or L of trachea which ↑ on attempts to swallow.
 Dysphagia
 Drooling of saliva → seen in cases of total obstruction. Saliva may be aspirated
 Resp. distress → impacted foreign body in the upper esophagus compresses trachea post. wall
causing resp. obstruction especially in children. Laryngeal edema can develop.
 Substernal or epigastric pain → due to esophageal spasm or incipient perforation

Signs
 Tenderness in the lower part of neck on the right or left of trachea.
 Pooling of secretions in pyriform fossa on indirect laryngoscopy that do NOT disappear on swallowing.
 Foreign body may be seen protruding from the esophageal opening in the postcricoid region.

Diagnosis
 Plain X-rays
 Fluoroscopy→ radiolucent foreign bodies are not seen on plain X-rays. They can be diagnosed
on fluoroscopy, when the patient is given a piece of cotton soaked in barium or barium filled
capsule to swallow and its passage is observed through the esophagus.

Management
1) Esophagoscopic removal → under general anaesthesia.
2) Cervical esophagotomy → impacted foreign bodies or those with sharp hooks such as partial
dentures located above thoracic inlet may require removal through an incision in the neck and
opening of cervical esophagus
3) Transthoracic esophagotomy → For impacted foreign bodies of thoracic oesophagus, chest is
opened at the appropriate level

Operative interference may be required when:

 Patient complains of pain and tenderness in abdomen.
 Foreign bodies are not showing any progress on serial X-rays taken at a few days interval.
 Foreign body is 5 cm or longer (e.g. hair pin) in a child below 2 years. It is unlikely to pass
through the turns of the duodenum
 Presence of pyloric stenosis
Topic 19. Diseases of the salivary glands  Parotid gland
 Submandibular gland
 2 major categories of diseases: infla. and non-infla.  Sublingual gland
 Usually involve major salivary glands
 Usually do not require extensive diagnostic workup → Inspection, Palpation, X-ray, US, CT,
MRI, Endoscopy, FNA

Symptoms of the diseases (acute or chr.)

 Swelling → acute infla., sialadenitis
 Pain → Sialadenitis, tumour
 Dryness → Sjogren’s
 Purulent discharge → sialadenitis, abscess
 Palsy of the facial n. → malignancies

The diseases
1) Trauma
2) Mumps and Viral Infections
3) Acute Suppurative Parotitis
4) Sialectasis
5) Granulomatous Diseases → Tuberculosis, sarcoidosis and actinomycosis
6) Salivary Calculi
7) Sjogren's Syndrome
8) Neoplasms

Trauma
 Parotid gland: sharp injuries are more frequent (knife, dog bite)
 Surgical intervention is requierd in case of facial nerve injury and reconstruction
 Danger of salivary fistule (microsurgical suture)

Mumps (Parotitis epidemica)

 Caused by paramyxoviruses, affect children (4-6 years old)
 75% bilateral, painful parotid swelling (may involve submandibular and sublingual glands),
malaise, fever, trismus
 Complications: sudden sensorineural hearing loss (SNHL) (CN VIII involvement), infertility
(with orchitis), encephalitis, pancreatitis, and nephritis
 Treatment: self limiting → requires only supportive care (hydration, analgesics), audiological
evaluation, vaccine is available

Other Viral Infec.: CMV, Coxsackievirus, influenza A…

Acute Suppurative Parotitis

Most commonly seen in the elderly, debilitated and dehydrated patients.
 Dry mouth due to any cause is a predisposing factor.
 S. aureus is the usual causative MO though other G(+) and anaerobic bact. can cause it
 Usual route of infec. is from the mouth through the Stensen's duct

Clinical features
 Sudden onset of severe pain and enlargement of gland.
 Movements of jaw aggravate the pain.
 Opening of the Stensen's duct is swollen and red and may be discharging pus or the latter can
also be expressed by gentle pressure over the gland.
 Patient is usually febrile and toxaemic
Investigations
 CBC → leukocytosis with ↑ in polymorphs.
 Blood and pus (from the opening of the parotid duct) culture

Treatment
Antibiotics, adequate hydration, measures to promote salivary flow and attention to oral hygiene.
If temp. does not subside and there is progressive induration of the gland, in spite of adequate tr. →
surgical drainage should be done

Sialectasis
Dilatation of the ductal sys., leading to stasis of secretions, which predisposes to infection.
Different degrees of dilatation of the ductal system → punctuate, globular or cavitary types.
Sialectasis may be congenital, associated with granulomatous disease or autoimm. disease such as
Sjogren's sy.

Granulomatous Diseases
Tuberculosis, sarcoidosis and actinomycosis may involve the salivary glands
 Tubercular infec. may involve parenchyma or L.N of the parotid and present as non-tender mass.
 Overlying skin may undergoes necrosis leading to a fistula formation.
 Surgical excision of the involved tissue and antitubercular treatment usually control the disease.

