NOSE &PARASANAL SINUSES

Septal abscess : Nasal septal abscess is a condition of the

nasal septum in which there is a collection of pus between the
mucoperichondrium and septal cartilage.
Etiology and symptoms
A nasal septal abscess is frequently a result of a secondary
bacterial infection of a nasal septal hematoma, follow furuncle
of nose. Patient may have severe bilateral nasal obstruction.
patients with this condition may also have fever, general
malaise and nasal pain, and tenderness over the dorsum of the
nose.
Complications
Potential complications of a nasal septal abscess include
cavernous sinus thrombophlebitis, meningitis septal
perforation, or saddle deformity due to cartilage necrosis.
Treatment
Treatment for a nasal septal abscess is similar to that of other
bacterial infections. Aggressive broad spectrum antibiotics
may be used after the incision and drainage of abscess from
one side..
2) Ozaena surgical treatment (Atrophic rhinitis). Surgical
interventions include:
Young's operation
Modified Young's operation

 Narrowing of nasal cavities, submucosal injection of

Teflon paste, section and medial displacement of the
lateral wall of the nose
Transposition of parotid duct to maxillary sinus or nasal
mucosa
Both the nostrils are closed completely just within the
nasal vestibule by raising flaps.
They are opened after 6 months or later. In these
cases,mucosa may revert to normal and crusting reduced.
Modified Young's operation. To avoid the discomfort of
bilate ral nasal obstruction , modified Young's ope ration
aims to partially close the nostrils. It is also claimed to
gi ve the same benefit as Young's.
a) Narrowing the nasal cavities. Nasal chambers are
very wide in at rophic rhinitis and air currents dry
up secretions leading to crusting. Narrowing the size
of the nasal airway helps to relie ve the symptoms.
Among the techniques fo llowed, some are:
(i) Submucosal injection to teflon paste.
(iil Insertion of fat, cartilage, bone or teflon strips
under the mucoperiosteum of the floor and lateral
wall of nose and the mucopenchondrium of the
septum.
(iii) Section and medial displacement of lateral wall
of nose.
3) Nasal bone fracture
A nasal fracture is one of the most common facial
injuries, comprising almost 40%

Synonyms: Fracture nasal bone, Broken nose, Nose

fracture, Facial fracture.
Introduction: Nose is the most prominent part of the
face, hence it is likely to be the most common structure
to be injured in the face. Although fractures involving
the nasal bones are very common, it is often ignored by
the patient.
Patients with fractures of nasal bone will have
deformity, tenderness, hemorrhage, edema, ecchymosis,
instability, and crepitation. These features may be
present in varying combinations.
Pathophysiology:
1. Nasal bones and underlying cartilage are susceptible
for fracture because of their more prominent and central
position in the face.
2. These structures are also pretty brittle and poorly
withstands force of impact.
3. The ease with which the nose is broken may help
protect the integrity of the neck, eyes, and brain. Thus
it acts as a protective mechanism.
4. Nasal fractures occur in one of two main patternsfrom a lateral impact or from a head-on impact. In
lateral trauma, the nose is displaced away from the
midline on the side of the injury, in head-on trauma, the
nasal bones are pushed up and splayed so that the upper
nose (bridge) appears broad, but the height of the nose
is collapsed (saddle-nose deformity). In both cases, the
septum is often fractured and displaced.
5. The nasal bone is composed of two parts: A thick
superior portion and a thin inferior portion. The

intercanthal line demarcates these two portions.

Fractures commonly occur below this line.
Types of nasal bone fractures: Fractures involving nasal
bones are divided into three categories depending on the
degree of damage, and its management.
Class I fractures: Very little force is sufficient to cause a
fracture of nasal bone. It has been estimated to be as
little as 25-75 pounds / sq inch. Class I fractures are
mostly depressed fractures of nasal bones. The fracture
line runs parallel to the dorsum of the nose and naso
maxillary suture and joins at a point where the nasal
bone becomes thicker. This point is about 2/3 of the
way along its length. The fractured segement usually
regains its position because of its attachement along its
lower border to the upper lateral cartilage. The nasal
septum is not involved in this particular injury. Class I
fractures donot cause gross lateral displacement of nasal
bones, though a persistent depressed fragment may give
it the appearance. In children these fractures could be
of green stick variety and a significant nasal deformity
may develop subsequently during puberty when nasal
growth accelerates.
Clinically this fracture will present as a depression
over the nasal bone area. There may be tenderness and
crepitus over the affected nasal bone. Radiological
evidence may or may not be present. Infact class I
fracture of nasal bone is purely a clinical diagnosis.
Class II fractures: These fractures cause a significant
amount of cosmetic deformity. In this group not only
the nasal bones are fractured, the underlying frontonasal

process of the maxilla is also fractured. The fracture

line also involves the nasal septum. This condition
must be recognised clinically because for a successful
result both the nasal bones as well as the septum will
have to be reduced. Since both the nasal bones and the
fronto nasal process of maxilla would have absorbed a
considerable amount of force, the ethmoidal labyrinth
and the adjacent orbit should be intact.
The precise nature of the deformity depends on the
direction of the blow sustained. A frontal impact may
cause comminated fracture of nasal bones causing gross
flattening and widening of the dorsum of the nose. A
lateral blow of similar magnitude is likely to produce a
high deviation of the nasal skeleton. The perpendicular
plate of ethmoid is invariably involved in these
fractures, and is characteristically C shaped (Jarjaway
fracture of nasal septum).

Class III fractures: Are the most severe nasal injuries

encountered. This is caused by high velocity trauma. It
is also known as naso orbital fracture / naso ethmoidal
fracture. Recent term to describe this class (Naso orbito
ethmoid fracture) indicates the clinical importance of
orbital component in these injuries. These fractures are
always associated with Le Fort fracture of the upper
face involving the maxilla also. In these fractures the
nasal bone along with the buttressing fronto nasal

process of maxilla fractures, telescoping into the

ethmoidal labyrinth. Two types of naso ethmoidal
fractures have been recognised:
Type I: In this group the anterior skull base, posterior
wall of the frontal sinus and optic canal remain intact.
The perpendicular plate of ethmoid is rotated and the
quadrilateral cartilage is rotated backwards causing a
pig snout defromity of the nose. The nose appears
foreshortened with anterior facing nostrils. The space
between the eyes increase (Telecanthus), the medial
canthal ligament may be disrupted from the lacrimal
crest.
Type II: Here the posterior wall of the frontal sinus is
disrupted with multiple fractures involving the roof of
ethmoid and orbit. Sphenoid and parasellar regions
may sometimes be involved. Since the dura is adherent
to the roof of ethmoid fractures in this region causes
tear in the dura causing csf rhinorrhoea.
Pneumocranium and cerebral herniation may
complicate this type of injury.
Management:
If fractures of nasal bones are left uncorrected it could
lead to loss of structural integrity and the soft tissue
changes that follow may lead to both unfavorable
appearance and function. The management of nasal
fractures is based solely on the clinical assessment of
function and appearance; therefore, a thorough physical
examination of a decongested nose is paramount.

Patients with fractures involving nose will have

intense bleeding from nose making assessment a little
difficult. Bleeding must first be controlled by nasal
packing. These patients also have considerable amount
of swelling involving the dorsum of the nose, making
assessment difficult. These patients must be
conservatively managed for atleast 3 weeks for the
oedema to subside to enable precise assessment of bony
injury. According to Cummins Fracture reduction
should be accomplished when accurate evaluation and
manipulation of the mobile nasal bones can be
performed; this is usually within 5-10 days in adults and
3-7 days in children.
Radiological investigations:
1. Plain xray nasal bones
2. Xray paranasal sinuses water's view
3. CT scan paranasal sinuses - This is a must in all cases
of class II and class III fractures of nasal bones for
precise estimation of damage.
Most class I fractures can be managed by closed
reduction and imobilisation by application of POP.
Digital pressure alone commonly does the job.

Photo showing digital pressure being applied to reduce

fractured nasal bones

If the fractured fragments are impacted then a

Welsham's forceps will have to be used to disimpact and
reduce the fractured nasal bone.

Welsham's forceps being used to reduce fractured nasal

bones
In the event of using Welsham's forceps to disimpact the
nasal bone, there will be extensive trauma to the nasal
mucosa causing epistaxis. The nasal cavity of these
patients must be packed with roller gauze, with
application of an external splint to stabilise the bone.
Class II septal fractures:
Closed reduction in these cases donot give optimal
results because the septal fracture is not corrected.
Since the fractured fragments of the perpendicular plate
of ethmoid and the septal cartilage fragments are not
repositioned the results of closed reduction are not
satisfactory. In these patients closed manipulation of
nasal bones should always be accompanied by open
correction of septal deformity.
Class III fractures: Must be treated with open reduction
and internal fixation. The problem here is eventhough
the nasal bones can be reduced the adjacent supporting
bones (components of the ethmoidal labyrinth) donot
support the nasal bones because of their brittleness. It is
always better to reconstruct and stabilise the anterior
table of the frontal bone so that other parts of nasal
skeleton can derive support from it. Formerly

transnasal wires were used to fix the nasal bones, but

with the advent of plates and screws the whole scenario
has undergone a dramatic change.
Ellis procedure of management of Class III fractures:
Aims of the procedure include:
1. Provision of adequate surgical exposure to provide an
unobstructed view of all components of the fracture.
2. The medial canthal ligament should be identified.
This is rarely avulsed and is usually attached to a large
fragment of bone. Once identified the ligament should
be reattached and secured to the lacrimal crest. This
step will avoid the future development of telecanthus.
3. Reduction and reconstruction of medial orbital rim.
This can be achieved by use of transnasal 26 gauge
wires. If plates are used they should be very thin
otherwise they will become conspicous once the wound
has healed.
4. Reconstruction of medial orbital wall and floor with
bone grafts
5. Realignment of nasal septum
6. Augmentation of dorsum of the nose by the use of
bone grafts
7. Accurate soft tissue readaptation should be
encouraged by placing splints.

Complications of nasal bone fracture:

1. Cosmetic deformity (saddle nose, pig snout
deformity)
2. Persistent septal deviation
3. CSF leak
4. Orbital oedema / complications
5. Nasal block / compromise of nasal functions
Nasal polyps.
2) Nasal polyps are usually classified into antrochoanal
polyps and ethmoidal polyps. Antrochoanal polyps arise from
the maxillary sinuses and are the much less common,
ethmoidal polyps arise from the ethmoidal sinuses.
Antrochoanal polyps are usually single and unilateral whereas
ethmoidal polyps are multiple and bilateral.
Symptoms of polyps include nasal congestion, sinusitis,
anosmia (loss of smell), and secondary infection leading to
headache.[1] They may be removed by surgery, but are found
to recur in about 70% of cases. Sinus surgery requires great
amount of precision as this involves risk of damage to orbit
matter.
Causes
The pathogenesis of nasal polyps is unknown. Nasal polyps
are most commonly thought to be caused by allergy and rarely
by cystic fibrosis although a significant number are associated
with non-allergic adult asthma or no respiratory or allergic
trigger that can be demonstrated. Nasal mucosa, particularly
in the region of middle meatus becomes oedematous due to
collection of extracellular fluid causing polypoidal change.

Polyps which are sessile in the beginning become

pedunculated due to gravity and excessive sneezing.
In early stages, surface of nasal polypi is covered by ciliated
columnar epithelium, but later it undergoes metaplastic
change to squamous type on atmospheric irritation.
Submucosa shows large intercellular spaces filled with serous
fluid.
These polyps have no relationship with colonic or uterine
polyps. Irregular unilateral polyps particularly associated with
pain or bleeding will require urgent investigation as they may
represent an intranasal tumour.
There are various diseases associated with polyp formation:
1. Chronic rhinosinusitis
2. Asthma
3. Aspirin intolerance/salicylate sensitivity
4. Cystic fibrosis
5. Kartagener's syndrome
6. Young's syndrome
7. Churg-Strauss syndrome
8. Nasal mastocytosis
Exposure to some forms of chromium can cause nasal polyps
and associated diseases.
Treatments

Nasal polyps are most often treated with steroids or topical,

but can also be treated with surgical methods.
Pre-post surgery, sinus rinses with a warm water (240 ml / 8
oz) mixed with a small amount (teaspoon) of salts (sodium
chloride & sodium bicarbonate) can be very helpful to clear
the sinuses. This method can also be used as a preventative
measure to discourage the polyps from growing back and
should be used in combination with a nasal steroid.
. The surgery can be done under general or local anaesthesia,
and the polyps are removed using endoscopic surgery..
Mometasone furoate, commonly available as a nasal spray for
treating common allergy symptoms, has been indicated .
3)Nasal septum.
The nasal septum separates the left and right airways in the
nose, dividing the two nostrils. The fleshy external end of the
nasal septum is sometimes also called columella. The nasal
septum contains bone and hyaline cartilage
The nasal septum is composed of five structures:
perpendicular plate of ethmoid bone
vomer bone
cartilage of the septum
crest of the maxillary bone
crest of the palatine bone
The nasal septum derives its blood supply from the sphenopalatine and the anterior and
posterior ethmoid arteries with the added contribution of the superior labial artery (anteriorly)

and the greater palatine artery (posteriorly). The Kiesselbach plexus, or the Little area,
represents a region in the anteroinferior third of the nasal septum, where all 3 of the chief
blood supplies to the internal nose converge.
Veins in the nose essentially follow the arterial pattern. They are significant for their direct
communication with the cavernous sinus and for their lack of valves; these features potentiate
the intracranial spread of infection
Lymphatics arise from the superficial mucosa and drain posteriorly to the retropharyngeal
nodes and anteriorly to the upper deep cervical nodes and/or submandibular glands
Clinical significance

The nasal septum can depart from the centre line of the nose
in a condition is known as a deviated septum caused by
trauma. However, it is normal to have a slight deviation to one
side.
A perforated nasal septum can be caused by an ulcer, trauma
due to an inserted object, excessive nose-picking, long-term
exposure to welding fumes,[3] or cocaine use. There is a
procedure that can be of help to those suffering from
perforated septum. A silicone button can be inserted in the
hole to close the open sore. An operation to the nasal septum
is known as a septoplasty.
The nasal septum can be affected by both benign (fibroma,
inflammatory hemangioma of the nasal septum"bleeding
polyp" etc.) and malign tumors (squamous cell carcinoma,
esthesioneuroblastoma etc.)

