MBBS (Prefinal) OtolaryngologyMarch 2010

Question paper with solutions

Dr T Balasubramanian

www.drtbalu.co.in

MBBS (Prefinal) Otolaryngology March 2010

Essay – 2x15

a. What is cholesteatoma? Describe its etiology, pathogenesis,clinical features and management

Definition:

Cholesteatoma is defined as a cystic bag like structure lined by stratified squamous epithelium on a

fibrous matrix. This sac contains desquamated squamous epithelium. This sac is usually present in

the attic region. Cholesteatoma is also referred to as “skin in the wrong place”. Histologically

cholesteatoma is known to contain all the layers of cutaneous epithelium. The basal layer

(germinating layer) is present on the outer surface of the sac directly in contact with the middle ear

mucosa.

Theories explaining the etiopathogenesis of cholesteatoma:

Various theories have been postulated explaining the etiopathogenesis of cholesteatoma.

These include:

Cawthrone theory : This theory was proposed by Cawthrone in 1963. He suggested that

cholesteatoma always originated from congenital embryological cell rests present in various areas of

temporal bone.

Tumarkin's theory of immigration : This theory suggested by Tumarkin suggests that cholesteatoma

was derived from migration of squamous epithelium from the deep portion of the external auditory

canal into the middle ear cleft. This migration usually took place through a marginal perforation or

total perforation of the ear drum which includes even the annulus (due to necrotizing otitis media).

Toss theory of invagination : Toss postulated that presence of persistent negative pressure in the

attic region causes invagination of pars flaccida causing a retraction pocket. This pocket later

becomes filled with desquamated epithelial debris, which later forms the nidus for infection.

Common organism that are known to infect this keratin debris include pseudomonas, Ecoli, Proteus

etc. Toss also graded the attic retraction in to 4 grades.

Grade I – The retracted pars flaccida is not in contact with the neck of the malleus.

Grade II – The retracted pars flaccida is in contact with the neck of the malleus to such an extent that

it seems to cloth the neck of malleus.

Grade III – In addition to the retraction pocket being in contact with the neck of the malleus, the outer

attic wall (scutum) shows limited erosion.

Grade IV – In this stage in addition to all the changes described in the previous three stages there is

severe erosion of outer attic wall.

Wendt theory of metaplasia – This theory was suggested by Wendt in 1873. According to Wendt the

attic area of the middle ear cavity is lined by pavement epithelium which undergoes metaplastic

transformation to stratified squamous epithelium in response to infection. This metaplasia forms

a nidus for infection.

Of all these theories the theory of invagination appears to the most plausible one which could

account for all the features of cholesteatoma.

Clinical features:

The following are the clinical features of acquired cholesteatoma:

Ear discharge – It is usually scanty and foul smelling in these patients. The odor has been classically

described as musty in nature. The probable cause for this odor is the presence of osteitic reaction

and saprophytes within the cholesteatomatous cavity.

Hearing loss – Highly variable. Commonly patients with attic choleateatoma present with

conductive hearing loss. Normal hearing is also possible even in patients harboring a large

cholesteatomatous mass in the middle ear cavity. This is probably due to the bridging effects

of the cholesteatoma mass. Sensorinerual hearing loss is also possible in these patients.

Probable causes for SN loss in these patients include:

a. Absorption of bacterial toxins into the inner ear via the round window

b. Erosion of the bony labyrinth by the cholesteatomatous mass causing contamination of the

inner ear fluids.

c. Administration of topical antibiotics which could be ototoxic

Ear ache – In these patients is due to the presence of coexisting otitis externa. If the ear ache is

intense and worse during night then the presence of extradural abscess should be ruled out.

Tinnitus – If present in these patients indicate imminent sensorineural hearing loss.

Vertigo – If present may indicate erosion of the lateral semicirular canal by cholesteatoma matrix.

Fistula test is invariably positive in these patients.

Fistula test – is positive if a third window is present in the labyrinth in addition to the round and

oval windows. This third window is usually caused by labyrinthine erosion caused by

cholesteatoma matrix. Dome of the lateral semicircular canal is commonly involved due to its

proximity to the floor of the aditus. This test is performed by using a snugly fitting Siegel's

pneumatic speculum and applying pressure to the ear drum by compressing the pneumatic bulb.

If labyrinthine fistula is present this pressure impulses would be transmitted to the labyrinthine

fluids causing giddiness and nystagmus. The presence of positive fistula sign in patients with

cholesteatoma always indicate erosion of labyrinth.

Facial nerve palsy – May be seen if facial canal is eroded and the facial nerve is involved by

cholesteatoma.

Theories proposed to explain the invasive nature of cholesteatoma:

a. Pressure theory – This theory states that the increase in the size of cholesteatoma may lead

to bone erosion due to pressure necrosis. Increasing pressure by the enlarging mass could

lead to ischemic necrosis of bone leading on to osteitic reaction.

b. Enzymatic theory – Histological studies have demonstrated the presence of osteoclasts and

histiocytes within the cholesteatoma matrix. These cells are known to release acid phosphatase,

Collagenase and other proteolytic enzymes. These enzymes have known to cause bone

erosion.

c. Pyogenic osteitis – Pyogenic bacteria present in the attic region may release enzymes which

may cause bone resorption.

Types of cholesteatoma:

Congenital

Acquired

Primary acquired – In this type of cholesteatoma there is no history of pre existant / previous

episodes of otitis media or perforation. Lesions arise from the attic region due to the presence

of retraction pocket.

Secondary acquired – This type of cholesteatoma follows active middle ear infection that manages

to destroy the annulus as well as a major portion of the ear drum. This condition is also known

as necrotizing otitis media which occurs following exanthematous fever like measles.

Management: Cholesteatoma is a surgical condition. The aims of surgical management include:

a. Removal of the disease

b. Exteriorizing the middle ear by creating a large cavity consisting of mastoid cavity, attic portion

middle ear cavity and external auditory canal.

c. Reconstruction of sound conduction mechanism if possible.

Recommended surgical procedure is Modified Radical Mastoidectomy. This procedure includes:

a. Exenterating the mastoid air cell system

b. Removing the outer attic wall / scutum with removal of cholesteatoma matrix

c. Making the attic, aditus, middle ear and mastoid in to one single cavity

d. Exteriorizing the cavity created by performing a sufficiently large meatoplasty

This is achieved by:

Opening up the mastoid cortex, removal of outer attic wall, removal of bridge and lowering of

facial ridge. This leaves behind a fairly large cavity which needs to be exteriorized by a

sufficiently large meatoplasty.

b. A male patient aged 60, chronic smoker, comes with c/o Hoarseness of voice of 1 year of 1 yr

duration. How do you investigate and treat him?