Salivary Calculi
Calculi may form in the ducts of submandibular or parotid glands.
They are formed by the deposition of Ca-phosphate on the organic matrix of mucin or cellular debris.
~ 90% of the stones are seen in submandibular and 10% in the parotid.
Stones may form in the duct or parenchyma of the gland.

Clinical features and diagnosis

 The presenting feature is intermittent swelling of the involved gland, and pain due to obstruction
to outflow of saliva.
 Sometimes, stone is visible at the duct opening or can be palpated.
 ~ 80% of the stones are radio-opaque and can be seen on appropriate X-rays
 Sialography may be required for radiolucent stones

Treatment
Stones in peripheral part of submandibular or parotid ducts can be removed intraorally, while those at
the hilum or in the parenchyma require excision of the gland

Sjogren's Syndrome (Sicca Syndrome)

Is an autoimm. disorder involving exocrine glands of the body. It may be 10 or 20

Primary Sjogren's sy.

Consists of xerostomia and xero-ophthalmia and is due to involvement of salivary and lacrimal gl.
 Parotid is most often involved.
 It has also been known as benign lymphoepithelial lesion of parotid or Mikulicz's disease.
 Both sexes are equally involved

Secondary Sjogren's sy.

Consists of 3 major components:
1) keratoconjunctivitis sicca → due to involvement of lacrimal gl.
2) xerostomia → due to involvement of salivary glands and mucous glands of the oral cavity
3) autoimmune CT disorder, usually the RA → bilateral swelling of the salivary glands
Presentation
 Fatigue, low grade fever, myalgias/arthralgias
 Other exocrine gl. involvement → dry nose, dry throat, xerotrachea, esophageal mucosal
atrophy, atrophic gastritis, subclinical pancreatitis, vaginal dryness
 Extraglandular involvement → Lungs, kidneys, vasculitis, nervous system

Diagnosis depends on raised ESR, (+) rheumatoid factor, (+) antinuclear Ab-s and biopsy from the
lower lip for evidence of involvement of minor salivary glands

Neoplasms of Salivary Glands

The tumours of major or minor salivary glands are either from epi. or mesenchymal tissues
Larger the size of salivary gland, more are the chances of a tumor being benign.
80% of parotid, 50-60% of submandibular and only about 25% of other minor salivary gland tumours
are benign → chance of malignant tu. in minor salivary glands is higher

Rapid growth, restricted mobility, fixity of overlying skin, pain and facial nerve involvement indicate
the possibility of tumor being malignant

Benign Malignant
Epithelial Epithelial
 Pleomorphic adenoma  Mucoepidermoid cc. (low/high grade)
 Adenolymphoma (Warthin's tumour)  Adenoid cystic carcinoma (cylindroma)
 Oncocytoma  Acinic cell carcinoma
 Other adenomas  Adenocarcinoma
 Malignant mixed tumour
Mesenchymal  Squamous cell carcinoma
 Haemangioma  Undifferentiated carcinoma
 Lymphangioma
 Lipoma Mesenchymal
 Neurofibroma  Lymphoma
 Sarcoma

Benign tumors

Pleomorphic Adenoma
"Mixed tumors" → both epithelial and mesenchymal elements are seen in histology
 Most common benign tumor, can arise from the parotid, submandibular or other minor salivary
glands. (in parotid it usually arises from its tail)
 Slow-growing tumors and may be quite large at initial presentation
 No facial nerve palsy
 Th: lateral lobectomy, total removal of the gland with preservation of the facial nerve.

Adenolymphoma (Warthin's Tumor)

 They are commonly seen b/w 5th-7th decade with preponderance in males
 They mostly involve the tail of the parotid and are bilateral in 10% of the patients.
 They may be multiple.
 Rounded, encapsulated tumour, at times cystic, with mucoid or brownish fluid.
 Treatment is superficial parotidectomy though they can be enucleated without danger of
recurrence
Haemangiomas
Haemangiomas are the most common benign tumors of the parotid in children
 predominantly affecting females
 Most of them are discovered at birth, grow rapidly in the neonatal period and then involute
spontaneously.
 Cutaneous haemangioma may co-exist in 50% of the patients.
 Soft and painless and ↑ in size with crying or straining.
 Overlying skin may show bluish discoloration.
 Surgical excision is indicated if they do not regress spontaneously

Lymphangiomas
 Are less common and may involve parotid and submandibular glands.
 On palpation, they feel soft and cystic.
 They do not regress spontaneously and are surgically excised

Malignant tumors
 Not painful
 Skin involvement
 Fixation
 No infla.
 Facial nerve involvement
 Th: radical removal, facial nerve resection+ND

Muco-epidermoid cc → slow growth, majority occurs in the parotid. It May transform into sqamous
anaplastic tumor.