4)Aspiration cytology of Paranasal sinuses

A variety of non-neoplastic and neoplastic conditions can
involve the sinonasal region. FNAC is a reliable diagnostic
procedure in a good number of cases, especially in the light of
clinico-radiological data

Reliable procedure in diagnosing non-specific inflammation,

fungal infection tuberculosis (, actinomycosis . Benign
cysts . Benign bone Malignant epithelial tumors like
squamous cell carcinoma , basal cell carcinoma , poorly
differentiated carcinoma and metastatic carcinoma .
5) Rhinitis caseosa
Rhinitis caseosa is a condition in which the nasal cavity
is filled with foul smelling, purulent discharge and
cheesy material
Epidemiology:
o It is an uncommon condition, mostly seen in males
Pathology:
o Chronic infection of sinus resulting in production of
purulent discharge and inspissated cheesy material
which gets collected in nasal cavity
o Bony destruction of the sinus walls may be present
o Hence it is necessary to differentiate this from
malignancy
Treatment:
o Removal of the discharge, debris and granulation
tissue to allow free drainage of sinuses
Prognosis is good
6) Olfaction is the sense of smell. This sense is mediated by
specialized sensory cells of the nasal cavity. In humans,

olfaction occurs when odorant molecules bind to specific sites

on the olfactory receptors. These receptors are used to detect
the presence of smell. They come together at the glomerulus,
a structure which transmits signals to the olfactory bulb
( directly above the nasal cavity and below the frontal lobe
For air-breathing animals, the main olfactory system detects
volatile chemicals, and the accessory olfactory system detects
fluid-phase chemicals Olfaction, along with taste, is a form of
chemoreception. The chemicals themselves that activate the
olfactory system, in general at very low concentrations, are
called odorants.
.
7) Rhinosporidiosis is a rare chronic granulomatous disease
caused by rhinosporidium seeberi. ..
Rhinosporidium seeberi is a fungus from the class
ofphycomycetes of family coccoidiodaceae.
Some authors recently postulated that etiological agent is not
a fungus but a prokaryotic cynobacterium called microcystitis
aeroginosa.However, the most accepted responsible agent
today is an aquatic protisan parasite belonging to a novel
group of fish parasites (Mesomycetozoa), located
phylogenetically between the fungal and animal divergence. It
commonly affects nose and nasopharynx. Occasionally the
conjunctiva, palate, lacrimal sac, maxillary antrum, larynx,
trachea, bronchi, urethra and skin are affected.
The disease is endemic in India and Sri Lanka, with only few
cases being reported from Africa, South America and other
parts of the world. In India, highest number of cases are
reported from southern states of Kerala and Tamil Nadu which
are on either side of western ghats. Rhinosporidiosis presents
with soft highly vascular sessile or pedunculated mass . Most
successful treatment is surgical excision with cauterization of
the base.Incomplete excision leads recurrences. Dapsone is

the only drug found to be of value in treating

rhinosporidiosisdrug found to be of value in treating
rhinosporidiosis
8) Kiesselbach's plexus, which lies in Kiesselbach's area,
Kiesselbach's triangle, or Little's area, is a region in the
anteroinferior part of the nasal septum where four arteries
anastomose to form a vascular plexus of that name. The
arteries are:[1]
Anterior ethmoidal artery (from the ophthalmic artery)
Sphenopalatine artery (terminal branch of the maxillary
artery)
Greater palatine artery (from the maxillary artery)
Septal branch of the superior labial artery (from the
facial artery)
Ninety percent of epistaxis occur in Little's area, as it is
exposed to the drying effect of inspiratory current.
10)- MUCOUS BLANKET
nasal mucosa is rich in goblet cells, mucous and serous
secretory glands. Their secretions form a mucous blanket
floating on top of cilia which a constantly beating to carry it
like a conveyer belt -Inspired bacteria, viruses and dust
particles are entrapped on the viscous mucous blanket and
carried to nasopharynx to be swallowed -Cilia beats 10-20
times/second at room temperature -The movement of mucous

is maintained in a single direction towards natural ostea

because of rapid effective stroke and slow recovery stroke

11)ALLERGIC RHINITIS
is an allergic inflammation of the nasal airways. It occurs
when an allergen, such as pollen, dust or animal dander
(particles of shed skin and hair) is inhaled by an individual
with a sensitized immune system. In such individuals, the
allergen triggers the production of the antibody
immunoglobulin E (IgE), which binds to mast cells and
basophils. IgE bound to mast cells are stimulated by allergens,
causing the release of inflammatory mediators such as
histamine (and other chemicals). This usually causes sneezing,
itchy and watery eyes, swelling and inflammation of the nasal
passages, and an increase in mucus production
Allergic rhinitis may be seasonal or perennial. Seasonal
allergic rhinitis occurs particularly during pollen seasons. It
does not usually develop until after 6 years of age. Perennial
allergic rhinitis occurs throughout the year. This type of
allergic rhinitis is commonly seen in younger children
Signs and symptoms
The characteristic symptoms of allergic rhinitis are: rhinorrhea
(excess nasal secretion), itching, and nasal congestion and
obstruction Characteristic physical findings include
conjunctival swelling and erythema, eyelid swelling, lower
eyelid venous stasis (rings under the eyes known as "allergic
shiners"), swollen nasal turbinates, and middle ear effusion.[6]

. Diagnosis
Laboratory tests:
Allergy skin tests (immediate hypersensitivity testing):
An in vivo method of determining immediate (IgEmediated) hypersensitivity to specific allergens
Radioallergosorbent test (RAST): Indirectly measures the
quantity of immunoglobulin E (IgE) serving as an
antibody to a particular antigen
Total serum IgE:
Total blood eosinophil count: Imaging studies used in the
diagnosis and evaluation of allergic rhinitis include the
following:
Radiography: Can be helpful for evaluating possible
structural abnormalities or to help detect complications
or comorbid conditions, such as sinusitis or adenoid
hypertrophy
Computed tomography scanning: Can be very helpful for
evaluating acute or chronic sinusitis
Management
The management of allergic rhinitis consists of the following
3 major treatment strategies:
Environmental control measures and allergen avoidance:
These include keeping exposure to allergens such as
pollen, dust mites, and mold to a minimum

 Pharmacologic management: Patients are often

successfully treated with oral antihistamines,
decongestants, or both; regular use of an intranasal
steroid spray may be more appropriate for patients with
chronic symptoms
Immunotherapy: This treatment may be considered more
strongly with severe disease, poor response to other
management options, and the presence of comorbid
conditions or complications; immunotherapy is often
combined with pharmacotherapy and environmental
control

11) Functions of Nose.

Breathing
The nasal passages allow air to flow in and out during normal
breathing. As a person inhales, the nose warms and humidifies
the air before it gets to the lungs. The lining in the nose has
many blood vessels at the surface. The warm blood flowing
through the nose helps warm the air.
Cleansing
The nose has many small hairs inside the nostrils. These hairs
serve to filter the air and remove dirt and particles before they
enter the lungs. Sneezing and nose blowing help remove the
particles out of the body.
Smell

Smell is one of the most important functions of the nose. The

olfactory nerves are pairs of cranial nerves that connect the
nose to the brain and assist in perceives and interpreting
smells
Taste
Although taste is a completely separate sense than smell, the
nose plays a role in the way the tongue perceives taste.
Individuals with a congested nose report a decreased sense of
taste. The aroma of the food plays a role in the taste
Voice
The air resonating in nose assists in giving the voice its
particular sound. This is why individuals suffering with a
stuffed nose sound differently than normal. The shape of the
septum also plays a role in the sound of the voice.
12) Septal perforation
The nasal septal mucoperichondrium provides the blood
supply to the septal quadrangular cartilage. Any insult (eg,
chemical, physical, iatrogenic) to this normal anatomy can
lead to the development of a perforation.
Causes
Traumatic causes of septal perforation may be divided into
external, External trauma includes nasal-septal fracture. A
septal hematoma results in elevation of the
mucoperichondrium from the quadrangular cartilage,
ischemia, and subsequent necrosis of the cartilage, with
resultant perforation
self-inflicted, Self-inflicted trauma, such as digital
manipulation, may cause a septal perforation.

iatrogenic causes Iatrogenic trauma includes a history of

septoplasty, nasal packing or cauterization for epistaxis, and
nasotracheal intubation.
Chronic use of vasoconstrictive nasal sprays and steroid nasal
sprays may cause septal perforations. In addition, the use of
cocaine may result in septal perforations.
Inflammatory diseases such as collagen vascular diseases,
sarcoidosis, and Wegener granulomatosis may cause septal
perforations.
In addition, infectious processes such as tuberculosis, syphilis,
and fungal diseases may result in septal perforations. Rarely,
septal perforation is the initial finding of sinonasal
malignancy.
Clinical findings
Septal perforations are usually asymptomatic. However, some
patients may present with a history of nasal obstruction,
crusting, intermittent episodes of epistaxis, malodorous
discharge from the nose, or a whistling sound during nasal
breathing
Management
13) Antrochoanal polyp. Definition: Antrochoanal polyp is
a benign solitary polypoidal lesion arising from the maxillary
sinus antrum causing opacification and enlargement of antrum
radiologically without any evidence of bone destruction. It
exits the antrum through the accessory ostium reaches the
nasal cavity, expands posteriorly to exit through the choana
into the post nasal space.
Incidence: It commonly affects children and young adults.
Polypoidal tissue from the maxillary antrum exits out through
the accessory maxillary sinus ostium according to some
workers. This accessory sinus ostium is placed posteriorly,

which could be the reason for the polyp to present posteriorly.

The accessory sinus ostium widens progressively, ultimately
at one stage merging with the natural ostium of the maxillary
sinus forming one huge opening into the maxillary antrum.
This disease is commonly seen only in non atopic persons. Its
etiology is still unknown. Infact this disorder is not associated
with nasal allergy.
Proetz theory: Proetz suggested that this disease could be due
to faulty development of the maxillary sinus ostium, since
it was always been found to be large in these patients.
Hypertrophic mucosa of maxillary antrum sprouts out through
this enlarged maxillary sinus ostium to get into the nasal
cavity. The growth of the polyp is due to impediment to the
venous return from the polyp. This impediment occur at the
level of the maxillary sinus ostium. This venous stasis
increases the oedema of the polypoid mucosa thereby
increasing its size.
Bernoulli's phenomenon: Pressure drop next to a constriction
causes a suction effect pulling the sinus mucosa into the nose.
Mucopolysaccharide changes: Jakson postulated that changes
in mucopolysaccharides of the ground substance could cause
nasal polyp.
Infections: Recurrent nasal infections have also been
postulated as the cause for nasal polyp
Vasomotor imbalance theory: This theory attributes polyp
formation due to autonomic imbalance
Clinical features: Since the disorder is unilateral
(commonly) the patient always present with

1. Unilateral nasal obstruction

2. Unilateral nasal discharge
3. Headache (mostly unilateral)
4. Epistaxis
5. Sleep apnoea
6. Rhinolalia clausa due to presence of polyp in the post nasal
space
7. Difficulty in swallowing if the polyp extends into the
oropharynx
Anterior rhinoscopy may show the polyp as glistening
polypoidal structures. They will be insensitive to touch. this
feature helps to differentiate it from a hypertrophied nasal
turbinate.
Postnasal examination will show the polyp if extending
posteriorly at the level of choana. If it fills up the
nasopharynx it will be visible there.
Xray paranasal sinuses will show a hazy mazillary antrum.
CT scan of paranasal sinuses is diagnostic. It will show the
polyp filling the maxillary antrum and exiting out through the
accessory ostium into the nasal cavity.
Histology: Shows respiratory epithelium over normal
basement membrane. The interstitial layer is grossly
oedematous, with no eosinophils. The interstial layer contains
other inflammatory cells.
Treatment:
This is a surgical problem. Formerly it was treated by
avulsion of the polyp transnasally. This method led to
recurrences. A caldwel luc approach was preferred in patients
with recurrences. In caldwel luc procedure in addition to the

polypectomy, the maxillary antrum is entered via the canine

fossa and the antral component is completely excised.
Endoscopic approach: With the advent of nasal endoscope
this approach is the preferred one. Using an endoscope it is
always easy to completely remove the polypoid tissue. The
uncinate process must also be completely excised.
Endoscopic approach has the advantage of a complete surgical
excision with negligible recurrance rates.
14) Rhinoliths are stone like calcareous deposits found
inside the nasal cavity. These are of two types:
Exogenous rhinolith and Endogenous rhinolith. These
concretions are common in the nasal cavities of females
than in men. They may also occur although rarely in the
naso pharynx. They are almost always single and
unilateral. These masses are more or less irregularly
spherical, they may also show prolongations according to
their directions of growth.
The surface of a rhinollith is mulberry like, may be grey
or brownish pink in color. Rhinoliths are friable, and they
crumble readily under pressure. They are chiefly made of
phosphates and carbonates of calcium. Sometimes
phosphate of magnesia, chloride of sodium and carbonates
of magnesia are also seen. These salts originate from the
nasal mucous secretions, tears, and inflammatory
exudates.
These salts have been found to be deposited around a
nucleus which could be inspissated mucous, blood clot or a
small foreign body. If concretions occur around a foreign
body then the rhinoloith is known to be exogenous in

nature and if if forms around a blood clot or inspissated

mucous plug then it is known to be endogenous in nature.
Gauze swabs inadvertantly left in the nose can also act as
a nidus for the formation of rhinolith.
Symptoms:
These patients have unilateral nasal discharge, which may
be serosanguinous in nature. As the rhinolith increases in
size, the symptoms of nasal obstruction become more
pronounced and the patient may manifest with unilateral
purulent nasal discharge. Swelling of the nose, face
epiphora could be some of the symptoms.
On probing the presence of a stony hard structure could be
identified. It is common in the inferior meatus
Management:
Complete removal of the offending mass is the dictum. If the
rhinolith is reasonably small it can be remove per via naturalis
without incision. If it is large attempt must be made to break it
to manageble pieces to facilitate per via naturalis removal. If
attempts to break the mass fail then lateral rhinotomy should
be resorted to for complete removal of the mass.
Once successfully removed it does not recur.
14) Chronic atrophic rhinitis is a chronic inflammation of
nose characterised by atrophy of nasal mucosa, including the
glands, turbinate bones and the nerve elements supplying the
nose. Chronic atrophic rhinitis may be primary and secondary.
Special forms of chronic atrophic rhinitis are rhinitis sicca
anterior and ozaena.
Primary Atrophic rhinitis

Etiology
Heredity factors: the disease runs in families
Endocrine imbalance: the disease tends to start at puberty
and mostly involves females
Racial factors: whites are more susceptible than natives
of equatorial Africa
Nutritional deficiency: vitamins A or D, or iron[citation needed]
Infection: Klebsiella ozaenae, diphtheroids, Proteus
vulgaris, E. coli, etc.
Autoimmune: viral infection or some other unidentified
insult may trigger antigenicity of the nasal mucosa