Introduction:

Vocal cord undergoes changes due to exposure to pollutants and cigarette smoke. Cigarette smoke

is supposed to contain carcinogens which causes the vocal folds to undergo excess keratinization.

This excess keratinization causes whitish thickening of the vocal folds with loss of normal mucosal

wave pattern leading on to hoarseness of voice. It should be borne in mind that hoarseness of voice

in a chronic smoker should always be viewed with caution as there is likelihood of malignancy.

Investigations:

Videolaryngoscopy – This is performed under local anesthesia. It helps in the assessment of vocal

fold status in real time. Thickening of the vocal folds can be clearly documented and recorded.

Mobility of vocal cords can be assessed. Hyperkeratosis of the vocal folds / carcinoma in situ can

only be identified after studying the histopathology of the lesion for which biopsy of the suspicious

looking lesion is a must.

Direct laryngoscopy under GA / LA should be performed if there is a suspicious looking lesion in

the vocal fold as seen in videolaryngoscopy examination.

Smoker's laryngitis – This is chronic inflammation of vocal folds commonly seen in chronic smokers.

Since these patients have bronchitis they constantly keep coughing putting the vocal folds under

tremendous amount of stress. This causes inflammation of vocal folds leading on to hoarseness of

voice. These patients will benefit from cessation of smoking and improved hydration.

Hyperkeratosis of vocal folds – can be managed by cessation of smoking, encouraging the patient to

consume lots of fluids and providing absolute rest to the voice. Keratotic patches can be stripped

away from the vocal folds by performing microlaryngeal surgery under general anesthesia.

This condition also goes by the term leukoplakia.

Premalignant conditions – Vocal fold dysplasias should be considered as premalignant lesion. If the

biopsied material from the vocal fold is reported as dysplasia then the whole suspicious looking

lesion should be surgically removed. If necessary the whole mucosal lining of the vocal fold can be

stripped leaving it bare for fresh mucosa to regenerate. Management of these premalignant lesions

should include complete abstinence from smoking.

Carcinoma in situ – This is the early malignant change which takes place on the surface of the vocal

folds. This lesion if treated properly carries the best prognosis. Since these patients develop

hoarseness of voice they seek treatment at an early stage. This type of lesion is limited to the

epithelial layer of the vocal fold and doesn't show invasion of lamina propria. Since vocal cords don't

have lymphatic supply metastasis to regional nodes is not a risk at all. Regional metastasis is

possible only when the lamina propria is breached and the lesion comes into contact with vocalis

muscle. These lesions are best managed by vocal cord stripping. This is performed using a Direct

laryngoscope under general anesthesia. Laser when used for this purpose reduces the morbidity

and mortality of the surgery. Irradiation is not indicated in these patients as these borderline lesions

may undergo malignant transformation when exposed to it. Major clinical difference between

carcinoma in situ and carcinoma of vocal fold is that in carcinoma in situ the affected cord is still

mobile since the vocalis muscle is not involved. In carcinoma of vocal fold the cord is fixed due to

involvement of vocalis muscle. This vocalis muscle is richly supplied with lymphatics and hence

involvement of this muscle could lead to nodal metastasis.

Malignant growth vocal cord – In this condition the vocal cord appears fixed. This is due to the fact

that vocalis muscle is involved by the lesion. If there is just restriction of mobility of the cord with no

involvement of anterior commissure area then cordectomy can be performed with reasonable degree

of assured clearance.

Total laryngectomy should be resorted to if there is involvement of paraglottic space / anterior

commissure area is suspected. In addition these patients should be subjected to conventional

curative doses of radiotherapy in order to sterilize the potential cervical nodal metastasis.

Short notes: 10x5= 50

1. Middle ear cleft – The middle ear cleft is also known as Tympanum, Middle ear proper. The

middle ear cleft includes: Middle ear cleft proper, mastoid air cell system and the eustachean tube.

Definition – The middle ear cleft is defined as an irregular air filled space present within the temporal

bone. In simple terms the middle ear cleft could be considered as a box with four walls with a roof

and floor. The corners of this hypothetical box are not sharp.

Contents of middle ear cleft proper -

Air

Three ossicles (Malleus, Incus, and Stapes).

Two muscles (Stapedius and tensor tympani).

Lateral wall – This wall is partly bony and partly membranous. The central portion of this wall is

formed by tympanic membrane. Above and below the pars tensa portion of this membrane lie the

attic and hypotympanum respectively. The portion of ear drum covering the lateral wall of attic lacks

the middle fibrous layer and hence known as parsflaccida. The lateral wall of attic is partly bony and

this portion is known as the outer attic wall or scutum. This wall is eroded in patients with attic

cholesteaoma. The lateral wall of hypotympanum is also partly bony. There are three openings seen

on the medial surface of the bony portion of the lateral wall. The first opening is the posterior

canaliculus for the chorda tympani nerve. This opening is situated at the junction of the lateral and

posterior walls of the tympanic cavity. This opening is usually present at the level of upper end of the

handle of malleus. This opening leads to a bony canal which descends through the posterior wall of

the tympanic cavity. Since the chorda tympani nerve traverses this canal it is known as the canal of

the chorda tympani nerve. The second opening is the petrotympanic (Glasserian fissure). This

opening anteriorly receives the anterior malleolar ligament. The third opening is for the canal of

Hugier. This canal lies medial to the Glasserian fissure. The chorda tympani nerve enters through

this.

Roof – Of the middle ear cavity is formed by the tegmen tympani which separates it from the dura of

middle cranial fossa.

Floor – This portion of middle ear is narrower than that of the roof. It overlies the jugular bulb. At the

junction of the floor and medial wall of middle ear there is an opening through which the tympanic

branch of glossopharyngeal nerve enters the middle ear cavity.

Anterior wall – Of middle ear cavity is narrow because of the convergence of medial and lateral walls

here. This wall can be divided for the sake of convenience into a large lower portion and a smaller

upper portion. The lower portion is related to the internal carotid artery as it enters the skull. This

portion of the anterior wall has two openings i.e. for the entry of superior and inferior carotico

tympanic nerves. The smaller upper part of this wall has two tunnels placed one above the other.

The superior tunnel is for tensor tympani muscle and the inferior one is for the bony portion of the

eustachean tube.

Medial wall – This wall separates the middle ear from the inner ear. The most prominent portion of

the medial wall of middle ear is the promontary which overlies the basal turn of the cochlea.

The promontary has numerous grooves over its surface on which lies the tympanic plexus of nerves.

Behind and above the promontary lies the oval window also known as fenestra vestibuli. This oval

shaped opening connects the middle ear cavity to the vestibule. This window is closed by the foot

plate of stapes.