Adenoid cyst cc → mainly in minor salivary glands of the hard palate, they may perforate the
perineural spaces, causing pain and difficult to remove totally.

Acinic cell cc: its cells resemble the normal serous cells of the glands → Good prognosis
Topic 20. Stenosis in the larynx and upper respiratory tract. Treatment of this disease

Laryngeal stenosis is a congenital or acquired narrowing of the AW

May affect supraglottis, glottis, and/or subglottis (subglottis is the most common site)

Congenital Subglottic Stenosis

Results from failure of the laryngeal lumen to recanalize.
During normal development, the laryngeal lumen is obliterated to give rise to the epi. lamina, which
later recanalizes. By 10th week of gestation → laryngeal lumen is reestablished following recanalization.
Incomplete recanalization results in various degrees of glottic and/or subglottic stenosis.
 3rd most common laryngeal anomaly
 Congenital laryngeal atresia represents the most severe form

Types
1. Membranous → circumferential, thickened mucous glands or fibrous tissue
2. Cartilaginous → abnormal shelf on cricoid or a trapped 1st tracheal ring
3. Mixed

Grades
I. <70% obstruction
II. 70–90%
III. 91–99%
IV. Complete obstruction

Clinical presentation
 biphasic stridor (insp. and exp.) in first few months of life, may mimic croup or recurrent URI
 Cry is normal
 failure to thrive

Diagnosis
Made when subglottic diameter is < 4 mm in full-term neonate (normal 4.5-5.5 mm) or 3 mm in
premature neonate (normal 3.5 mm).
 Endoscopy, CXR, neck plain films, flexible nasopharyngoscopy to assess vocal fold motion

Treatment
Many cases of congenital stenosis improve as the larynx grows but some may require surgery
May require tracheotomy (decannulation by 2–3 years old)
Grade I–II → consider endoscopic management (CO2 or KTP laser excision with dilation)
Grade III–IV → open Procedures
 Anterior Cricoid Split → no graft required, indicated to wean off of a ventilator before a
tracheotomy is performed, indicated for a trapped first tracheal ring
 Posterior Cricoid Split → indicated for posterior stenosis, may use costal graft, usually requires
a stent, may also be used concurrently with an anterior cricoid split
 Anterior Laryngofissure with Anterior Lumen Augmentation → requires an anterior graft
 Laryngofissure with Division of Posterior Cricoid Lamina → required if posterior glottis
involvement, upper tracheal stenosis, or complete glottis stenosis
 Laryngofissure with Division of Posterior Cricoid Lamina with ant. and post. grafts
 Segmental Resection with End-to-End Anastomosis
 Hyoid Interposition
 Rotary Door Flap
 Epiglottic Reconstruction
Acquired Laryngeal Stenosis
1) ET tube → pressure necrosis results in ulceration and cart. exposure, healing result in fibrosis
2) Postoperative → pressure necrosis from a high tracheotomy or from a cricothyroidotomy
3) Granulomatous Disease → TB, sarcoidosis, rhinoscleroma (Klebsiella), Wegener’s
granulomatosis
4) Infectious → leprosy (epiglottic and vocal fold ulceration), syphilis, histoplasmosis…
5) Idiopathic
6) Trauma → foreign body, caustic ingestion, blunt trauma, hematoma, thermal injury
7) Systemic → CT disorders, GERD, radiation effects
8) Neoplasia → chondroma, fibroma, malignancy

 Symptoms: inspiratory or biphasic stridor, dyspnea, cough

 Diagnosis: flexible nasopharyngoscopy, endoscopy, or videostroboscopy, CT of neck

Supportive therapy
 Administer humidified oxygen and monitor airway closely in a supervised setting.
 Symptomatic patients benefit from preoperative systemic steroids.
 Treat gastroesophageal reflux aggressively.
 When the stenosis is due to infections or inflammatory disorders, appropriate management in the
form of antibiotics and/or steroids is important.
 Steroid injection into posterior glottic or subglottic scars has had mixed results and is not used
routinely.
 Inhalational steroids (dexamethasone) are sometimes used to reduce formation of granulation
tissue in the airway.