Pathology
The ciliated columnar epithelium of the nasal mucosa is
replaced by stratified squamous epithelium. Atrophy of
mucosa, turbinal bones and seromucinous glands tends to
occur, due to obliterative endarteritis causing decreased blood
supply, hence the supplying area atrophies.
Clinical manifestations
The disease is most commonly seen in females, and tends to
appear during puberty. It can occur, however, as early as 12
months of age. The nasal cavities become roomy and are filled

with foul smelling crusts which are black or dark green and
dry, making expiration painful and difficult. Microorganisms
are known to multiply and produce a foul smell from the nose,
though the patients may not be aware of this, because their
elements (responsible for the perception of smell) have
become atrophied. Patients usually complain of nasal
obstruction despite the roomy nasal cavity, which can be
caused either by the obstruction produced by the discharge in
the nose, or as a result of sensory loss due to atrophy of nerves
in the nose, so the patient is unaware of the air flow. In the
case of the second cause, the sensation of obstruction is
subjective. Bleeding from the nose, may occur when the dried
discharge (crusts) are removed. Septal perforation and
dermatitis of nasal vestibule can occur. The nose may show a
saddle-nose deformity. Atrophic rhinitis is also associated
with similar atrophic changes in the pharynx or larynx,
producing symptoms pertaining to these structures. Hearing
impairment can occur due to Eustachian tube blockage
causing middle ear effusion.
Permanent loss of smell and impairment of taste may also be a
result of this disease, even after the symptoms are cured.
Secondary atrophic rhinitis
Specific infections, such as syphilis, lupus, leprosy and
rhinoscleroma, may cause destruction of the nasal structures
leading to atrophic changes. Atrophic rhinitis can also result
from long-standing purulent sinusitis, radiotherapy of the nose
or excessive surgical removal of turbinates.
Unilateral atrophic rhinitis
Extreme deviation of nasal septum may be accompanied by
atrophic rhinitis on the wider side

Treatment of atrophic rhinitis can be either medical or

surgical.
Medical measures include:
Nasal irrigation using normal saline
Nasal irrigation and removal of crusts using alkaline
solutions
25% glucose in glycerine can be applied to the nasal
mucosa to inhibit the growth of foul-smelling proteolytic
organisms
Local antibiotics, such as chloramphenicol (Kemicetine)
Estradiol and vitamin D2
Estradiol spray
Systemic streptomycin
Oral potassium iodide
Placental extract injected in the submucosa
Surgical interventions include:
Young's operation
Modified Young's operation
Narrowing of nasal cavities, submucosal injection of
Teflon paste, section and medial displacement of the
lateral wall of the nose

 Transposition of parotid duct to maxillary sinus or nasal

mucosa
15) Describe the pathology, signs, symptoms and
management of Antro chonal polyp.

The antrochoanal polyp is uncommon. It is usually unilateral

and commences as oedematous lining in the maxillary sinus.
This prolapses, usually via a posterior accessory ostium, into
the nasal cavity and enlarges toward the posterior choana and
naspoharynx. The patient, commonly a young adult,
complains of unilateral nasal obstruction, which is worse on
expiration due to the ball valve effect of
the polyp in the posterior choana. If significantly large it may
block both choanae and cause otological symptoms due to
obstruction of the Eustachian tube (Fig. 2). Patients
occasionally present so late that the polyp has enlarged behind
the soft palate and hangs visibly in the oropharynx.
Treatment is surgical by pernasal excision with removal of the
cystic antral portion endoscopically via an antrostomy.
Recurrences may require a CaldwellLuc approach to the
antrum to remove the roots of the cyst
Antrochoanal polyp. Definition: Antrochoanal polyp is a
benign solitary polypoidal lesion arising from the maxillary
sinus antrum causing opacification and enlargement of antrum
radiologically without any evidence of bone destruction. It
exits the antrum through the accessory ostium reaches the
nasal cavity, expands posteriorly to exit through the choana
into the post nasal space.
Incidence: It commonly affects children and young adults.

Polypoidal tissue from the maxillary antrum exits out through

the accessory maxillary sinus ostium according to some
workers. This accessory sinus ostium is placed posteriorly,
which could be the reason for the polyp to present posteriorly.
The accessory sinus ostium widens progressively, ultimately
at one stage merging with the natural ostium of the maxillary
sinus forming one huge opening into the maxillary antrum.
This disease is commonly seen only in non atopic persons. Its
etiology is still unknown. Infact this disorder is not associated
with nasal allergy.
Proetz theory: Proetz suggested that this disease could be due
to faulty development of the maxillary sinus ostium, since
it was always been found to be large in these patients.
Hypertrophic mucosa of maxillary antrum sprouts out through
this enlarged maxillary sinus ostium to get into the nasal
cavity. The growth of the polyp is due to impediment to the
venous return from the polyp. This impediment occur at the
level of the maxillary sinus ostium. This venous stasis
increases the oedema of the polypoid mucosa thereby
increasing its size.
Bernoulli's phenomenon: Pressure drop next to a constriction
causes a suction effect pulling the sinus mucosa into the nose.
Mucopolysaccharide changes: Jakson postulated that changes
in mucopolysaccharides of the ground substance could cause
nasal polyp.
Infections: Recurrent nasal infections have also been
postulated as the cause for nasal polyp
Vasomotor imbalance theory: This theory attributes polyp

formation due to autonomic imbalance

Clinical features: Since the disorder is unilateral
(commonly) the patient always present with
1. Unilateral nasal obstruction
2. Unilateral nasal discharge
3. Headache (mostly unilateral)
4. Epistaxis
5. Sleep apnoea
6. Rhinolalia clausa due to presence of polyp in the post nasal
space
7. Difficulty in swallowing if the polyp extends into the
oropharynx
Anterior rhinoscopy may show the polyp as glistening
polypoidal structures. They will be insensitive to touch. this
feature helps to differentiate it from a hypertrophied nasal
turbinate.
Postnasal examination will show the polyp if extending
posteriorly at the level of choana. If it fills up the
nasopharynx it will be visible there.
Xray paranasal sinuses will show a hazy mazillary antrum.
CT scan of paranasal sinuses is diagnostic. It will show the
polyp filling the maxillary antrum and exiting out through the
accessory ostium into the nasal cavity.
Histology: Shows respiratory epithelium over normal
basement membrane. The interstitial layer is grossly
oedematous, with no eosinophils. The interstial layer contains
other inflammatory cells.
Treatment:

This is a surgical problem. Formerly it was treated by

avulsion of the polyp transnasally. This method led to
recurrences. A caldwel luc approach was preferred in patients
with recurrences. In caldwel luc procedure in addition to the
polypectomy, the maxillary antrum is entered via the canine
fossa and the antral component is completely excised.
Endoscopic approach: With the advent of nasal endoscope
this approach is the preferred one. Using an endoscope it is
always easy to completely remove the polypoid tissue. The
uncinate process must also be completely excised.
Endoscopic approach has the advantage of a complete surgical
excision with negligible recurrance rates.
17) Discuss etiology clinical features Management and
chronic maxillary sinusitis
Chronic sinusitis is defined as chronic inflammation of
mucosal lining of paranasal sinuses lasting for more than 3
weeks.
Pathology: The mucosal lining of para nasal sinuses shows
evidence of chronic inflammatory changes. The cilia of the
lining epithelium are damaged, causing inadequate
drainage of sinus cavity. This is especially more common
in maxillary sinuses. Pent up secretions start to
accumulate within the sinuses. This retained secretions
again predispose to secondary infections and reinfections
causing a vicious cycle. There is also associated
hypertrophy of the lining mucosa leading to polypoidal
changes.
Clinical features:
Symptoms:

1. Nasal obstruction: This could be due to the result of

underlying pathology like a deviated nasal septum / septal
spur, polypoidal changes of nasal mucosa, hypertrophied
turbinates. The patient infact complains of stuffy nose.
2. Nasal discharge:The patient complains of excessive
nasal discharge, which could be mucoid to begin with and
may later get purulent due to super added infections. This
also leads to post nasal drip causing irritation of throat
and formation of granular pharyngitis.
3. Abnormalities of smell: Patients may complain of
diminished acuity of smell. Patient may also present with
cacosmia or parosmia
4. Headache: is another important feature of chronic
sinusitis. Pent up secretions within the sinus cavity leads to
head ache.
5. Epistaxis:Hyperemia of nasal mucosa due to repeated
infections may lead to epistaxis.
6. Sinus tenderness could also be present
Investigations:
Xray para nasal sinuses water's view - shows hazy sinuses
CT scan paranasal sinuses plain both axial and coronal
cuts are diagnostic
Management:
Medical:
1. Antibiotics: Amoycillin is the drug of choice.
Erythromycin can be considered in patients allergic to
amoxycillin
2. Pain killers like acetaminophen can be used
3. Nasal decongestant drops like xylometazoline can be

used
4. Antihistamines can be considered if allergy is suspected
to be the cause
Surgical:
1. Antral lavage
2. Middle meatal antrostomy
3. FESS
18) Describe the etiology, signs, symptoms &management
of Acute maxillary sinusitis.
SinusitisCan be defined as inflammation of the mucosa
lining the paranasal sinuses Can be classified into acute
and chronic Allergic & infective types Pan sinusitis is the
term used to indicate inflammation of all the paranasal
sinuses
. Acute sinusitis Acute inflammation of mucosa lining
paranasal sinuses of less than 4 weeks duration. Infection
is said to be closed if the inflammatory exudate cannot
escape from the sinus because of blocked ostium or viscous
secretion Infection is said to be open if the exudate escapes
from the sinuses due to normal functioning mucociliary
clearence mechanism
Pathophysiology Acute sinusitis is caused when the normal
defence mechanisms like lysozymes and mucociliary
clearance mechanism is breached due to viral infection. After
the defences are breached, secondary bacterial infection
follows.
. Aetiology InfectionsSwiming / bathingTrauma to
paranasal sinuses As a component of general disease.
InfectionsNasal infectionsPharyngeal infectionsDental
infections

Swiming / bathingInfected pool / pondsChemical

rhinitisBacterial sinusitis due to water contamination
Trauma to sinusesCompound fractures involving sinuses
Foreign bodies involving sinuses Barotrauma - aerosinusitis
General diseases Influenza Measles Whooping cough
Pneumonia
. Contributing factors Unhygenic environment Low
resistence to infections Over crowding Anatomical
obstructions Conditions like Kartagener's syndrome
Osteomeatal complex block
. Importance of OMCIt represents an important anatomic
site where the drainage channels of maxillary,frontal and
ethmoidal sinuses drain Bounded by middle turbinate
medially, basal lamella posteriorly and superiorly and lamina
papyracea laterallyIt drains anteriorly and inferiorly Blockage
in this zone causes bacterial sinusitis
Microbiology Viruses include Rhinovirus, Parainfluenzae
I and II, Coxsackie, and Respiratory syncitial virusBacteria
include Pneumococci, streptococci, staphylococci, H
influenzae, E coli, MicrococcusSpecific infections Fungi,
syphilis, tuberculosis and leprosy
. Pathological stages Catarrhal stage Exudative stage
Suppurative stage Stage of complications Stage of resolution
Criteria to suggest bacterial sinusitis Diagnosis of bacterial
sinusitis requires two major / one major or two or more minor
criteria History should be strongly suggestive of bacterial
sinusitis Gold standard investigations would be pus culture
and sensitivity

Major criteria Facial pain / tenderness Facial fullness &

congestion Nasal congestion & obstruction Purulent nasal
discharge / post nasal drip Hyposmia / anosmiaFever
16. Minor criteriaHeadache Halitosis Fatigue Cough
Dental pain Ear fullness / ear pain
. Clinical types Acute catarrhal type Earliest stage. There
is oedema, mucous secretion, presence of leukocytes. There is
no destruction of mucous membrane lining the sinuses.
Acute suppurative type Inflammation is very severe. Large
number of leukocytes seen. Pus could be seen accumulating
due to suppuration. The mucous membrane may be necrotic
and polypoidal
Symptoms General symptoms Malaise, headache, mild
fever, facial pain, sorethroat and periorbital oedema.
Local symptoms Nasal block, loss of vocal resonance,
reduction in sense of smell, nasal discharge, post nasal drip,
cough, pain over sinus area
. Features of pain Antral pain Occurs along the
infraorbital margins, and is referred to upper teeth Ethmoidal
pain Over bridge of nose, and inner canthus of eye. May be
referred to parietal eminenceFrontal sinus pain Localized to
forehead. Shows classic periodicity Sphenoidal pain
Occipital in nature. May radiate to the neck
Signs swelling over cheek swelling over lower eyelids /
upper eyelids swelling over inner canthus of eye Tenderness
over affected sinus anterior rhinoscopy Congested nasal
mucosa, sometimes discharge from middle meatus

. Investigations Radiology Culture sensitivity Routine

hematology
Treatment Purely medical
Antibiotics
Nasal decongestants
Anti histamines
Anti inflammatory drugs
Surgery very rare Indicated only in cases of impending
complications
Complications
Osteomyelitis of the surrounding bone.
Orbital cellulitis.
Orbital abscess formation.
Intracranial complications
cavernous sinus thrombosis,
meningitis, and
intracranial abscess
Ch sinusitis
Middle ear infections
Laryngitis,
oroantral fistula,

mucoceles

LARYNX AND TRECHEA

Essays:
1. Discuss etiology and management of Hoarseness of
voice.
2. Describe the clinical symptoms, signs etiological factors,
diagnosis and treatment of Airway obstruction problems
of all ages.
3. Mention the neoplastic benign tumours of the larynx and
discuss about juvenile papillomatosis of the larynx.
4. Describe etiology, symptoms, signs, and management of
carcinoma of larynx.
5. What are the indications of trecheostomy? complications
of this procedure.
Short notes
1. Stridor.
2. Supraclavicular lymphadenitis.
3. Thyro-glossal cyst.
4. Complications of Tracheostomy.
5. Hoarseness of voice.
6. Vocal nodules (singers nodules).
7. Indications for Tracheostomy.
8. Multiple juvenile papillomatosis.
9. Bilateral abductor palsy.

10.
11.
12.
13.
14.
15.
16.
17.

Acute laryngitis.
Laryngeal polyp.
Causes of left vocal cord paralysis.
Branchial sinus in the neck.
Tic-doloreaux (trigeminal neuralgia).
Carina.
Laryngocoele.
Acute epiglottitis.