Above the oval window lies the canal through which the facial nerve traverses.

The round window also known as fenestra cochlea lies below and behind the oval window. In life it is

closed by the secondary tympanic membrane. The nerve supplying the ampulla of the posterior

semicircular canal (singular nerve) lies close to the secondary tympanic membrane. Thus the

secondary tympanic membrane proves to be a useful landmark to identify singular nerve during

singular neurectomy procedures performed to treat intractable vertigo. These two windows i.e. round

and oval are separated by posterior extension of promontory and is known as the subiculum.

The middle ear cleft is ventilated via the eustachean tube.

Posterior wall – This wall is wider above than below. In its upper part is present an important

opening known as the aditus through which the middle ear cavity communicates with the mastoid air

cell system. Below this opening lies a small depression known as the fossa incudis which houses

the short process of incus. Below the fossa incudis lies the pyramid out of which the stapedial

tendon exits to get attached to the neck of the stapes. The stapedial muscle lies entirely within the

pyramid. Between the promontory and tympanic annulus lie the facial recess area.

Facial recess: This is bounded medially by the facial nerve and laterally by the tympanic annulus.

The chorda tympani nerve runs between these two walls with varying degrees of obliquity. This

nerve always lie medial to the ear drum.

Cholesteatoma may lurk in this area and can lead to recurrence of CSOM. Drilling in this area

between the facial nerve and annulus in the angle formed by the chorda tympani nerve will

lead into the middle ear cavity. This is the commonly used approach to reach the round window

while performing cochlear implant procedures. Hypotympanum may also be reached through this

approach.

Sinus tympani – This is a small depression present at the border between the posterior and medial

walls of tympanic cavity. This depression always lie between the round and oval windows. It is

bounded laterally by the facial canal and pyramidal eminence. This sinus is important from the stand

point of residual cholesteatoma.

The chain of three ossicles i.e. malleus, incus and stapes conduct sound vibrations from the ear

drum and transmits it to the inner ear via the oval window.

Malleus – is the largest of the three ossicles and is shaped like a hammer. It has a head, neck and

three processes arising below the neck. Its head lies in the attic region effectively dividing it into

anterior and posterior portions. During surgical procedures for the management of cholesteatoma

the whole attic can be visualized only after clipping the head of the malleus. The head of the malleus

articulates with incus.

Incus – Is the second largest of the three ossicles and is shaped like an anvil. It has a body and two

processes. It articulates with the head of the mallues. Its short process lodges in the fossa incudis

while its long process articulates with the head of the stapes.

Stapes – Is the smallest of the three ossicles. It has a head, neck, two crura and a base. The base

is also known as the foot plate and it closes the oval window in life there by transmitting the

soundwaves into the inner ear fluids.

2. Physiology of nose – The physiological role played by the nose have always be conjectural.

Several hypothesis have been made. For easier understanding it may be grouped under three

heads: Structural theory, evolutionary theory and functional theory.

Structural theory: This is also known as Fallopio's theory. This was proposed way back

during the 16th century by Fallopio who hypothesized that the paranasal sinuses perform an

important function of making the skull bone lighter thereby effectively reducing the load on neck

musculature. He also suggested that these sinuses contribute to the maintenance of equilibrium

and the positioning of the head by lightening the anterior portion of the cranium.

Proetz theory: This theory suggested by Proetz suggests that the paranasal sinuses play a

role in remodeling of facial bones.

Evolutionary theory: This theory was proposed by Hardy. He considered paranasal sinsues

to be evolutionary response of anthropomorphic monkeys to shift from terrestrial environment to an

aquatic one. This was a necessity as they had to swim vast stretches of water 6.5 million years ago

when the whole continent of Africa was surrounded by sea. Hardy also suggested that this evolution

could have occurred by natural selection.

Functional theory:

Bartholini' s theory – Bartholin considered these cavities to be organ of resonance adding

resonance to the voice.

Cloquet's theory – Cloquet hypothesised that nose and paranasal sinuses functioned as a

single olfactory unit. This has been proved to be false as olfactory epithelium has not been

demonstrated in the sinus cavities.

Ventilatory function: The inspired air travels through the nasal cavity which is lined by ciliated

columnar epithelium which also contains mucoid glands. This epithelium adds moisture to the

inspired air making it fit for respiration. It also filters the dust particles from the inspired air due to the

turbulance caused to the air due to the presence of turbinates.

Immune defense: The mucosa of nose and paranasal sinuses play a vital role in protecting the lower

airways from infections. This defense mechanism can be divided in to nonspecific (which is

phylogenetically older) and specific (phylogenetically newer). The older nonspecific immunity is

brought about by factors like: lysosomes (destroys bacterial wall), interferon, complement and

enzymes. Specific immunity is provided by the presence of macrophages, immunoglobulin secreting

lymphocytes from NALT (Nose associated lymphoid tissue). The immunity provided by this specific

mechanism is against specific microbes.

Olfaction: Nasal cavity is endowed with olfactory epithelium which plays an important role in

the perception of smell. This happens to be one of the primitive and phylogenetically oldest

sensation.

3. Glue ear: This condition is also known as secretory otitis media, serous otitis media, Non

infective otitis media.

Definition: This condition is defined as chronic accumulation of mucous within the middle ear

cavity. This condition can also rarely involve the mastoid air cell system. This accumulation causes

conductive hearing loss.

Pathophysiology: The pseudostratified ciliated columnar epithelium of respiratory tract

extends up the eustachean tube. It also extends to involve the inferior portion of the middle ear

cavity (Hypotympanum). Goblet cells capable of secreting mucous are seen in the midst of this

epithelial lining. Otitis media with effusion (glue ear) is caused by inflammation of this epithelium

lining the eustachean tube and hypotympanum. In patients with glue ear the cuboidal epithelium of

the rest of the middle ear cavity and mastoid gets replaced by pseudostratified ciliated columnar

epithelium. The cilia of these cells have found to be ineffective in propelling the secretions into the

eustachean tube. The submucosa appears oedematous and inflammed with dilated blood vessels

and increased number of macrophages and plasma cells.

Etiology:

1. In most of the children glue ear is often preceded by an episode of acute otitis media. This is more

so because children are more prone to upper respiratory infection. Commonly viral infections cause

this problem as they cause extensive damage to the mucosa of the eustachean tube.

2. Craniofacial abnormalities: Children with cleft palate due to their deficient functioning of palatal

muscles have pre existing eustachean tube function which predisposes to the development of

chronic glue ear. .

3. Allergy: Nasal allergy has been postulated to be an important cause for the development of glue

ear.