Surgical treatment
Overall, the trend in management of glottic and subglottic stenosis is shorter stenting periods and
less-invasive techniques
Endoscopic excision (laser) or dilation for thin webs (thicker webs require ext. approaches)
Topic 21. Differential diagnosis of dysphonia

The term Dysphonia refers to voice disorders characterized by hoarseness, weakness or even loss of
voice (aphonia)

Types of dysphonia
Organic dysphonia
Occurs due disorders such as laryngitis, tumor, trauma, endocrine (Hypothyroidism / hypogonadism),
Haematological (Amyloidosis), Iatrogenic (inhaled corticosteroids)

Functional dysphonia
It is a functional disorder mostly seen in emotionally labile females in the age group of 15-30. Mostly
occurring due to psychogenic, vocal misuse or idiopathic causes
 Aphonia is usually sudden and unaccompanied by other laryngeal symptoms.
 Patient communicates with whisper.
 On examination, vocal cords are seen in abducted position and fail to adduct on phonation;
however adduction of vocal cords can be seen on coughing, indicating normal adductor function.
Even though patient is aphonic, sound of cough is good.
 Treatment given is to reassure the patient of normal laryngeal function and psychotherapy.

Spasmodic dysphonia → used by the excessive tension in the laryngeal muscles

Symptoms
 Characterized by intermittent, involuntary tightening or constriction of the larynx (voice box)
during phonation.
 The interruption of air flow results in staccato, jerking, labored speech.
 Occasionally, vocal spasms can abduct or separate the vocal folds, resulting in breathy voice
breaks (abductor spasmodic dysphonia).

Chronic dysphonia
Can occur in people such as teachers who use their voices a lot, and in people who have experienced
trauma or surgery that affected the larynx.
It can also start out as a virus that causes chronic laryngitis.
In some cases, gastro-esophageal reflux can cause chronic hoarseness.

Diagnosis
Some voice changes can signal disorders such as vocal cord polyps or the onset of cancer or other
diseases, so it is important to pinpoint the source of the problem promptly. To do so, the physician can
refer you to an ENT specialist who can perform a diagnostic procedure called indirect or direct
laryngoscopy, or video-laryngoscopy.

Treatment
 Conservative treatment includes avoiding vigorous use of the voice (singing, shouting) and throat
lozenges.
 Acute laryngitis from a virus should resolve on its own, while acute laryngitis from a bacteria may
be improved with an antibiotic.
 In GERD, treatment with an acid blocker (PPI or H2-blocker) may be effective.
 Some cases of dysphonia may require surgical intervention.
Differential diagnosis
1) Inflammations
 Acute → Acute laryngitis usually following cold, influenza, exanthematous fever, laryngo-
tracheo-bronchitis, diphtheria
 Chronic→ Chronic laryngitis, atrophic laryngitis, TB, syphilis, scleroma, fungal infections
2) Tumors
 Benign → Papilloma (solitary and multiple), haemangioma, chondroma, fibroma, leukoplakia
 Malignant → Carcinoma
 Tumor-like masses → Vocal nodule/polyp, angiofibroma, amyloid tu., contact ulcer, cysts,
laryngocele
3) Trauma → Submucosal haemorrhage, laryngeal trauma (blunt and sharp), foreign bodies,
intubation
4) Paralysis → Paralysis of recurrent, superior laryngeal or both nerves
5) Fixation of cords → Arthritis or fixation of cricoarytenoid joints
6) Congenital → Laryngeal web, cyst, laryngocele
7) Miscellaneous → Dysphonia plica ventricularis, myxoedema, gout
8) Functional → Hysterical aphonia
Topic 22. Palpation of the neck and its consequences in the practice.

Examination of neck nodes is important, particularly in head and neck malignancies and a
systematic approach should be followed.
Neck nodes are better palpated while standing at the back of the patient.
Neck is slightly flexed to achieve relaxation of muscles

The nodes are examined in the following manner so that none is missed:
1) Upper horizontal chain → examine submental, submandibular, parotid, facial, postauricular
and occipital nodes.
2) External jugular chain → lies superficial to sternomastoid.
3) Internal jugular chain → examine the upper, middle and lower groups. Many of them lie
deep to sternomastoid muscle which may need to be displaced posteriorly.
4) Spinal accessory chain.
5) Transverse cervical chain.
6) Anterior jugular chain.
7) Juxtavisceral chain → Prelaryngeal, pretracheal and paratracheal nodes.

When a node or nodes are palpable, look for the following points:
 Location, number and size of nodes
 Consistency
- metastatic nodes are hard
- lymphoma nodes are firm and rubbery
- hyperplastic nodes and nodes of metastatic melanoma are soft.
 Discrete or matted nodes.
 Tenderness → infla. nodes are tender.
 Fixity to overlying skin or deeper structures→ mobility should be checked both in the vertical
and horizontal planes.

Thyroid Gland
1. Inspect the neck looking for the thyroid gland. Note whether it is visible and symmetrical. A
visibly enlarged thyroid gland is called a goiter.
2. Move to a position behind the patient.
3. Identify the cricoid cartilage with the fingers of both hands.
4. Move downward 2-3 tracheal rings while palpating for the isthmus.
5. Move laterally from the midline while palpating for the lobes of the thyroid.
6. Note the size, symmetry, and position of the lobes, as well as the presence of any nodules. The
normal gland is often not palpable.