1. Discuss etiology and management of

Hoarseness of voice.
Definition:
Hoarseness of voice is defined as any change in the quality of
human voice (lay terms). This term utmost be considered to
be a nonspecific one. This term could imply breathiness,
roughness, voice breaks or unnatural pitch changes.
Dysphonia is the corresponding term used by
otolaryngologists to describe this condition.
Hoarseness is a symptom of utmost significance
and calls for a separate consideration as a subject because
of the frequency of its occurrence as a distant signal of
malignancy and other conditions
Chevalier Jackson
Causes of hoarseness of voice:
Inflammatory causes including acute injuries
Mucosal disorders of vocal folds

 Benign tumors of vocal folds

Malignant tumors of vocal folds
Laryngeal foreign bodies
Neurogenic causes affecting larynx
A useful Mnemonic to remember the causes of hoarseness of
voice:

VINDICATE
VVascular(thoracicaneurysm)
IInflammation
NNeoplasm
DDegenerative(Amyotrophiclateralsclerosis)
IIntoxication(smoking/alcohol)
CCongenital
AAllergies(angioneuroticoedema)
TTrauma/Thyroidsurgery
EEndocrinology(Reidel'sstruma)
Inflammatory causes:
This is one of the commonest causes of hoarseness of voice.
Inflammatory causes could either be acute / chronic.
Acute inflammatory causes: include acute laryngitis, acute

epiglottis, acute laryngotracheal bronchitis, diphtheria etc.

Chronic inflammatory causes include: chronic non specific
laryngitis (due to gastro oesophageal reflux disorders, vocal
abuse etc).
Chronic specific laryngitis (tuberculous / syphilitic laryngitis).
Acute vocal cord injuries can lead to vocal fold tears /
hematoma causing hoarseness of voice. This condition
resolves with complete voice rest.
Mucosal fold disorders:
Laryngeal oedema, Reinke's oedema.
Vocal nodule
Vocal cord polyp
Vocal cord cysts
Benign tumors:
Papilloma
Fibroma
Adenoma
Chondroma
Precancerous lesions:

Hyperkeratosis
Pachydermia
Leukoplakia
Malignant tumors of larynx:
Carcinoma vocal cords
Congenital conditions:
Congenital vocal cord webs
Foreign bodies

Vocal cord paralysis

Acute vocal fold tear

Hematoma of vocal cord

Reinke's oedema

Possible clinical presentations in patients with hoarseness

of voice:

1. Change in voice
2. Cough
3. Fever
4. Vocal fatigue
5. Irritation / soreness of throat
6. Weight loss
7. Painful vocalization

8. Difficulty in swallowing
9. Breathy voice
10.

Neck swelling

11.

Painful swallowing

12.

Heart burn / vomiting

13.

Haemoptysis

14.

Noisy respiration

Diagnosis:
Evaluation of hoarseness of voice should include:
Assessment of
Anatomy
Physiology
Behavioral factors
A complete history should be elicited.
Laryngeal visualization :
Indirect laryngoscopy / Direct laryngoscopy
Objective voice assessment: simplest method would be a
tape recording of the voice in question. This method should
be considered to be subjective.
Acoustic analysis: In this test voice is examined as electrical

signals. The term fundamental frequency is used to measure

the number of vocal fold vibrations per second. A normal
adult male vocal cord vibrates between 100 - 130 Hz, where
as in females it vibrates at the rate of 200 230
Hz.Abnormally high fundamental frequencies corrected for
age and sex changes would indicate hyper contraction of
cricothyroid muscle representing a functional pathology or
compensatory dysphonia.
Aerodynamic analysis:
The quality of voice is dependent on breath support.Even
subtle respiratory problems can lead to changes in voice
.Aerodynamic measurements play a role in quantifying
airflow during respiration and phonation. Pulmonary function
tests may play a role in identifying subtle respiratory
problems.
Maximum phonation time: This is a measurement of the
amount of time a patient can sustain a vowel sound in one
breath.
Normal values range between 15 - 25 seconds. Decreased
values indicate incomplete glottic closure or insufficient lung
support.
Glottal air flow: This sensitive test captures the amount of
air flowing through the glottis during phonation. This is
measured in cc/second by dividing the total volume of air
flowing through the glottis by the amount of time in seconds.
This gives information about the lung capacity and the
efficiency of vocal folds. Increased glottal flow is associated
with incomplete closure of glottis.
The voice in patients with increased glottal flow is usually

breathy / whispering in nature.

Decreased glottal air flow is seen in patients with
spasmodic dysphonia due to hyperadduction of vocal folds.
Management:
1. Absolute voice rest - very useful in acute conditions
2. Speech therapy - useful in chronic disorders
3. Antibiotics
4. Anti inflammatory drugs
5. Treatment of GERDS
6. Surgical intervention
What is stridor? Enumerate the causes of stridor. Describe briefly
the management modalities of stridor.
Definition: Stridor is defined as high pitched sound caused due to
turbulent airflow in the upper airway due to obstruction. This is
actually an emergency and airway should be secured at the earliest in
order to save the patient
.Classification of stridor:
Inspiratory stridor in case of airway obstruction above the level of
vocal cords
Expiratory stridor in case of obstruction at the level of bronchi
(Bronchial asthma)
Biphasic stridor stridor is present during both during inspiratory
and expiratory phases. This is classically caused due to tracheal
obstruction. (Tracheomalacia is the classic example).
Causes for stridor in infants and adults are different and variable.
Causes of stridor :Causes for stridor can be grossly classified into:
Laryngeal causes extralaryngeal causes

Laryngeal causes of stridor include varying disorders affecting

laryngeal airway leading onto obstructive airway pathology
.Congenital causes These conditions cause stridor in infants. They
include:
1. Infantile larynx causing laryngomalacia
2. Laryngeal web / stenosis
3. Laryngomalacia
4. Congenital cysts / hemangioma
Neoplasms:Includes both benign and malignant lesions
.Papillomas two types juvenile and adults.
Juvenile papilloma are multiple and their adult counterpart is single.
Juvenile papilloma has a high recurrence rate while adult papillomas
after removal are not known to recur
.Cysts These are benign and can be surgically removed
Tumors Benign / malignant.
Malignant tumors involving larynx causes stridor due to
1. Obstruction to the airway
2. Paralysis of both vocal cords
3. Fixity of both arytenoids
4. Laryngeal oedema following irradiation
Inflammatory causes:These include Acute laryngitis very rarely
they cause stridor
Diptheria Membrane dislodges and obstructs laryngeal inlet
Angioneurotic oedema Steroids will help in these patients Acute
laryngotracheal bronchitis common in children
Foreign bodies: Aspiration of foreign bodies are rare causes of
stridor. More common in children
.Neurological:
Vocal cord paralysis Bilateral abductor paralysis will cause stridor.
This can be caused due to involvement of recurrent laryngeal nerve
on both sides due to thyroid malignancy / or due toinjury following
total thyroidectomy. Hypocalcemic tetany can also lead to stridor in
rare cases.

Trauma This includes birth trauma, burns and scalds etc.

Extralaryngeal causes of stridor:
Congenital:
PIERRE ROBIN SYNDROME: This congenital condition is
associated with facial anomalies which include an unusually
small mandible (Micrognathia), posterior displacement of
tongue (glossoptosis) causing an upper airway obstruction.
Tracheo oesophageal fistula Can be congenital / acquired.
This is a surgical emergency.Inflammatory causes:
Ludwig's angina Submental oedema causing tongue to fall
back obstructing the airway.
Retropharyngeal abscess Surgical emergency
Foreign body cricopharynx A big foreign body at the level
of cricopharynx can cause upper airway obstruction due to
attendant airway oedema.
Neoplasm: Enlarged thymus causing compression over upper
trachea
.Cystic hygroma causing airway obstruction due to
involvement of tongue (or fall back of it).
Enlarged prelaryngeal / cervical lymphnodes causing airway
compression
.Management: Priority should be given to securing the
airway as early as possible.Depending on the probable cause
of stridor the management modality can be decided.
Attempting to oxygenate the patient: This is done on an
immediate basis as a first aid procedure.
Oxygen can be administered either by nasal prongs / face
mask. Nasal prongs are better tolerated by patients.
Intubation- This is the easiest way to secure the airway on an
immediate basis. This may not work if stridor is caused due to
tumors / oedema of larynx. Attempting to intubate these
patients would do more harm than good in these patients.
Contraindications for intubation:

1. Presence of hoarseness of voice in addition to stridor This

indicates coexistant malignancy.Larynx of these patients
should be examined before attempting intubation. This can be
performedby indirect laryngeal examination / video
laryngoscopic examination.
2. Absence of laryngeal crepitus This again indicates either
the presence of foreign body at thelevel of cricopharynx or
growth at the level of cricopharynx. Intubation should not be
attemptedin these patients.
3. Extralaryngeal causes of stridor is a contraindication for
intubation.tracheostomy should be performed as a life saving
procedure in these patients if intubation failsor if it is
contraindicated. Before taking up the patient for tracheostomy
the following investigations are a must:
Xray soft tissue neck
lateral view to assess the adequacy of subglottic air column.
For a successful tracheostomy a patient must have an
adequate subglottic air column. This x raywill also show any
foreign body at the level of cricopharynx, retropharyngeal
abscess etc. Surgically securing the airway can be performed
by any of these following methods:
Percutaneous tracheostomy
Criothyroidotomy
Tracheostomy
The aim of all these procedures is to secure the airway by
surgically by passing the obstructing airway lesion.
2. Mention the differential diagnosis of white patch in
tonsil
Causes of white patch seen over the tonsil can be classified
according to their etiology
.Infections: Could be viral, bacterial and fungal.
Viral infections:
Viral infections causing a white patch in the tonsil include:

Infectious mononucleosis This infection is caused by EB

virus. This infection commonly cause unilateral enlargement
of tonsil. The involved tonsil is covered with membrane
(pseudomembrane).These patients also have cervical adenitis
and hepatosplenomegaly.
Paul Bunnel test is positive.
Herpes simplex infections involving the tonsil will be seen
as ulcerative lesions which are covered with membranous
slough. Initially these lesions appear as multiple shallow small
ulcers. These ulcers coalesce to form a large ulcer covered
with membranous slough.
HIV infection Membranous tonsillitis in these patients
occur due to secondary infections.
Bacterial infections :Can be further subclassified into:
Acute non specific type
Acute specific type
Chronic non specific type
Chronic specific type
Acute non specific type This type is caused by a variety of
bacteria.
Acute follicular tonsillitis belongs to this category.
Organism involved include streptococci, H influenza,
pneumococci etc.
The dirty white membrane which is formed over the crypts of
the tonsil can easily be peeled off the tonsil without any
bleeding. In this condition membrane is seen only over the
tonsil and not over any other portion of the oral cavity.
Staphylococcal pseudo membranous tonsillitis is another
condition in which a membrane is seen over the tonsil.
Membrane formed is pseudomembrane type and can easily be
peeled off without bleeding. These patients commonly
manifest with cutaneous lesions characteristic of
staphylococcal infection

.Acute specific type:

Faucial diphtheria Caused by corynebacterium diphtheria.
Membrane could be seen extensively covering the tonsil,
uvula and soft palate. The membrane formed is true
membrane. It doesn't strip easily. Even when attempted to be
removed it leaves behind raw area which bleeds.Significantly
pain is absent in faucial diphtheria.
Swab taken from the membrane demonstrates
corynebacterium diphtheria.
Schick test is positive in these patients.
Vincent's angina This infection is caused by two organisms
namely Fuciform bacillus and spirocheta denticulata. These
patients have foul smelling breath, high grade fever and
cervical adenitis in addition to membranous tonsillitis. Smear
from the membrane is diagnostic. Membrane when peeled
causes considerable loss of tissue
.Chronic non specific type:
Keratosis of tonsil In this condition keratin could be seen
coming out of the crypts of tonsil. They appear as whitish
plaques. There are also associated keratosis seen over the
posterior 1/3 of tongue and posterior pharyngeal wall. These
patients are asymptomatic and the whole condition is an
incidental finding.
Chronic specific type This type include tuberculous and
syphilitic tonsillar infections.
In tuberculosis the whole tonsil along with their pillars show
ulceration. Smaller ulcers coalesce to form large ones covered
by dirty colored slough which appears like a membrane.
Swab taken from membrane shows mycobacterium
.Secondary syphilis involving the tonsil appears as white
colored painless mucosal patch. Ulcers seen over the tonsil
appear like snail tracks and hence they are known as snail

tract ulcers.These ulcers are the characteristic feature of

syphilitic tonsillitis.
Fungal infections: involving the tonsil appear as whitish
patches if the infecting fungus happens to be candida. This
condition is also known as the oral thrush. Fungal infections
involving thetonsil are seen in immunocompromised
individuals.
Autoimmune conditions causing whitish patch over the
tonsil Include Lichen planus and wegener's granulomatosis.
These conditions are caused by autoimmunity for mucous
membrane covering the tonsil.
Traumatic causes of membrane formation over tonsil
These include surgical trauma, thermal injuries, foreign body,
corrosive poisoning and post irradiation.
Premalignant conditions presenting as a patch over the tonsil
include Leukoplakia and submucosal fibrosis. These
conditions are painless and non inflammatory in nature.
Tumor and tumor like conditions causing whitish patch over
tonsil include:
Tonsillar cyst Painless and incidental finding
Tonsillolith Painless commonly and incidental Papilloma
Painless and incidental Fibroma of tonsil Painless and
incidental
Malignancy of tonsil Pain may be present. Associated JD
node enlargement can be seen.
Systemic conditions causing membrane over tonsil include
:Leukemia
Agranulocytosis
Aplastic anaemia
Blood dyscrasias
These conditions can be ruled out by performing routine
blood smear examination.infection causes membranous
tonsillitis.