4. GERD: Gastrooesophageal reflux has been identified in a majority of children affected by glue ear.

Analysis of middle ear fluid has demonstrated the presence of significant quantities of pepsin which

could have come only from the gastric secretions.

5. Parental smoking: Exposure to parental smoking has been implicated as one of the cause for the

development of glue ear in children.

Age of occurrence: Glue ear classically shows bimodal distribution. The first peak is seen

around 2 years of age while the second is seen at about 5 years of age (school going age). It is

during these phases of growth the child is more prone for respiratory infections.

Seasonal association: Glue ear commonly occurs during winter season when there is more

likelihood of respiratory infections due to closer contact with infected children. In fact it has been

suggested that every child with upper respiratory infection should have their ears examined

otoscopically. This is more so in children living in temperate zones. Children living in tropics are

more prone to get glue ear during monsoon season.

Clinical features: A high index of suspicion is necessary in order to diagnose this condition.

Every child with upper respiratory infection should have an otoscopic examination done.

Otoscopic findings:

Bulging / retracted tympanic membrane

Distorted cone of light

The ear drum may be yellow/blue/dirty white in color

Pneumatic otoscopy may reveal restricted mobility of ear drum

Investigations:

Pure tone audiometry – Demonstrates mild /moderate conductive deafness

Tympanogram – Tympanometry is used as a screening test to identify patients with glue ear.

Commonly type B tympanograms are seen.

Free field audiometry: Is performed in infants and can identify deafness.

Management:

Conservative – Antibiotics (Amoxycillin is the drug of choice followed by cephalosporins).

Nasal decongestants – Oxymetazoline / xylometazoline can be used

Balloon blowing (autoinflation of eustachean tube) may help

Steroid nasal spray may help to tackle resistant cases

Surgical management: This includes adenotonsillectomy in an effort to remove focal infection

and Grommet insertion to drain the middle ear cavity.

4. Retropharyngeal abscess:

Definition: It is defined as collection of pus between the posterior pharyngeal wall and the

fascia and muscles covering the cervical vertebrae.

Classification – Retropharyngeal abscess occurs in two forms which differ in etiology

Acute retropharyngeal abscess – Common in infants

Chronic retropharyngeal abscess – Common in adults

Acute retropharyngeal abscess – Is more dangerous type and is seen in infants between age

groups ranging from 3 months to 3 years. Predisposing factors for this condition include malnutrition,

gastroenteritis, poor hygiene etc.

Etiology:

1. May follow general deblitating illnesses like scarlet fever, measles etc.

2. Infections from tonsils / adenoids / nasopharynx may extend to this area causing absess

3. Impacted foreign bodies like bone bits / pin (rare)

Pathophysiology – This disorder begins with suppuration of retropharyngeal lymph node of

Henle. These nodes are usually situated on either side of midline between the posterior pharyngeal

wall and the aponeurosis over the bodies of second and third cervical vertebrae. These nodes

receive lymphatics from the post nasal space, pharynx, nose, eustachean tube and middle ear.

These nodes usually undergo atrophy during the 3rd to 5th year, hence it is uncommon in children

above the age of 5. This node of Henle first gets infected from the lymphatic drainage area causing

adenitis first. Later there is development of periadenitis and suppuration. This suppuration is usually

localized to one side of the posterior pharyngeal wall. If it does not rupture / nor evacuated this

abscess may spread in different directions – towards larynx, angle of the jaw or even into the

external auditory canal. The purulent material is usually foul smelling and may contain streptococci

and more rarely staphylococci / pneumococci.

Chronic retropharyngeal abscess – Has a different etiopathology and commonly occurs in

adults. This is commonly caused by tuberculosis involving the cervical vertebrae (Pott's spine). This

infection later spreads to the retropharyngeal space. Primary syphilis of oral cavity may also lead on

to the formation of retropharyngeal abscess. This abscess is usually present on the midline in

contrast to the acute retropharyngeal abscess which is present on either side of the midline. As the

size of the swelling increases it can spread to either side.

Clinical features:

1. Painful swallowing (odynophagia) – Young infant may refuse feeds

2. Drooling of saliva

3. Adults may hold their head straight in order to avoid pain

4. Infants may have torticollis

5. Stridor may occur due to airway compromise

6. Constitutional symptoms like fever and toxicity are common in acute retropharyngeal

abscess

Investigations:

X-ray soft tissue neck AP/Lat - Will show prevertebral soft tissue widening. It should be

borne in mind that the normal prevertebral soft tissue thickening is about half the size of

corresponding cervical vertebra. There is always straightening of cervical spine (Ram Rod spine)

due to the presence of cervical paraspinal muscle spasm. In almost all these patients a small air

pocket could be seen above the prevertebral soft tissue mass in the lateral view. This air shadow

could be caused due to entrapment of swallowed air, or due to gas formed by organism like

clostridia.

CT Scan / MRI – Really clinches the diagnosis. CT scan helps in differentiating cellulitis from

abscess. It should ideally be performed using contrast. Contrast CT will show a hypodense lesion in

the posterior pharyngeal wall with ring enhancement along with obliteration of normal fat planes.

Management:

1. Incision & drainage should be performed at the earliest if it is acute retropharyngeal

abscess. It should ideally be performed under local anesthesia taking precaution that the child

doesn't aspirate pus during the procedure.

2. If the abscess points in the neck then it should be incised through the neck and the incision

should ideally be sited behind the sternomastoid muscle.

3. In chronic retropharyngeal abscess if tuberculosis is suspected then surgery is deferred and

the patient is immediately started on anti TB drugs.

4. After surgical drainage a course of antibiotics should be ideally started. The drug of choice

being drugs belonging to cephalosporin group. Metronidazole should also be administered because

of its efficacy against anaerobes.

Complications:

The following complications may occur if these patients remain untreated.

1. Mediastinitis

2. Airway compromise

3. Atlanto occipital dislocation

4. Jugular venous thrombosis

5. Cranial nerve deficits – especially the last three nerves

6. Hemorrhage secondary to involvement of carotid artery

5. Extracranial complications of csom: Includes

1. Facial nerve paralysis - Since the facial nerve courses extensively inside the temporal bone

it can very easily be damaged in infections involving the middle ear cavity. Damage can occur due to

oedema compromising its nerve supply, erosion of facial nerve canal with involvement of the nerve

itself. This causes a lower motor neuron type of facial palsy. These patients should undergo mastoid

exploration in order to clear the disease, and decompression of the facial nerve.

2. Suppurative labyrinthitis - This is infection of the inner ear due to bacterial pathogen and

toxin from the middle ear cavity. This commonly causes vestibular manifestation (vertigo), cochlear

manifestation (hearing loss) or both. Organism usually enters the inner ear via either round window

or erosion of the bony labyrinth. Suppurative labyrinthitis is of two types.