3. Write short notes

. FESS

Introduction:
FESS is an acronym for Functional Endoscopic Sinus Surgery.
This surgery aims at restoring the normal function of paranasal
sinuses
.Indications for FESS:
1. Chronic sinusitis resistant to medical management
2. Repeated acute exacerbations of chronic sinusitis
3. In order to remove resistant focal infections from the paranasal
sinuses
4. In the management of fungal sinusitis in an effort aimed at
ventilation of paranasal sinuses
Aim of FESS - is to remove paranasal sinus drainage block there by
facilitating faster recovery of the mucociliary mechanism of nose and
paranasal sinuses. Experiments have shown that drainage of sinuses
always occur through their natural ostium because cilia always beat
towardstheir natural ostium
.Procedure:This surgery is usually performed under local / general
anesthesia.The nasal cavity is packed with 4% xylocaine mixed with 1
in 100,000 units of adrenaline. Xylocaine anesthetizes the nasal
mucosa while adrenaline decongests the nasal mucosa thereby
increasing the dimensions of nasal cavity and reduces bleeding during
surgery.
0 degree nasal endoscope is used to perform the surgery
.Steps of surgery:
1. Medialization of the middle turbinate. This is done gently
using a freer's elevator. Infiltratingthe root of middle
turbinate with cc of 2% xylocaine mixed with 1 in
100,000 units adrenaline will ensure anesthesia of the
middle meatus which is the area of surgery.
2. Uncinectomy: Uncinate process is identified and
medialized using a probe. It is completely removed using a
sickle knife / back biting forceps. It is important that the
uncinate process is removed completely including its
inferior horizontal portion. Natural ostium of maxillary
sinus can be seen when the horizontal portion of inferior

part of uncinate is removed. The natural ostium can be

widenedusing a back biting forceps.
Clearance of frontal recess area comes next. The frontal recess area
can be widened after bulla ethmoidalis is de roofed.The horizontal
portion of middle turbinate separates the anterior ethmoidal cells from
the posterior group. If the posterior group of ethmoidal cells are found
to be involved then they can be accessedafter breaching the basal
lamella. The idea is to remove the diseased mucosa, widening
thedrainage channels of paranasal sinuses there by allowing them to
be ventilated normally. This ensures faster regeneration of the ciliated
columnar epithelium and restoration of normal ciliary motility
.Complications of FESS:
1. Bleeding
2. CSF leak
3. Injury to orbit and its contents
4. Synechiae formation
. Stapedial reflex
: Introduction: Contraction of stapedial muscle occurs under normal
conditions when a loud acoustic stimulusis presented to the auditory
system. This muscle contraction causes a stiffening of the ossicular
chain and decreases the compliance of the middle ear system. This
change in the middle ear compliance can be recorded by
tympanometry.
This reflex is binaural and simultaneously occurs in both the ears.
This reflex is activated in normal adults when the sound pressure
levels range between 70-105 dBHL.
Stapedial muscle contraction in response to intense sound signal
occurs bilaterally because the reflex pathway has both ipsilateral and
contralateral projections. Acoustic reflex thresholds areusually
estimated in response to stimuli of 500, 1000, 2000, and 4000 Hz. For
screening purposes it is sufficient if recording is made at 1000 Hz
.Reflex pathway:Any reflex pathway by definition should include:
1. Sensory limb Input
2. Central integration
3. Motor limb Output

This stapedial reflex is designed to be protective in nature that limits

the damage caused by high intensity sound. The sensory signals travel
to the cochlear nuclei via the auditory component of the 8th cranial
nerve. From the cochlear nucleus signals travel to the superior olivary
complex bilaterally, and from there to the lower motor neurons in the
facial nucleus which innervates the stapedius muscle.
Indications:
A)Objective assessment of hearing Range of acoustic reflex in
persons with normal hearing averages between 70-100dB
sound pressure level.
i)
In conductive hearing losses, greater the loss
greater becomes the acoustic threshold reflex.
ii) Where as in sensori neural hearing loss
theacoustic reflex threshold may be within normal
range, this is true in patients with mild to
moderate levels of sensorineural hearing losses
with recruitment
B) Can be used as a topognostic test in patients with facial
nerve paralysis
C). Can be used in identifying deafness in infants
D). Acoustic neuroma diagnosis
Contraindications:
1. In infants under the age of 7 months due to extreme
pliability of external canal
3. In the presence of wax as the results may not be reliable.
Scarlet fever:
Introduction :Also known as scarlatina. It is an exo-toxin mediated
disease arising from group A Beta hemolyticstreptococcal infection.
This condition usually evolves from tonsillar / pharyngeal focal
infection.
Bacteriology: Group A Betahemolytic streptococci are known to
secrete a number of enzymes of toxins. One such toxin is known as
the erythrogenic toxin which is responsible for the pathognomonic
rash of scarlet fever. These organisms are known to survive extremes
of temperature and are spread via fomites.During the 18th century

scarlet fever was one of the most dreaded epidemics. With the advent
of excellent antibiotics this condition is not threatening anymore.
Incidence: This condition frequently affects children between 4-8
years. This infection is rare in children under the age of 2 because of
the presence of maternal antibodies
.Clinical features:Scarlet fever has an incubation period ranging from
1-4days. Evolution and presentation of thisdisease is usually dramatic.
These patients complain of: Sudden onset fever Throat pain Malaise
Myalgia Characteristic skin rash appears within 12 48 hours after
the onset of fever.If these patients are untreated the fever peaks by 48
hours.Condition abates within a couple of days after starting treatment
with appropriate antibiotics.
On examination :Exudative tonsillitis usually precede this
condition.Tonsillar infections are usually accompanied by
erythematous oral mucous membrane along with petechiae / punctate
red macules over hard palate/soft palate/uvula. These spots are known
as Forchheimer's spots. The tongue appears coated and reddish
raspberry tongue.
Features of skin rash:1. Rash generally appears within 12 48 hours
after the onset of fever. In the beginning it appearsas erythematous
patches below the pinna, chest and axilla. Dissemination to the trunk
andextremities occur within the first day.
2. The rashes typically consist of scarlet macules over generalized
erythema (Boiled lobster appearance).
3. The skin lesion later evolves to become more diffuse, and later turn
punctate resembling sunburn / goose pimples.
4. Fragile capillaries under the skin ruptures displaying arrays of
petechiae known as (Pastialines).
5. Circumoral pallor is another distinguishing feature seen in these
patients.
6. Peeling of skin occurs in the skin of axilla, groin, and toes
.Blood count shows predominant leucocytosis. Eosinophilia
develops during the first week of infection.Throat culture is
diagnostic. It also helps in deciding the sensitivity of the organism to
the specific ntibiotic.
Management:The goals in managing this disease are
1. Prevention of acute rheumatic fever

2. Reducing the spread of infections

3. Prevention of suppurative complications
4. Shortening the course of ailment
Antibiotics:Penicillin is the drug of choice. Could be administered
either orally / parenterally. Amoxycillin has gradually replaced
penicillin as the first choice antibiotic in these patients.
. Septal hematoma
Introduction:
Septal hematoma is defined as collection of blood between the
perichondrium of nasal septum and the septal cartilage. Since nose is
the most prominent part of the face it is more prone to injurieswhich
could lead to septal hematoma formation.
Pathophysiology:The submucosal blood vessels present under the
mucosal lining of nasal septum may be damaged due to sharp
buckling forces to which nasal septum could be subjected to in case of
trauma. If the mucosa is intact then blood will collect under the
perichondrium leading on to hematoma formation.This will strip the
muco perichondrial layer away from the septal cartilage causing a
bulge which could be seen in the nasal septal area. If the trauma is
severe enough to cause fracture of nasal septal cartilage then blood
may seep to the opposite side also stripping the muco- perichondrial
layer on the opposite side also. This condition can be identified by the
presence of bilateral septal swelling. This bilateral septal hematoma is
really critical because it can compromise the nourishment of the septal
cartilage which occurs only when the perichondrium is in contact with
it.This nutritional compromise can lead to liquifaction necrosis of the
septal cartilage leading on to pig snout deformity. Cartilage resorption
starts to occur from the third day of vascular compromise.If the septal
hematoma is unilateral and small it may cause localized necrosis of
cartilage leadingon to fibrosis and thickening of cartilage in that area.
Signs & symptoms: The predominant symptom is nasal obstruction.
If the hematoma is unilateral then nasal obstructiontoo is unilateral, if
the same is bilateral then nasal block is also bilateral.
Examination:Should be carried out without the introduction of nasal
speculum. The nasal septum can be clearly viewed by just lifting up
the tip of the nose. Examination will reveal a smooth rounded
unilateral /bilateral rounded swelling extending up to the lateral nasal

wall. The swelling will be fluctuantand may blanch on application of

gentle pressure. Long standing septal hematoma can lead to formation
of septal absess. Presence of pain and tenderness indicate abscess
formation.
Management:Early evacuation of hematoma will definitely reduce
the risk of cartilage necrosis, hence it is alwaysworth while trying it
out. Evacuation can be performed under local anesthesia via a
hemitransfixation incision. This incision is sited at the lower border of
the septal cartilage. The septal hematoma would have already elevated
the mucoperichondrial flap away from the septal cartilage, hence
evacuation of hematoma would be pretty straight forward. If the
cartilage show evidence of necrosis it should be immediately removed
and homograft cartilage should be used to cover the defect.The
homograft cartilage are sourced from patients who have undergone
submucosal resection nasal septum. This cartilage can be stored in
0.1% sodium mercurothio-salicylate solution.Nowadays cartilage
banks are commonly available. Antibiotics and anti inflammatory
drugs should be prescribed for these patients as a routine inorder to
prevent development of septal abscess.
Complications
:1. External deformity of nose The dorsum of the nose derives its
support from the septal cartilage.If this support is lost then it would
lead on to the formation of saddle nose deformity. If this injury occurs
during early childhood then it would cause under development of the
whole of middle third of face causing maxillary hypoplasia.
2. Septal abscess Blood is an excellent culture medium and hence
could get infected leadingon to abscess formation. The presence of
septal abscess will lead on to constitutionalsymptoms like fever,
toxemia etc.
3. Septal deviation Unilateral septal hematoma can cause local
thickening of nasal septum there bycausing deviation of nasal
septum.e.
CROUP:
Synonyms: Acute laryngotracheal bronchitis, Viral laryngotracheal
bronchitis
Introduction: This clinical syndrome is characterized by:
a. Hoarseness of voice

b. Stridor which could be inspiratory or biphasic

c. Barking cough
d. Fever
e. Malaise
Pathophysiology: This condition is usually caused by mucosal
oedema of larynx and trachea. The lining mucosa of larynx and
trachea is pretty lax in infants, and hence can swell up rapidly causing
airway compromise. Inflammation and oedema occurs in the
subglottic area and trachea commonly.
Children of age between 6 months and 3 years are affected commonly.
Peak age of occurrencehappens to be 2 years.
Causative organism:
Viruses have been implicated as the common cause.
They include: Parainfluenza type I virus, Parainfluenza type II virus,
Respiratory syncitial virus and Influenzatype A and type B viruses.
Management:Since it is a self limiting disease reassurance and
supportive therapy may be all that is needed. The Child usually
improves dramatically within the first 24 hours and complete recovery
occurs within4 days even without treatment.
If the affected child has acute airway obstruction then hospitalization
is a must. Coexistent measles infections and bronchopneumonia may
complicate the issue.
Croup scores:
Grading croup will help us in deciding the optimal management
modality of these patients:
Commonly used grading system is the Westley scale.
Westley scale:This scoring system helps the examiner in assessing the
degree of respiratory compromise.Usually the following five factors
are taken in to consideration in this scoring system:
Inspiratory stridor: None 0 points
Upon agitation 1 point
At rest 2 points
Chest retractions:Mild 1 point
Moderate 2 points
Severe 3 points
Air entry:Normal 0 points
Mild decrease 1 point

Marked decrease 2 points

Cyanosis:None 0 points
Upon agitation 4 points
At rest 5 pointsLevel of consiousness:Normal 0 pointDepressed
5 points
Over all score: Less than 3 mild
3-6 moderate6 and
above is severe
DD:Ideally croup should be differentiated from conditions causing
stridor. They include:Allergic reaction, angioneurotic oedema,
subglottic tumors, neck space infections etc.
plain x-ray chest Shows classic steeple sign in the laryngotracheal
air column. The shadow resembles steeple of a church. This is due to
significant subglottic narrowing seen in these patients.Arterial blood
gas estimations are not routinely done. They are indicated only in
patients with significant amount of cyanosis.The child should be
made as comfortable as possible. Moist air will help these children to
recover faster.
Injection dexamethazone in doses of 0.15mg/kg if administered
within 2-4 hours of attackcan alleviate symptoms because of its
antiinflammatory effects.
In patients with severe distress administration of nebulized L
epinephrine will help. This acts by constriction of precapillary
arterioles causing a reduction in the capillary hydrostatic pressure.
Heliox an inert gas inhaled in combination with oxygen causes greater
laminar flow in the respiratory tract ensuring better gas exchange.
Antibiotics are not indicated in these patients.
. Lateral wall of Nasal cavity
Introduction:With the advent of nasal endoscopes and use of
endoscopes in nasal surgeries the anatomy of the lateral nasal wall has
been re-written. The current description of anatomy of lateral nasal
wall is infact the endoscopic anatomy of lateral nasal wall only.
Turbinates: These are the most prominent features of the lateral nasal
wall. They are usually three or sometimes four in number. Out of
these turbinates the inferior turbinate is a separate bone whilethe other
turbinates are part of ethmoidal complex. These turbinates are delicate
scrolls of bone covered by ciliated columnar epithelium. Sometimes

these turbinates may contain a large air cell in which case they are
termed as concha. These turbinates are named according to their
positions: Superior turbinate Middle turbinate Inferior turbinate
Supreme turbinate rarely A prominence can be seen commonly
anterior to the attachment of middle turbinate. This is known as
aggernasi. This projection usually over lie the lacrimal sac. This
prominence may be of varying shapes in different individuals. This
prominence is considered to be remnants of nasoturbinal bones seen
in animals.Under each of these turbinates and lateral nasal wall a
space is enclosed. The space between inferior turbinate and lateral
nasal wall is known as the inferior meatus. The nasolacrimal duct
drains into the inferior meatus in its anterior third. This opening is
covered by mucosal valve known as Hassner's valve. The course of
the nasolacrimal duct lie under the agger nasi cell.Middle meatus:This
critical space lies between the middle turbinate and the lateral nasal
wall . In this space opens the drainage channels of the anterior group
of paranasal sinuses.
These include:1. Frontal sinus
2. Maxillary sinus
3. Anterior ethmoidal sinus
4. Middle group ethmoidal sinus It is this space which is critical in the
pathophysiology of sinusitis. It is this space that is relevant in
functional endoscopic sinus surgery.
Uncinate process: This boomerang shaped (L) shaped bone forms the
first layer (lamella) of middle meatus. This bone should be removed
in its entirety in order to visualize the natural ostium of maxillary
sinus and frontal sinus drainage channel.
Ethmoidal infundibulum: This is a cleft like three dimensional space
in the lateral wall of the nose.This space is bounded medially by the
uncinate process and the mucosa covering it. Major portion of its
lateral wall is bounded by lamina papyracea, and the frontal process
of maxilla to a lesser extent. Defects in the medial wall of
infundibulum is covered with dense connective tissue and periosteum.
These defects are known as anterior and posterior fontanelles
.Hiatus semilunaris: This lies between the anterior wall of bulla and
the free posterior margin of uncinate process. This hiatus semilunaris
leads to the ethmoidal infundibulum.

Osteomeatal complex:This term is used by the surgeon to indicate to

indicate the area bound by middle turbinate medially,lamina
papyracea laterally and the basal lamella superiorly and posteriorly. It
is through this area the anterior group of sinuses drain. This area
happens to be a cess pool of secretions from all the anterior group of
sinuses.
g. Atrophic rhinitisDefinition:
Atrophic rhinitis is defined as a chronic nasal disease characterized by
progressive atrophy of nasal mucosa along with the underlying bones
of turbinates. There is also presence of viscid secretions which gets
dried up leading on to the formation of foul smelling crusts. The
characteristic foetid odour emanating from these crusts is known as
ozaena. The nasal cavity in these patients appear to be abnormally
patent. The patients with this condition are fortunately unaware of this
condition because of the coexisting presence of anosmia (Merciful
anosmia).
Etiology :Still remains obscure. Numerous pathogens have been
implicated. The most important of them are:a. Coccobacillusb.
Bacillus mucosusc. Coccobacillus foetidis ozenaed. Diptheroid
bacillie. Klebsiella ozenae Even though these organisms have been
repeatedly isolated from the nasal cavity of these patients they have
not been categorically proved to be the cause
.Other predisposing causative factors include:
a. Chronic sinusitis
b. Excessive destruction of nasal mucosa and turbinates (overzealous
nasal surgeries)
c.Nutritional deficienciesd.
d. Syphilise.
e. Endocrine imbalances (This disease is known to worsen with
pregnancy)
f. Hereditary
g. Autoimmune mechanisms According to Faud these patients have
altered cellular immunityleading on to intolerance to nasal tissues.
This immune intolerance can be caused by viral infections
.Fraenkel triad:Dr Bernhard Fraenkel described a classic triad of
symptoms seen in these patients. According toFraenkel the presence

of this triad is a must for the diagnosis of atrophic rhinitis. This triad
include:
1. Fetor
2. Crusting
3. Atrophy
Age of onset This disorder commonly occurs at puberty. Females are more
commonly affected than males Bernat postulated that iron deficiency could
probably cause this condition.
Histopathology:
1. Metaplasia of ciliated columnar epithelium into squamous epithelium
2. There is a decrease in the number and size of nasal compound alveolar glands
3. Dilated capillaries can be seen
Pathologically atrophic rhinitis has been divided into two types:
Type I This is characterized by the presence of endarteritis and periarteritis of
terminal arterioles.Usually this type could be caused by chronic infections.
These patients benefit from the vasodilator effects of oestrogen. Majority of
these patients belong to this categoty.
Type II This type is characterised by vasodilatation of capillaries and these
patients are likely to worsen with oestrogen therapy. The endothelial cells of
these capillaries contain more cyto-plasm than those of normal capillaries.
These cells also show active reaction for alkaline phosphatase indicating rapid
bone destruction.
Clinical classification of atrophic rhinitis:
Clinically atrophic rhinitis can be classified into primary and secondary types
.Primary atrophic rhinitis:This is the classic form of atrophic rhinitis and is
supposed to arise denovo. Diagnosis of this type of atrophic rhinitis is by the
process of exclusion. All the known causes of atrophic rhinitis should be ruled
out before branding the patient to be suffering from primary atrophic rhinitis.
The causative organisms in these patients are usually klebsiella ozenae.
Secondary atrophic rhinitis:This is the most common form of atrophic rhinitis
seen in developed countries. The most common causes of this form of atrophic
rhinitis include:
1. Extensive destruction of nasal mucosa and turbinates during nasal surgery
2. Following irradiation
3. Following granulomatous infections like syphilis, leprosy and tuberculosis
Clinical features:
1. Nasal obstruction
2. Epistaxis
3. Anosmia (Merciful)
4. Foul smelling greenish yellow crust can be seen inside the nasal cavity
5. Roomy nasal cavity due to atrophy of nasal mucosa and turbinate bones

6. These patients are psychologically depressed because of the foul smelling

crusts in the nose
Reason for nasal obstruction despite the presence of roomy nasal cavity:The
nasal cavity is filled with sensory nerve endings close to the nasal valve
area.These receptors sense the flow of air through this area thus giving a sense
of freeness in the nasal cavity. These nerve endings are destroyed in patients
with atrophic rhinitis thus depriving the patient of this sensation. In the absence
of these sensation the nose feels blocked.
Radiographic findings:This is more or less the same for both type I and type II
atrophic rhinitis.
Plain x-rays paranasal-sinuses show:
1. Lateral bowing of nasal walls
2. Thin / absent turbinates
3. Hypoplastic maxillary sinuses
CT scan findings:1. Mucoperiosteal thickening of paranasal sinuses
2. Loss of definition of osteomeatal complex due to destruction of bulla
3. Hypoplastic maxillary sinuses
4. Enlargement of nasal cavity with erosion of lateral nasal wall
5. Atrophy of inferior and middle turbinates
Management:
Conservative:Nasal douching Patient is encouraged to douch the nasal cavity
at least twice a day with solution prepared with: Sodabicarb 28.4 g2.
Sodium diborate 28.4 g3. Sodium chloride 56.7 g mixed in 280 ml of luke
warm water.
The greenish yellow crusts can be removed by suction or by teasing with
forceps.
Glucose glycerine drops:25% glucose dissolved in glycerine can be
administered into the nasal cavity. Glycerine is an hygroscopic agent hence
moistens the nasal cavity there by softening the crusts. 25% glucose inhibits
proteolytic organisms which are commonly present in the nasal cavity of these
patients.
Patients with histological type I atrophic rhinitis could benefit from nasal
topical administration of oestradiol in arachis oil in concentrations of 10,000
units / ml.Another topical medication that could benefit these patients is
Kemecitine antiozena solution.Kemecitine antiozena solution contains:
1. Chloramphenicol 90 mg
2. Oestradiol dipropionate 0.64 mg
3. Vitamin D2 900 IU
4. Propylene glycol
5. Isotonic saline 1 ml
Oral administration of potassium iodide has been tried in an effort to increase
nasal secretions with varying degrees of success.

Systemic administration of placental extracts have also been attempted in these

patients
.Surgical management
:Submucous injection of paraffin - This happens to be one of the procedures that
displaces thelateral nasal wall medially. Various materials are being used for this
procedure. This medicalization procedure is also known as Lautenslauger's
operation.
Recently teflon strips / autogenouscartilages are being inserted after elevating
the flaps in the lateral wall and floor of the nasal cavity.
Wilson's operation: Submucosal injection of 50% teflon in glycerine paste. This
not only narrowsthe nasal cavity but also helps in dislodging the crusts.
Stellate ganglion blocks: This helps to some extent in increasing the glandular
secretions of the nasal cavity. Sometimes this process may need to be repeated
more than once for optimal benefit.
Young's operation:This procedure aims at closing the nasal cavity by raising
mucocutaneous flaps. In this method mucocutaneous flaps are raised all around
inside the nasal cavity. This flap is then sutured insuch a way that the whole
nasal cavity is obliterated. The nasal cavity is kept blocked for a period
of 9 months during which time the nasal mucosa would have regenerated. After
9 months thenasal mucosa can be assessed by performing a post nasal
examination. If it had regenerated then the sutured flaps can be released and the
nasal cavity reopened. This procedure shouldbe performed on one side first,
then after opening up the nasal cavity after 9 months the other sideshould be
attempted.
Modified young's operation:In this procedure a small hole measuring 3 mm is
left while the flaps are being sutured. This hole helps the patient to breath
normally through the nasal cavity. The healing process can also be monitored by
performing periodical nasal endoscopic examination via the opening
.h. Physiology of hearing
In the study of physiology of hearing the role played by external ear, middle ear
and internal ear should be discussed separately.
Role played by external ear: Because of its funnel shape the external ear helps
in capturing sound waves and focuses it on the ear drum. The portions of
external ear which play an important role in sound conduction are: Pinna,
concha and external auditory meatus.
Functions of external ear:
1. By acting as an resonator it increases the pressure of sound at the level of
ear drum in a frequencyspecific manner. It is known to resonate better in
the frequency range of 2-5 Khz
.2. It helps in sound localization
3 The pinna conchal system acts like a trumpet focussing the sound to the
ear drum for transmission

4 Role of ear drum in sound conduction:The ear drum conducts sound from
external ear to middle ear. According to Bekesey the ear drum moves like
a stiff plate up to the frequency levels of 2 KHz. Above this frequency the
vibrating pattern gets broken up and becomes more complex. The ear
drum serves to conduct sound preferentially in the frequency ranges
between 2-5 Khz. The handle of the malleus is attached to the centre of
the ear drum. This relationship helps in conduction of sound from the
external ear to the middle ear.
Role of middle ear in sound conduction:The middle ear serves to couple
sound energy to the fluids of cochlea. It should be borne in mind that sound gets
reflected from the interface separating two media with different impedances.
Thisis true of the middle and inner ear interface because the cochlear fluids
have higher impedanceto sound when compared to that of air in the middle ear
cavity. In order to conduct sound efficiently without loss, the middle ear should
function as an impedance matcher. The middle ear serves to convert low
pressure high displacement vibrations to high pressure low displacement ones
which is favorable for sound conduction via cochlear fluids. The middle ear
apparatus couples sound preferentially to one window of the cochlea there by
creating differential pressure between the oval and round windows which
pushes the cochlear fluid in a forward direction
.Components of middle ear transformer mechanism:
1. The surface area of ear drum is 55 mm
2. , while the surface area of foot plate of stapes is
3. 3.2 mm 2. The difference between these surface areas happens to be
roughly 17 times. Thus the forces collected by the ear drum are
concentrated over a small area causing movementof cochlear fluids
towards round window
4. .2. Ossicular lever ratio. This roughly works out to 2.1 times. The incus is
shorter than the malleusand this is very important for lever action of
ossicles. This lever action increases the force and decreases the velocity
at the level of stapes.
5. 3. Buckling effect of ear drum: The ear drum curves from its rim to its
attachment to the manubrium.This buckling effect causes greater
displacement of the ear drum and lesser displacement of the
manubrium.This middle ear transformer mechanism ensures that at least
50% of the incident sound energy gets transmitted to the cochlea
.Role played by cochlea:Sound traveling through cochlea causes a
mechanical traveling wave which forms the basisof frequency selectivity.
Features of cochlear traveling wave:
1. As the wave travels along the cochlea it reaches a peak and dies down
rapidly
2. The basilar membrane vibrates at a constant frequency for all low
frequency sounds and drops abruptly above certain frequency levels.It has

been shown that basal turn of cochlea responds best to high frequency
sounds and the apex of cochlea responds better to low frequency sounds
.Role of auditory fibers:In response to stimulus, neurotransmitter is
released in the synapses at the base of inner hair cells.This gives rise to
action potentials in the auditory nerve fibers. Single auditory nerve
stimuli is always excitatory and never inhibitory. This action potential is
conveyed to the auditory centers of brain by the auditory division of the
8th nerve.The following are the proposed theories of hearing
:Place theory of Helmontz - This theory proposes that frequency
resolution occurs at the levelof basilar membrane. The various zones of
basilar membrane are sensitive to different frequenciesand this spatial
relationship play a role in frequency resolution.
Telephone theory of Rutherford This theory assumes that the whole
cochlea responds as a whole to all the frequencies. This theory assumes
that cochlea reacts to various frequencies like a telephone cable.
Volley theory of weaver This theory proposed by Wever assumes that
several neurons acting as a group can fire in response to the frequency to
which they are sensitive to.
Place theory of Lawrence Lawrence combined both volley and place
theories to explain how sounds are perceived.
Traveling wave theory of Bekesy This theory assumes that frequency
coding took place at the level of cochlea.Auditory center of brain is
located at the superior gyrus of temporal lobe
.Functions of auditory center:Sound localization and lateralization
Speech discrimination Auditory performance with competing acoustic
signals
Auditory performance with degraded signals
.. Pure tone audiometry
Introduction:This procedure is performed to measure the auditory
threshold of an individual. The instrument used for this purpose is known
as the audiometer.
Components of a pure tone audiometer:Oscillator:The function of an
oscillator is to generate electronically standardized sound whose
frequencies liewithin + / - 3% of their supposed value.
The frequencies generated include: 125, 250,500, 750,1000,1500, 2000,
3000, 4000, 6000 and 8000 Hz
.Interrupter switch: This switch helps in turning on and off the sounds
which are presented to the patient from the oscillator. This is important
because presenting a continuous tone to a patient may cause auditory
decay causing problems with interpretation of results. This switch
provides the option of presenting the sound in a continuous / interrupted
manner.

Equalization circuit:This circuit contains resistors which helps in

equalization of the sound generated. This process is important because
the threshold of human hearing is not uniform and it is very good
for frequencies around 2 kHz. Above and below this level the sensitivity
of human hearing varies.
Output power amplifier:The signals generated by the oscillator needs to
be amplified. The vital feature of any power amplifier is that it should
have a good signal to noise ratio and should produce very little
distortion.In most audiometers the power amplifier is run at constant high
signal output levels.
Hearing level attenuator:This controls the level of signal from the
audiometer within a range of 110-120 dB. This attenuator can be varied in
steps of 5 dB. The basic reference point is marked as 0. This point
technicallyindicates -5 to -10 dB hearing threshold levels. The attenuator
steps should be accurate.
Output transducers:These are of three types:a. Ear phonesb. Bone
vibrator c. Loud speaker The ear phones of an audiometer are real special.
They cannot be changed / replaced withoutrecalibrating the whole
equipment. A good ear phone should have long term stability, should have
aflat frequency response, and should have the ability to deliver high
output sounds.Bone vibrators unlike ear phones has a limited frequency
range. It cannot be used to reliablyrecord frequencies above 4 kHz
because it wont vibrate beyond this range. At low frequencies itshows
distortions and is incapable of transmitting high frequencies.Loud
speakers are used in free field audiometry.Technique of measurement of
hearing acuity:Air conduction threshold of a patient is measured using ear
phones. It can be measured from goingfrom an inaudible to an audible
stimulus intensity. This is known as the ascending method of evaluation
of air conduction threshold. There is one other method that uses the
descending methodof threshold estimation. In this method the air
conduction threshold is assessed by going fromaudible to inaudible signal
intensity. The patient should be instructed to raise his / her indexfinger
even if the sound is mildly audible.Care should be taken to ensure that the
headphones are properly seated over the externalauditory canal, because
patient's pinna may be in different shapes and sizes. Improper
placementof headphones will lead to threshold variations of 15 20 dB.
Before placing the ear phones on thepatient, wax free ear canal should be
ensured because the presence of wax could cause adiscrepancy of about
30 dB. While plotting the values red color ink is used to plot results
of right ear and blue color is used to plot the results of left ear.