They include:

1. Toxic labyrinthitis – Due to diffusion of bacterial toxin into the inner ear via round window

membrane, internal acoustic meatus, and cochlear aqueduct. This type of labyrinthitis produces mild

high frequency sensorineural hearing loss and mild vestibular dysfunction which is self limiting. This

condition can be managed by antibiotics and myringotomy may be resorted to if the drum is bulging

due to pent up middle ear secretions.

2. Suppurative labyrinthitis – Due to bacterial infection of the inner ear. This goes through

classically 4 stages:

Serous / irritative labyrinthitis- In this stage there is production of Immunoglobulins in

the perilymph fluid. These patients have irritative labyrinthine symptoms like nystagmus to the side

of lesion. This condition is potentially reversible if treatment is initiated immediately.

Acute purulent labyrinthinthitis- In this stage suppuration starts in the inner ear due to

bacterial infections. This stage is associated with end organ necrosis and hence is irreversible.

Since the labyrinth has lost its function this stage is also known as dead labyrinth. These patients

have giddiness and severe degree of sensorineural hearing loss.

Fibrous labyrintitis – In this stage proliferation of fibroblasts and formation of granulation

tissue occludes periphymphatic space.

Osseous labyrinthitis – Also known as sclerotic labyrinthitis. This stage is characterized

by new bone formation.

Suppurative labyrinthitis should be considered to be a medical emergency. These patients

should be treated with antibiotics preferably parenteral. This is done in order to prevent infection

from migrating to intracranial tissues.

3. Labyrinthine fistula – This is a pathological communication between the fluids of inner ear

and the air filled middle ear cavity. This is caused due to erosion of the bone of inner ear by

cholesteatomatous matrix. Erosion is commonly seen over the lateral semicircular canal. Initially

this causes a serous labyrinthitis and gradually progresses to purulent labyrinthitis. These patients

manifest with vertigo and sensorineural hearing loss.

4. Subperiosteal abscess- This is collection of pus under the periosteal lining of the mastoid

process. This commonly occurs in patients with block in the aditus due to cholesteatoma. This is

usually caused due to hyperemic decalcification of the mastoid cortex with coalescence of air cells

due to destruction of their walls. These patients have pain and swelling behind the ear. There may

be mild to moderate conductive deafness. There is sagging of the posterosuperior meatal wall these

patients. Incision and drainage should be performed in these patients to alleviate pain.

5. Post aural fistula- Spontaneous rupture of subperiosteal abscess in the presence of

continuing infection involving the mastoid air cell may lead to excessive bone destruction in the

mastoid cortex area causing post aural fistula.

6. Petrositis – This is infection of air cells surrounding the petrous apex. For this to happen

these patients should have well pneumatized petrous apex. Diagnosis is usually based on deep

seated retro orbital pain, temporal headache, diplopia due to 6th cranial nerve palsy. The triad of

symptoms which include diplopia (due to lateral rectus palsy), otorrhoea, and retro orbital pain is

known as Gradenigo's syndrome. Retro orbital pain is usually caused due to involvement of 5 th

cranial nerve. If these patients do not respond to conservative medical management surgical

decompression should be resorted to.

6. Ethmoidal polyposis – Polyp is defined as simple oedematous hypertrophic nasal mucosa.

Ethmoidal polypi mostly arise from ethmoidal labyrinth. They project into the middle meatus as they

keep increase in size. Ethmoidal polypi are commonly seen in adults and are multiple in nature.

They are also bilateral. They polypi keep enlarging in size due to increase in their fluid content.

Gravity also plays a role in it increase in size.

Factors responsible for development of polypi in ethmoid air cells:

a. Ethmoidal air cells give rise to polypi due to their complex anatomy, poor blood supply and a

combination of adverse mucosal reaction at the cellular level.

b. Allergy has been attributed as one of the causative features due to its propensity for

causing odema of the mucosal lining of ethmoid air cells. This in turn leads to poor ventilation and

accumulation of secretions. Allergy due to the presence of bacterial toxins due to nasal sepsis have

also been known to contribute.

c. Bernoulli's phenomenon – This phenomenon states that when gases pass through a

constriction it causes a negative pressure area in the vicinity causing a suction effect which causes

prolapse of mucosa. This prolapsed mucosa undergoes oedematous changes and leads to polypi

formation.

d. If ethmoidal polypi are seen in children then mucoviscidosis should be rule out.

Clinical features:

a. Nasal obstruction usually bilateral

b. Anosmia in cases with severe ethmoidal polyposis

c. Watery rhinorrhoea

d. Head ache due to obstruction of sinus drainage channels

e. Broadening of nose due to polypi causing flaring / splaying of the bones causing frog faced

deformity.

Anterior rhinoscopy – Shows multiple glistening grape like masses which are painless and

insensitive to touch. These polypi can be probed all around.

Posterior rhinoscopy – Polypi involving the posterior ethmoid air cells and sphenoid air cells

can be seen coming out of the choana. This can be seen occluding the choana when posterior

rhinoscopy is performed.

Differential diagnosis -

1. Meningocele

2. Inverted papilloma

3. Enlarged turbinates

4. Angiofibroma

Management – Administration of antihistamines and steroids will help in shrinking the polypi

thereby increasing the comfort level of these patients. Endoscopic removal of these polypi is the

most preferred surgical management modality.

7. Hearing loss : Is also known as difficulty in hearing / hard of hearing.

Types of deafness:

1. Conductive – This type deafness is caused due to a disruption in the sound conduction

mechanism.

2. Sensorineural – This type of deafness is caused due to pathology involving the end organ of

hearing (cochlear hair cells) or nerves conducting the sound to brain or sound perception centers of

brain.

3. Mixed – In this type of hearing loss both conductive and sensorineural mechanisms are

involved.

Conductive deafness: Causes are enumerated here

Tests to identify conductive deafness:

1. Tuning fork tests – This includes Rinne and weber's test. These tests are usually performed

using tuning forks vibrating at the following frequencies – 256, 512, and 1024 Hz.

Rinne test - This tuning fork test is used to clinically evaluate hearing deficiencies in patients.

This test is designed to compare air conduction threshold with that of bone conducted threshold. In

patients with normal hearing air conduction is supposed to be better than bone conduction. This

test is ideally performed using tuning forks vibrating at 256, 512, and 1024 Hz. The tuning fork is

struck at the junction of upper 1/3 and lower 2/3 of the fork. As soon as the tuning fork starts to

vibrate it is placed over the mastoid process of the patient. The patient is instructed to raise the hand

as soon as the sound is not heard. Then the vibrating fork is shifted immediately and held close to

the external auditory canal in such a way that the vibrating prongs vibrate in an axis parallel to that of

the acoustic axis of the ear that is being tested. In normal hearing persons the fork will still be heard

when it is held close to the external auditory canal. This is known as positive Rinne test. In patients

with conductive hearing loss the fork will not be heard on being shifted close to the external auditory

canal. This is known as negative Rinne. Negative Rinne indicates conductive deafness.

Weber test - This test is very sensitive in identifying unilateral hearing loss. A vibrating fork is

placed over the forehead of the patient and is asked to indicate in which ear the tuning fork is heard

better. Under normal circumstances the fork will be heard in the midline. In patients with conductive

hearing loss it will be better heard in the ear with loss because the bone conducted sound is heard

better because the ambient noise is not heard in that ear. This is known as lateralization of weber's

test. This test is so sensitive that it can pick up a difference in hearing of even 5 dB between two

ears.

Sensorineural hearing loss:

Causes of sensorineural hearing loss

Management – Depends on the cause of hearing loss. Conductive hearing loss has the best

prognosis.

Impacted wax – if present should be removed.

Perforations involving ear drum should be repaired.

If the stapedeal foot plate is fixed then stapedectomy should be performed

If the middle ear ossicles are damaged then ossiculoplasty should be performed.

It is difficult to manage sensorineural hearing losses. Hearing aids may be beneficial. In

patients with severe degree of sensorineural hearing loss cochlear implants are the only way out.

8. Vocal nodule – Also known as Singers nodule / Teacher's nodule.

This disorder frequently affects children and adults. In children it appears as spindle shaped

thickenings of the edges of the vocal cords, whereas in adults they appear as more localised

thickenings, varying from small points - nodules. These nodules typically appear at the junction of the

anterior and middle 1/3 of the vocal cords. They appear almost aways symmetrically.

Pathophysiology – Vocal nodules are caused by a combination of overtaxing and incorrect use

of the voice. This is also aggravated by the presence of infections in the para nasal sinuses, tonsils,

and adenoids. Patients with habitual dysphonia frequently encounter this condition. This condition

can be effectively prevented or cured by voice rest or by using the voice properly. Infact the nodules

can appear and disappear in a matter of weeks. If the aggravating factors persist for a long time then

these nodules become permanent.

Stages of vocal nodule formation :

Stage of transudation - Oedema occurs in the submucosal plane in this stage. This occur

during the acute phase of the disorder. This stage is reversible in nature and may become normal on

giving voice rest.

Stage of ingrowth of vessels - In this stage neovascularisation of the area occur. This phase is

also reversible, but takes a long time to become normal.

Stage of fibrous organization - In this stage the transudate in the submucosal area is replaced

by fibrinous material. This stage is more or less resistant to conservative line of management.

These stages can be clearly observed by laryngoscopy under stroboscopic light. Local

oedematous swelling of recent onset vibrates in phase with the whole vocal fold, whereas an older

and more fibrous swelling can impede the vibrations so much that only a part of the cord is seen to

vibrate. The improvement in the vibration pattern or signs of recovery are picked up early during

stroboscopic examination.

Clinical features:

a. Change in voice

b. Fatiguability of voice

c. Decreased pitch range

Management:

a. Voice rest

b. Speech therapy

c. Treating focal infections of tonsils / sinuses etc.

d. Fibrous nodule should always be excised using Microlaryngeal technique

9. Deviated nasal septum -

Introduction – Septal deviations are pretty common occurrence. In fact a dot central nasal

septum is a clinical curiosity.

Aetiology:

Direct trauma - Many septal deviations are a result of direct trauma and this is frequently

associated with damage to other parts of the nose such as fractures of nasal bone.

Birth molding theory - Many patients with septal deviation do not give history of trauma. Birth

molding theory was propounded by Gray. According to him abnormal intrauterine posture may result

in compression forces acting on the nose and upper jaws. Displacement of septum can occur in

these patients due to torsion forces that occur during parturition. Dislocations are more common in

primipara and when the second stage of labour lasted for more than 15 minutes. Dislocations are

generally to the right in the case of left occipitoanterior presentations and to the left with right

occipitoanterior presentations. Subsequent growth of nose accentuates these asymmetries.

Differential growth rates of nasal septum and palate - This is the most acceptable theory

today. When the nasal septum grows faster in certain individuals than the palate then the nasal

septum starts to buckle under pressure.

Figure showing differential growth rates between nasal septum and hard palate showing

septal deviation.

Classification -

Deformities involving the nasal septum can be classified into:

1. Spurs

2. Deviations

3. Dislocations

Spurs - These are sharp angulations seen in the nasal septum occurring at the junction of the

vomer below, with the septal cartilage and / or ethmoid bone above. This type of deformity is the

result of vertical compression forces. Fractures that occur through nasal septum during injury to the

nose may also produce sharp angulations . These fractures heal by fibrosis that extend to the

adjacent mucoperichondrium. This increases the difficulty of flap elevation in this area.

Deviations - May be C shaped or S shaped. These can occur in either vertical or horizontal

plane. It may also involve both cartilage and bone.

Dislocations - In this the lower border of the septal cartilage is displaced from its medial

position and projects into one of the nostrils.

In patients with septal deviation a compensatory hypertrophy of the turbinates and bulla may

occur on the side opposite to the deviation. If compression forces are involved the septal deviations

are often asymmetrical and may also involve the maxilla, producing flattening of the cheek, elevation

of the floor of the affected nasal cavity, distortion of the palate and associated orthodontic

abnormalities. The maxillary sinus is usually slightly smaller on the affected side.

Effects of septal deviation:

Nasal obstruction - This is always found on the side of the deviation, and can also be present

on the opposite side as a result of hypertrophic changes of the turbinates.

Mucosal changes - The inspiratory air currents are abnormally displaced and frequently gets

concentrated on small areas of nasal mucosa, producing excessive drying effect. Crusting will occur

and the separation of the crusts often produces ulceration and bleeding. Since the protective mucous

layer is lost the resistance to infection is reduced. The mucosa around a septal deviation may

become oedematous as a result of Bernouilli's phenomenon. This oedema further increases nasal

obstruction.

Neurological changes - Pressure may be exerted by septal deviations on adjacent sensory

nerves can produce pain. This was first explained by Sluder and the resultant condition became

known as 'the anterior ethmoidal nerve syndrome'. In addition to these direct neurological effects,

reflex changes perhaps may result from septal deformities which affect the nasopulmonary and nasal

reflexes.