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 acombination 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 rhinorrhoead.
d. Head ache due to obstruction of sinus drainage channelse
e. . Broadening of nose due to polypi causing flaring / splaying of the bones
causing frog faceddeformity
.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
Retropharyngeal abscess:
Definition: It is defined as collection of pus between the posterior pharyngeal
wall and thefascia 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 pharyngealwall 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 3rdto 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 usuallylocalized 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 streptococciand 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 onto 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 feed
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 labscess
Investigations:
X-ray soft tissue neck AP/Lat - Will show prevertebral soft tissue widening. It
should beborne 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 likeclostridia.
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
retropharyngealabscess. It should ideally be performed under local anesthesia
taking precaution that the childdoesn'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 andthe patient is immediately started on anti TB drugs
.4. After surgical drainage a course of antibiotics should be ideally started. The
drug of choicebeing drugs belonging to cephalosporin group. Metronidazole
should also be administered becauseof 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
Hemorrhage secondary to involvement of carotid artery
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 smokeis 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 toconsume 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 thebiopsied 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 vocalfolds. 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'thave
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 degreeof
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.
.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 pars flaccida. 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
thehandle 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 throughthis.
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 tympanicbranch 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
caroticotympanic 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.
.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 areinvolved.Conductive deafness
:Causes are enumerated here
Vocal nodule Also known as Singers nodule / Teacher's nodule.This disorder
frequently affects children and adults. In children it appears as spindle
shapedthickenings 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 conditioncan 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 ongiving voice rest
.Stage of in growth 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
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
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 vocalcord 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 lesionsinvolving the recurrent laryngeal nerve the abductors
paralyze first followed by the adductors. Whenrecovery 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 isalso 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
nucleusambiguus.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 changeb.
b. Diplophoniac. Aspiration in severe cases
c. 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.
d. Vocal cord lateralization procedures should be performed in patients with
bilateralabductor palsy.

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.
.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.
.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 postcricoid region. It commonly affects females and this
condition is considered to be premalignant innature because of increasing
incidence of post cricoid malignancy in these patients
..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.
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.

Describe the diagnosis, complications and treatment of acute

follicular tonsillitis
.Acute follicular tonsillitis is a severe form of tonsillar infection
caused by infections by virulent organisms like streptococcus
hemolyticus / Haemophilus influenza. Initially the tonsillar crypts get
inflammed. From the crypts inflammation spreads to the surrounding
tonsillar follicles.The inflammed follicles appear reddish and swollen.
This type of tonsillar infections are commonin adults.
Appearance:The involved tonsils appears irregular with prominent
crypts. These crypts appear to be filled with whitish to yellow
exudate. This exudate may coalesce to form a coating over the tonsil
giving the appearance of the presence of a membrane. This membrane
is a false membrane. Thiscondition is now termed as acute
membranous tonsillitis.
Clinical features:High grade fever General malaise / bodyache
Odynophagia Dry cough Sorethroat
Signs:Tonsils enlarged congested and oedematous Follicles swollen
Crypts filled with pusPus can coalese to form membrane over the
tonsil (membranous tonsillitis)
Enlarged tender jugulo-digastric node
The presence of pseudomembrane in follicular tonsillitis should be
differentiated from that of diptheritic tonsillitis.
Membrane formed in diptheretic tonillitis is true membrane.

acute follicular tonsillitis

acute diphtheria

Age

between 6-20

Children under the

age of 10

onset
Temperature
Throat pain
Toxiemia
Pulse rate

Acute onset
Very high temperature
Severe throat pain
No evidence of toxemia
proportionate to rise in
bodytemperature

Membrane

Formation of dirty white

pseudomembranelimited
to the tonsil only
It can easily beremoved
and does'nt leave raw
areas

Throat swab

Thorat swab demonstrates

bacteria likestreptococci,
H influenza etc
in neck enlarged and
tender

Slow onset
High temperature
Mild throat pain
Toxemia present
Bradycardia
common
In early stages
of myocarditis
tachycardia is
pssible
Extensive
membrane
formation on
tonsils,pillars and
uvula. Can be
removed only
withdifficulty. On
removal leaves
behind rawbleeding
areas
Throat swab shows
corynebacterium
diphtheria
Massive cervical
adenopathy (Bull's
neck)
test positive

JD nodes

Schick test
Schick test negative
^No albuminuria Albuminaria present

Treated with antibiotics

Treatment with antidiphthertic serum
Complications:1. Peritonsillar abscess2. Parapharyngeal abscess3.
Chronic tonsillitis4. Focal infections involving the ear 5. Rheumatic
fever 6. Acute glomerular nephritis
Investigations:1. Throat swab for culture and sensitivity
2. Peripheral smear
3. Paul Bunnel test to rule out infectious mononucleosis
4. X ray paranasal sinuses to rule out focal sepsis
5. X-ray soft tissue nasopharynx to rule out adenoid hypertrophy
Treatment:Since this is an acute condition antibiotic therapy is
advisable.Surgery is contraindicated.
Penicillin is the drug of choice if the infecting organism is
streptococcus
Beta lactamase producing organism should be treated with
amoxycillin clavulanic acid combination.In patients with
hypersensitivity to penicillins then Erythromycin is the preferred
antibiotic.
Tablet paracetomol can be administered in patients with fever.
Ibuprofen can be given incombination with paracetomol if the pain in
the throat is unbearable
Nasal cholesteatoma:
This is another name for Rhinitis caseosa. The term Rhinitis
caseosa was coined by Duplay in1868. Eggston and Wolff after a
detailed study in 1947 concluded that this condition could
occur secondarily following pent up secretions in the sinus cavities.
Their studies revealed that thiscondition is more common in patients
with extensive bilateral ethmoidal polyposis. The presenceof polypi in
the nasal cavities caused obstruction to the normal drainage
mechanism of the paranasalsinuses. This led to accumulation of
secretions. Whitish to yellow cheesy material were foundwithin the
nasal cavities of these patients behind the nasal polypi. This cheesy
material also causedexpansion of sinus cavities, erosion of bone and
extension into orbit.Eggston used the term pseudocholesteatoma to
describe this condition which resembledcholesteatoma only
morphologically. Histologically squamous elements could not be
identified inthem. Histologically this tissue comprises of

inflammatory tissue, granulation mixed with mucoiddebris.Presently

allergic fungal sinusitis also resembles this condition and hence
included under this category
.Clinical features:
1. Nasal obstruction
2. Presence of nasal polypi
3. Telecanthus
4. Swelling over medial canthal region
5. Proptosis with the eye being pushed downwards and laterally6.
These patients may present with loss of vision due to involvement of
optic nerve
7. Intracranial extension due to erosion of anterior cranial fossa skull
base is also seen
This disease could be considered to be end stage manifestion of sinus
inflammation.
Hence the use of the term Rhinitis caseosa syndrome makes lot of
sense.
Pinus theory of nasal cholesteatoma:According to Pinus a majority of
patients suffering from nasal cholesteatoma also suffered from dental
cysts which obliterated the entire maxillary sinus cavity
.Management:Rhinitis caseosa can be managed by debridement
followed by regular douching using normal saline
Antrochoanal polypSynonyms:Antrochoanal polyp, Killian's polyp,
Nasal polyp.History:In 1753 Palfyn first described an antrochoanal
polyp in a female patient. The polyp wasfound filling the nasopharynx
extending up to the uvula of the patient. Palfyn believed that thispolyp
arose from the choana. It was Killian in 1906 who demonstrated that
this polyp arose fromthe maxillary sinus
antrum.Definition:Antrochoanal polyp is a benign solitary polypoidal
lesion arising from the maxillarysinus antrum causing opacification
and enlargement of antrum radiologically without any evidenceof
bone destruction. It eixts the antrum through the accessory ostium
reaches the nasal cavity,expands posteriorly to exit through the choana
into the post nasal space.Incidence:It commonly affects children and
young adults.Etiopathogenesis:This disease is commonly seen only in
non atopic persons. Its etiology is stillunknown. Infact this disorder is
not associated with nasal allergy.Proetz theory: Proetz suggested that

this disease could be due to faulty development of themaxillary sinus

ostium, since it was always been found to be large in these patients.
Hypertrophicmucosa of maxillary antrum sprouts out through this
enlarged maxillary sinus ostium to get into thenasal cavity. The
growth of the polyp is due to impediment to the venous return from
the polyp.This impediment occur at the level of the maxillary sinus
ostium. This venous stasis increases theoedema of the polypoid
mucosa thereby increasing its size.Bernoulli's phenomenon:Pressure
drop next to a constriction causes a suction effect pulling thesinus
mucosa into the nose.Mucopolysaccharide changes:Jakson postulated
that changes in mucopolysaccharides of the groundsubstance could
cause nasal polyp.Infections:Recurrent nasal infections have also been
postulated as the cause for nasal polypVasomotor imbalance
theory:This theory attributes polyp formation due to autonomic
imbalancePolypoidal tissue from the maxillary antrum exits out
through the accessory maxillary sinus ostiumaccording to some
workers. This accessory sinus ostium is placed posteriorly, which
could be thereason for the polyp to present posteriorly. The accessory
sinus ostium widens progressively,ultimately at one stage merging
with the natural ostium of the maxillary sinus forming one
hugeopening into the maxillary antrum.Possible reasons for migration
of antrochoanal polyp in to the post nasal space:1. The accessory
ostium through which the polyp gets out of the maxillary antrum is
presentposteriorly.2. The inspiratory air current is more powerful than
the expiratory air current thereby pushes thepolyp posteriorly.3. The
natural slope of the nasal cavity is directed posteriorly, hence the
polyp always slips
posteriorly.4. The cilia of the ciliated columnar epithelial cells lining
the nasal cavity always beatsanteroposteriorly pushing the polyp
behind.Histology:Shows respiratory epithelium over normal basement
membrane. The interstitial layer isgrossly oedematous, with no
eosinophils. The interstial layer contains other inflammatory
cells.Clinical features:Since the disorder is unilateral (commonly) the
patient always present with1. Unilateral nasal obstruction2. Unilateral
nasal discharge3. Headache (mostly unilateral)4. Epistaxis5. Sleep
apnoea6. Rhinolalia clausa due to presence of polyp in the post nasal

space7. Difficulty in swallowing if the polyp extends into the

oropharynxAnterior rhinoscopy may show the polyp as glistening
polypoidal structures. They willbe insensitive to touch. this feature
helps to differentiate it from a hypertrophied nasal turbinate.Postnasal
examination will show the polyp if extending posteriorly at the level
of choana. If it fillsup the nasopharynx it will be visible there.Xray
paranasal sinuses will show a hazy mazillary antrum.CT scan of
paranasal sinuses is diagnostic. It will show the polyp filling the
maxillary antrum andexiting out through the accessory ostium into the
nasal cavity.The antrochoanal polyp is dumb bell shaped with three
components i.e. antral, nasal andnasopharyngeal.Treatment:This is a
surgical problem. Formerly it was treated by avulsion of the polyp
transnasally. Thismethod led to recurrences. A caldwel luc approach
was preferred in patients with recurrences. Incaldwel luc procedure in
addition to the polypectomy, the maxillary antrum is entered via the
caninefossa and the antral component is completely
excised.Endoscopic approach:With the advent of nasal endoscope this
approach is the preferred one.Using an endoscope it is always easy to
completely remove the polypoid tissue. The uncinateprocess must
also be completely excised. Endoscopic approach has the advantage
of a completesurgical excision with negligible recurrance rates.
Rhinoscleroma
This is a chronic granulomatous condition of the nose and upper
airway. This condition is caused byinfection by the bacilli Klebsiella
rhinoscleromatis. It is also known as Firsch bacilli (as an honor tovon
Firsh who described this organism).Pathophysiology: This condition
is contracted by direct inhalation of droplets / contaminatedmaterial.
This infection usually prefers transitional epithelial zones (like
vestibule of nose where thesquamous epithelium changes in to ciliated
columnar epithelium and supraglottic area of larynx).Clinical
features:1. Nasal obstruction2. Rhinorrhoea3. Epistaxis4. Nasal
deformity5. Anesthesia of palate6. AnosmiaClassically this condition
passes through three stages:Catarrhal stage: This initial stage begins
with non specific rhinitis progressing on to formation of foul smelling
thick discharge and crusting of the nasal mucosa.Granulomatous
stage: This stage is also known as hyperplastic stage. Nasal mucosa
shows rubberynodules / polypoidal lesion. Epistaxis may be present.

The nasal cavity appears enlarged withdestruction of nasal cartilages.

Involvement of maxillary antrum is common in this stage and
mayform the reservoir.The soft palate appears to be thickened at its
junction with that of hard palate. If the lesion presentslike a tumor
with evidence of tissue destruction it is known as pseudotumerous
rhinoscleroma.Sclerotic stage: This stage is characterised by sclerosis
and fibrosis. In this stage the nodules presentin the nasal mucosa gets
replaced by fibrous tissue.Management: Antibiotics. Tetracycline
happens to be the drug of choice. Ciprofloxacillin andrifampicin have
also found to be effective.Steroids can be administered inorder to
prevent excessive scarring of tissues.Surgery is indicated in patients
with extensive scarring of the nose.
Allergic rhinitis
Allergic rhinitis is defined as inflammation of nasal mucous
membrane caused by abnormalreaction to exposure to
allergens.Symptoms:RhinorroheaSneezingNasal congestion
Itching of nose and eyesDue to itching these patients keep twiddling
with the nose. This twiddling of the nose is known asallergic salute.
Thus a horizontal line can be seen over the dorsum of the nose
Darriers line.Since the mucous membrane lining the nasal cavity
also lines the nasopharynx and the middle ear cavity.There are two
types of allergic rhinitis:Seasonal rhinitis: this condition occurs during
pollen seasons. This type of allergic rhinitis does'ntdevelop till the
patient is 6 years of age.Perennial rhinitis: this condition occurs
throughout the year and is commonly seen in younger children.The
symptoms begin minutes after exposure to the offending antigen. It
causes nasal congestion byimpeding venous return from the nasal
mucosa. There is also increased vascular permeability andincreased
secretion of nasal mucous glands.Management:1. Avoiding exposure
to allergen2. Antihistamines3. Topical steroids4. Nasal decongestants
during acute phase5. Immunotherapy in troublesome cases
Chronic retropharyneal abscess:
Retropharyngeal abscess is a collection of pus between the posterior
pharyngeal wall and the fasciaand muscles covering the cervical
vertebrae. It occurs in two forms - 1. The acute
primaryretropharyngeal abscess which is common in infants, and 2.