Symptoms - The symptoms caused by septal deviations are entirely the result of their effects

on nasal function. The dominent symptom being nasal obstruction, but this is rarely severe enough to

cause anosmia.

Signs - Septal deviations are evident on anterior rhinoscopy. This should be done without the

use of nasal speculum because the insertion of speculum is sufficient to straighten the nasal septum.

When the tip of the nose is lifted septal deviation become evident. Nasal obstruction may also be

present on the opposite side (paradoxical nasal obstruction). This is due to the presence of

hypertrophied turbinates. If the hypertrophy is limited to turbinate mucosa alone then it will shrink

when decongestant drugs are used in the nasal cavity. If the hypertrophy is bony then decongestant

drops is useless.

Septal deviations in the region of the nasal valve area cause the greatest obstruction, since

this is the narrowest part of the nasal cavity. This can be identified by the cottle test. A positive cottle

test will confirm the fact that narrowing is present in the nasal valve area. This is done by asking the

patient to pull the cheek outwards and this manuver is supposed to open up the area thus reducing

the block. The septum should not be considered in isolation and it is necessary to do a careful

examination of the lateral wall of the nasal cavity. When ever sinus complications like sinusitis is

suspected due to obstruction to the drainage channel of the sinuses by the deviation xray sinus must

be taken.

Septal deviation in new born is associated with asymmetry of the nostrils, an oblique columella

and tip which points in the direction which is opposite to the deviation. Most of these patients are

diagnosed by the use of Gray's struts. These struts are 4mm wide and 2mm thick and after

lubrication, are inserted into the nostrils and then gently pushed backwards along the floor of the

nasal cavity, hugging the nasal septum. Normally these struts can be introduced for a distance of 4 -

5 cms, but in cases of septal deviation a frank obstruction is encountered, usually 1 - 2 cms from the

nostril.

Cottle's classification of septal deviation: Cottle has classified septal deviations into three

types.

Simple deviation: Here there is mild deviation of nasal septum, there is no nasal obstruction.

This is the commonest condition encountered. It needs no treatment.

Obstruction - There is more severe deviation of the nasal septum, which may touch the lateral

wall of the nose, but on vasoconstriction the turbinates shrink away from the septum. Hence surgery

is not indicated even in these cases.

Impaction - There is marked angulation of the septum with a spur which lies in contact with

lateral nasal wall. The space is not increased even on vasoconstriction. Surgery is indicated in these

patients.

Management : SMR / Septoplasty.

Indications for SMR:

1. Marked septal deviation occurring behind the vertical line passing between the nasal

processes of the frontal and maxillary bones. This deviation must be the cause for the patient's

symptoms. 2. Closure of septal perforations

3. Source of grafting material

4. To obtain surgical access in hypophysectomy, and vidian neurectomy

Figure showing the cottle's line

Procedure:

Submucosal resection of nasal septum is ideally performed under local anaesthesia. 4%

xylocaine is used as topical anesthetic agent by nasal packing. 2% xylocaine is used as infiltrative

anesthetic agent. It is mixed with 1 in 1 lakh adrenaline. Infiltration is done at the mucocutaneous

junction on both sides just behind the columella. The floor of the nasal cavity is also infiltrated on the

concave side. Killian's incision is preferred for SMR operations. Killian's incision is the commonly

used incision. It is an oblique incision given about 5mm above the caudal border of the septal

cartilage.

The cartilagenous and bony nasal septum is exposed by elevation of mucoperichondrial and

mucoperiosteal flaps on both sides. This is done by slicing the septal cartilage just above the

columella to access the opposite side. Flaps are elevated on both sides of the nasal septum. the

cartilage is fully exposed from both sides and is remove using a Luc's forceps or a Ballanger's swiwel

knife. The flaps are allowed to fall back in place and wound is closed with catgut. Bony deviations

along the floor of the nose if any are also chissled out before wound closure.

SMR should not be performed in growing children because it would affect growth of middle

third of face.

Complications of SMR:

1. Septal hematoma

2. Septal abscess

3. Septal perforation

4. Nasal deformities due to excessive removal of dorsal strut

5. Removal of columellar cartilage will cause pig snout deformity

Septoplasty - This is a more conservative procedure. The anesthesia is the same as described

for SMR operation. The incision is always sited on the concave side of the septum. Freer's

hemitransfixation incision is preferred. This is made at the lower border of the septal cartilage. A

unilateral Freer's incision is sufficient for septoplasty. Three tunnels are created as shown in the

figure.

Figure showing various tunnels raised during septoplasty

Exposure - The cartilagenous and bony septum are exposed by a complete elevation of a

mucosal flap on one side only. Since flap is retained on the opposite side the vascularity of the

septum is not compromised.

Mobilisation and straightening: The septal cartilage is freed from all its attachments apart from

the mucosal flap on the convex side. Most of the deviations are maintained by extrinsic factors such

as caudal dislocation of cartilage from the vomerine groove. Mobilisation alone will correct this

problem. When deviations are due to intrinsic causes like the presence of healed fracture line then it

must be excised along with a strip of cartilage. Bony deviations are treated either by fracture and

repositioning or by resection of the fragment itself.

Fixation - The septum is maintained in its new position by sutures and splints.

Advantages of Freer's incision:

1. The incision is cited over thick skin making elevation of flap easy.

2. There is minimal risk of tearing the flap

3. The whole of the nasal septum is exposed.

4. If need arises Rhinoplasty can be done by extending the same incision to a full transfixation one .

Advantages of Septoplasty: 1. More conservative procedure

2. Performed even in children

3. Less risk of septal perforation

4. Less risk of septal hematoma

10. Vocal cord paralysis :

Definition - Vocal cord paralysis is caused by paralysis of intrinsic muscles of larynx. This is a

symptom of an underlying disorder and not a disease by itself. The intrinsic muscles of the vocal

cord are supplied by the vagus nerve. The term vagus means "wanderer" which is the apt term to

describe this nerve becuase of its long anatomical course.

Unilateral vocal fold paralysis occurs due to dysfunction of recurrent laryngeal or vagus nerve causes a

breathy voice. The breathiness of voice is caused by glottic chink which allows air to escape when the patient

attempts to speak. Normal voice production is dependent on proper glottal closure resulting from bilateral

adduction of the vocal cords. This adduction of vocal folds combined with subglottic air pressure causes the

vocal folds to vibrate causing phonation.

Pathophysiology: The physiologic function of larynx is adversely affected by vocal fold paralysis.

Interference with the protection of the tracheobronchial tree and respiration are more serious and life

threatening than interference with voice production. In recurrent laryngeal nerve paralysis the vocal folds may

assume a number of positions. Six positions have been described. They are median, paramedian, cadaveric

(intermediate), gentle abduction and full abduction. The various positions of the vocal cords cannot be

recorded precisely.

Theories that explains the varying positions assumed by the paralyzed cord:

Semon's law - This theory proposed by Rosenbach and Semon in 1881, depends on the concept that

abductor fibres in the recurrent laryngeal nerves are more susceptible to pressure than the adductor fibers.

After a number of amendments this law is stated as " In the course of a gradually progressing organic lesion

involving the recurrent laryngeal nerve three stages can be observed. In the first stage only the abductor fibers

are damaged, the vocal folds approximate in the midline and adduction is still possible. In the second stage the

additional contracture of adductors occur so that the vocal folds are immobilized in the median position. In the

third stage the adductors become paralysed and the vocal folds assume a cadaveric position".

This theory is fraught with clinical and experimental inconsistencies. It was assumed that the

nerve fibers supplying the abductors of the vocal folds lie in the periphery of the recurrent laryngeal

nerve and any progressive lesion involves these fibers first before involving the deeper fibers that

supply the adductors. It was even suggested that adductors being phylogentically older are more

resistant to insults than the newer abductors. According to this theory in all progressive lesions

involving the recurrent laryngeal nerve the abductors paralyze first followed by the adductors. When

recovery takes place the first muscle group to recover will be the adductors before the abductors

could recover.

Differential innervation theory: This theory was based on the anatomic fact that the recurrent

laryngeal nerve often branched outside the larynx. Injury to individual branches could cause

paralysis of specific groups of muscles accounting for the varying positions assumed by the

paralysed cord.

Bilateral innervation of interarytenoid muscle- In this theory the paramedian position of a

paralysed vocal cord is attributed to contraction of interarytenoid muscle which is supposed to

receive bilateral innervation. In reality this is not true as the interarytenoid muscle just helps to close

the posterior glottic chink.

Disturbance to autonomic nerve supply- This theory has no experimental evidence. It

suggests that the vocal cord position is determined by the laryngeal muscle tone due to autonomic

innervation.

Wagner Grossman theory - This is the most popular and widely accepted theory which could

account for the varying positions assumed by a paralysed vocal cord. This theory was first proposed

by Wagner and Grossman (1897). This theory states that in complete paralysis of recurrent

laryngeal nerve the cord lies in the paramedian position because the intact cricothyroid muscle

adducts the cord. (Because the superior laryngeal nerve is intact). If the superior laryngeal nerve is

also paralysed the cord will assume an intermediate position because of the loss of adductive force.

This theory has been confirmed by electro myological studies.

According to this theory, chest lesions should cause recurrent laryngeal nerve paralysis alone,

but in many patients with lung cancer the cord assumes a intermediate position. This has been

attributed to the phenomenon of retrograde atrophy of the vagus nerve up to the level of nucleus

ambiguus.

Paralysed vocal cords may demonstrate some movement due to the action of interarytenoid muscle

which gets bilaterally innervated.

Types of vocal cord paralysis – Congenital & acquired.

Acquired causes of vocal cord paralysis include:

1. Malignant disease – Involving lungs, thyroid, oesophagus and posterior cranial fossa

tumors.

2. Surgical trauma – Thyroid surgery, oesophageal surgeries, and surgeries of neck and

thorax.

3. Non surgical trauma – include penetrating injuries of neck and accidents.

4. Inflammatory causes – Tuberculosis is the commonest cause.

5. Neurologic causes – Brain stem ischemia, multiple sclerosis and head injury

6. Idiopathic cause – commonly involves left recurrent laryngeal nerve

Clinical features – Varies according to whether there is unilateral or bilateral recurrent

laryngeal nerve paralysis.

Unilateral vocal cord paralysis:

a. Voice change

b. Diplophonia

c. Aspiration in severe cases

Bilateral recurrent laryngeal nerve paralysis – Is an emergency. Patients present with stridor

and immediate control of air way should be the first priority. Tracheostomy should be performed at

the earliest. Vocal cord lateralization procedures should be performed in patients with bilateral

abductor palsy.

Short answers: 10x2=20

1. Perforations of ear drum – Occurs commonly in the pars tensa portion of the ear drum. If it

occurs in the pars tensa portion then it is known as central perforation and is considered to be a safe

disorder that does not cause complications. Patients with perforated ear drum present with hearling

loss. Perforated ear drums can be repaired using temporalis fascia graft. Perforations involving the

attic portion of the ear drum is considered to be unsafe type.

2. Gradenigo syndrome – This syndrome was first described by Gradenigo during 1907. The

classic features of this syndrome include: discharging ear, retro orbital pain, and abducent nerve

paralysis causing diplopia. This condition is caused due to unresolving mastoiditis in patients whose

petrous apex is pneumatized.

3. Otalgia – Is defined as pain in the ear.

Types of otalgia include -

Referred otalgia

Otalgia due to external ear causes

Otalgia due to middle ear causes

4. Nasopharyngeal tonsil – This is also known as adenoid. It is covered with furrows. On

palpation it feels like a bag of worms. It is lined by ciliated columnar epithelium. This tissue

undergoes enlargement till the child is about 3 years of age and progressively regresses later.

5. Complications of septal surgery – Septal hematoma, septal abscess, septal perforation and

nasal deformities.

6. Nasal myasis – This condition is characterized by the presence of maggots inside the nasal

cavity. Predisposing factors include – diabetics, leprosy involving the nasal mucosa and malignancy

involving the nasal cavity.

7. Heimlich maneuver – This is used as a first aid procedure for saving a patient's life. It is useful

in patients who has aspirated foreign body into the air way. This procedure is performed by standing

behind the patient and asking the patient to bend forward while pressure is being applied to the

abdomen. Sudden increase in intra thoracic pressure will push the foreign body out of the airway.

8. PV syndrome – This is also known as Plummer vinson syndrome. It is also known as

Patterson Brown Kelly syndrome. These patients have iron deficiency anaemia and web in the post

cricoid region. It commonly affects females and this condition is considered to be premalignant in

nature because of increasing incidence of post cricoid malignancy in these patients.

9. Juvenile papilloma larynx – This condition affects children. It is caused by Human papilloma

virus. It is multiple in nature and known to recur after surgical removal. Since it involves the larynx

these children have airway problems which should be addressed.

10. Tympanogram – This is generated using impedance audiometer. It determines the status of

ear drum and the middle ear ossicles. Jager classified tympanograms into 5 types. They include:

Type A curve – Normal middle ear function

Type As curve - Seen in stiffened middle ear function

Type Ad curve – Seen in flaccid ear drum and ossicular disruption

Type B curve – This is flat curve without any compliance peak

Type C curve – Suggests negative middle ear pressure.