Chronic retropharyngeal abscess whichis common in adults. These

two types of abscesses differ in their etiology and
management.Chronic retropharyngeal abscess commonly known to
occur in adults. This is usually caused bytuberculosis. The tuberculous
foci occur in the bodies of the cervical vertebrae( Pott's disease)which
later spread into the retropharyngeal space. Primary syphilis of the
mouth and pharynx mayalso cause retrophrayngeal abscess. This
abscess usually is present in midline and is free to spreadto either side
also. Rarely infections can spread from tonsils to involve this
space.Symptoms: These patients have excruciating pain while
swallowing (odynophagia). Young infantswith retrophryngeal abscess
will refuse feed, may have extensive drooling. In adults the head
maybe held straight. Torticollis is also common in these patients.
These patients may have difficulty inbreathing (stridor), in which case
tracheostomy must be considered to secure the airway in the
firstplace. Constitutional symptoms like fever / toxicity is very
common in acute retropharyngealabscess.Investigations:Complete
blood count show leucocytosis. Blood cultures can also be performed
to ascertain theappropriate antibiotics to be used.C reactive proteins
are also found to increased in these patientsXray soft tissue neck A.P. and lateral views.These pictures show prevertebral soft tissue
widening. This can be ascertained by estimating thesize of the
prevertebral soft tissue which is normally half the size of the body of
the correspondingvertebra. If the widening is more than half the body
size of the corresponding vertebra thenretropharyngeal abscess must
be considered. The cervical spine are straightend with loss of
thenormal lordosis (Ram Rod spine). Above the prevertebral shadow
air shadow is seen in almost allcases of retropharyngeal abscesses.
This gas shadow is caused by entrapped air which occur
duringbreathing. Some bacteria esp. Clostridium are known to form
gases which may be entrapped in theprevertebral space.If tuberculosis
is considered to be the cause of chronic retropharyngeal abscess then
surgery iscontraindicated. Anti tuberculous therapy is
initiated.Patients with non tuberculous chronic retropharyngeal
abscess need to undergo incision anddrainage under local anesthesia.
Local anesthesia is preferred in order to prevent aspiration
Killian's dehiscence:

Killian's dehiscence:Is the junction between thyropharyngeus and

cricopharyngeus muscles. This is a potentially weak area not
supported by other constrictor muscles. The cricopharyngeus muscle
isthicker and bulkier than the thyropharyneal component of inferior
constrictor. The pressuregenerated by the constriction of
cricopharyngeus muscle is sufficient to cause prolapse of
mucosallining through this potentially weak area.Posterior pharyngeal
diverticula is commonly seen in this area. Among the various types
of posterior pharyngeal diverticula, the posterior pulsion diverticulum
(Zenker's diverticulm) is morecommonly encountered.Diagram
showing Killian's dehiscence

Management of juvenile angiofibroma:

Depends mainly on the extent of the lesion. Surgery is the preferred
modality of treatment for all stages of the mass up to stage IVa
while radiotherapy is used for stage IVb.
Mainly three lines of treatment are available:1. Surgery
2. Irradiation
3. Hormonal (purely supportive in nature)
Surgery: Complete excision of an extensive JNA mass is a
desirable goal but is a surgical challenge because of the limited
field of work, inadequate visualisation and profuse bleeding during
surgery.Besides the deformity, scars and adhesions as a result of

prior surgery adds to this problem.Currently several approaches are

available to access the neoplasm.
They are:I Tumor removal - via naturalis:This approach is
preferred for very small tumors confined to nasopharynx. The
tumor can be removed by subperiosteal dissection after soft palate
retraction. Access is limited in this approach
.II Transpalatal approach:Wilson in 1951 described this approach.
This approach gives exposure to nasopharynx as well as extensions
into the sphenoid sinus and choana. It gives no visible scar and post
op healing is good.This approach is useful in dealing with masses
in the nasopharynx with minimal extension into the choana and
sphenoid sinus.
Procedure: Patient is put in tonsillectomy position. A forward
curved incision is made just in frontof the junction of hard and soft
palate. Mucoperiosteum is separated either way. Posterior spine
of the hard palate is removed. Incision is extended laterally and
downwards on either side along thepterygomandibular raphe. The
mucosa of the lateral pharyngeal wall is not divided and care
istaken not to damage the greater palatine vessels. A good view of
nasopharynx is achieved in thisprocedure. The mucous membrane
on the side of the growth is incised with a blunt knife. Thuswith
blunt dissection the periosteum is elevated, growth is separated and
finally avulsed in onepiece.
III. Lateral rhinotomy approach: This approach is suited for smaller
growth restricted to the nasalcavity. It is contraindicated for larger
masses and whose extensions and attachements cannot
beascertained
.IV. Trans hyoid approach: This is suitable for tumors localised to
nasopharynx without any extension into the surrounding structures.
The major disadvantage is that it requires a temporary
tracheostomy.
V. Transmandibular approach: (Kermen)
Incision is made vertically infront of the ear and carried down the
neck anterior to thesternomastoid muscle. Dissection is started in
the neck by exposing the carotid bifurcation at whichlevel the
external carotid artery is ligated. Lower pole of parotid is dissected
free. The insertions of masseter muscle is severed from the

mandible. Lateral aspect of the mandible is exposed by elevation of

the periosteum. Transection of mandible is done with a giglisaw at
a point 1 cm belowthe notch formed by coronoid and condyloid
processes. Separation of mandible exposes the tubemuscular wall
of nasopharynx which is incised longitudinally on its lateral wall so
that its lumen isentered. Tumor is exposed and dissected out.
VI. Sublabial midfacial degloving approach (Conley 1979): It is a
bilateral extended trans nasalmaxillary approach. There is no
visible scarring, adequate exposure of nasal complex,
nasopharynxand middle third of the face is obtained. Sublabial
incision is performed from one maxillary tuberosity to the other.
Intercartilagenous incisions are given to separate soft tissue of the
nose fromthe upper lateral cartilages. Incisions along the pyriform
aperture connects the circumferentialseptal vestibular incisions to
the sublabial incision. This allows total mid facial degloving up to
theroof of the nose and infra orbital foramen. The complication of
this procedure is vestibular stenosis.
VII. Transzygomatic approach (Sami & Girgis 1965): This
approach is useful for removal of tumor involving the temporal and
infra temporal regions.Combined approaches
:Depending on the size and extent of the mass a combination of
various approaches can be attemptedto extripate the mass in toto
.I. Transpalatal sublabial approach (Saldana 1965): This approach
is useful for tumors extendinginto pterygoid and infratemproal
fossa. A sublabial incision 'S' shaped is made extending to
themaxillay tuberosity. After elevation of mucoperiosteal flap, the
greater palatine neurovascular pedicle is preserved. The surgeon's
index finger is inserted into the pterygopalatine fossa and
bluntdissection is used to free the tumor from its lateral
attachement. The mass can be deliverd via thenasopharynx
.II. Combined transpalatal and lateral rhinotomy approach: This
approach is indicated for larger mass, recurrent JNA, and when
attachement and extensions of the tumor are not
predetermined.This approach gives excellent exposure and so the
chances of recurrence are minimal.
III. Triple approach of Hiranandani (1968): In this approach
transpalatal and lateral rhinotomy arecombined along with caldwel

luc. Complete exposure of pterygopalatine fossa is possible

byremoval of posterior wall of the maxillary antrum, after opening
the antrum through caldwel lucincision. Chances of recurrence are
minimised. Ligation of internal maxillary artery is done toreduce
the bleeding.
Radiotherapy:Radiotherapy can produce some amount of tumor
regression by radiation vasculitis and occlusion of vessels by
perivascular fibrosis. Radiotherapy should be reserved for selected
patients such as thosewith inoperable intracranial extensions and
recurrent tumors.
Disadvantages of radiotherapy:a. If the child is exposed to large
doses i.e. above 5000-6000 rads, there may be damage to
eyes,spinal cord and brain
.b. Small doses are ineffective in reducing the blood supply or the
size of the mass
.c. Radiotherapy may cause fibrosis and adhesions of surrounding
tissue. Later surgery upon thesepatients becomes difficult
.d. Sarcomatous changes can occur in the mass as a result of
irradiation.
Adjunctive treatment
:Hormonal therapy: Since JNA has been postulated as an endocrine
tumor testosterone receptor blocking drugs / estrogens have been tried
to reduce the mass. These hormones cause disaggreableside effects
such as increased breast size. Hormones could even act as
carcinogens.
Embolisation: Was first attempted by Robertson in 1972. This was no
tphonation meant to be therapeutic measure. After embolisation
bleeding is minimised during surgery. It is ideally carriedout a few
days before surgery. Hence it is a valuable preliminary to surgery. The
feeding vessels tothe tumor is identified. It is then deliberatly
occluded by means of materials injected through aselectively placed
catheter.Materials used:Autologous substances like fat, blood clot, or
chopped muscle fragments.Artifical materials: Gelfoam, Oxidised
cellulose, Tantalum powder, glass beads, polyvinyl
alcoholetc.Embolisation should always be preceded by angiography.
Subtraction films may be helpful in areascontaining complex bony
structures.Immediate complications of embolisation are pain,

embolisation of normal vessels,hypersensitivity. Delayed

complications include fever, pain and infections.
Cryosurgery and Lasers can also be used during surgery to minimise
bleeding.
1. Two important indications for total laryngectomy
:a. Malignant tumors of larynx with cartilage invasion
b. Malignant tumors involving larynx which has not responded
to irradiation
2. Four intra temporal complications of CSOM:
a. Facial nerve paralysis
b. Labyrinthitis
c. Lateral sinus thrombophlebitisd.
Petrositis
2. Epistaxis digitorum:Epistaxis digitorum is nasal bleed caused
by aggressive nose picking. This condition is common in
children. Bleeding usually begins from the little's area where
extensive anastomosis between thebranches of internal and
external carotid systems take place. This condition can be
managed bypinching the nose for about a minute.4.
3. Four important causes of referred otalgia:phonation
a. Tonsillitis
b. Temporomandibular joint disorders
c. Post tonsillectomy
d. Dental pain
5. Fistula sign:Fistula sign is the presence of giddiness and
nystagmus when the tragus is pressed and released alternatingly
or during siegalization of the ear. This sign is seen in conditions
which involve erosion of the bony labyrinth especially the
lateral semicircular canal
.6. Tonsillolith:Tonsillolith is a rare dystrophic calcification
occuring in the tonsil as a result of chronicinflammation. Most
commonly tonsilloliths are intratonsillar and are asymptomatic.
They have been identified incidentally. Commonly patients with
tonsillolith complain of foul breath and throat pain. Throat pain
is usually very intense during acts of swallowing. Also known as
tonsilconcretions or tonsillar stones.

7. Functional aphonia:This condition is due to under adduction

or non adduction of vocal volds while attempt is beingmade to
speak. The voice in these patients are rather weak. This
condition is seen in patients whoare depressed / under emotional
stress, shock etc.
8. :This is staphylococcal infection involving the hair follicles
of the vestibule of the nasal cavity. Thevestibule of the nasal
cavity is lined by skin bearing hair follicles. Furuncles involving
nose shouldbe aggressively treated with antibiotics. It should not
be squeezed because infecting organisms can traverse the facial
veins to reach the cavernous sinus causing cavernous sinus
thrombosis. These facial veins are devoid of valves hence the
risk of retrograde infection is more.
9. Two important clinical features in fungal sinusitis:Clinical
features of fungal sinusitis:HeadacheNasal block
9. Two common sites of CSF leak in nose:Cribriform plate
Roof of frontal sinus
11. Bleeding polypus septum:This is angioma involving nasal
septum. This is common in the antero inferior portion of the
nasalseptum. Nose picking in these patients can lead to troublesome
epistaxis.
12. Functions of nose:Conditioning of the inspired air Olfaction
13. Laryngeal papillomatous:This is caused by infections with
human papilloma virus. It is of two varieties. Adult and paediatric
types. Adult papillomas are solitary while papillomas involving the
children are oftenmultiple. This commonly occurs at the junction
where the transition between squamous epitheliumand columnar
epithelium occurs. These patients present with voice disturbances and
breathing difficulties
.14. Phonation:Phonation takes place at the level of larynx due to
vibration of vocal folds which occur due to air flowing from the lungs
through them. There are two theories currently accepted to explain the
process of phonation: Myoelastic theory and aerodynamic theory
.15. Aphthous ulcer:These are painful ulcers involving the mucosa of
the oral cavity. Aphthous ulcers are classifiedaccording to the
diameter of the lesion.Minor ulcersMajor ulcersHerpetiform

lesionsThese ulcers are commonly caused by herpetic infections of

the oral cavitphonationy mucosa.It is also common in individuals who
are excessively stressed.Trauma to the oral mucosa can also cause this
type of ulceration.
Discuss the etiopathology of malignant tumors of maxilla.
Add a note on itsinvestigations and surgical management
Causes of malignant tumors of maxilla include
:a. Exposure to hard wood dust (African Mahogany)
Adenocarcinomab.
Soft wood dust Squamous cell carcinomac.
Nickel refining (chromium workers) Cause squamous cell
carcinomad.
Leather and textile workerse.
Exposure to Isopropyl alcohol & volatile hydrocarbons
f. Snuff
e. Human papilloma virus exposure
About a quarter of malignant lesions of nose and paranasal
sinuses originate from the maxillary antrum.Commonest
malignant lesion involving the maxillary sinus is squamous cell
carcinoma. Other possible malignant lesions include: Basal cell
carcinoma,esthesioneuroblastoma, plasmocytoma,
lymphoreticular tumors, malignant tumors involving minor
salivary glands, adenocarcinoma, undifferentiated
carcinomas,sarcomas, inverted papilloma turning malignant and
malignant neurogenic tumors.
Harrison classified malignant tumors of the maxillary sinus into
four stages. This staging process facilitated assessment of
prognosis and deciding the optimal treatment modality.
T1- Tumor limited to antral mucosa without evidence of bone
erosion
T2- Tumor inside the antrum with evidence of bone erosion. The
facial skin, orbit,ethmoids and pterygopalatine fossa are not
involved
.T3- Involvement of orbit, ethmoids, facial skin
T4- Tumor extension to nasopharynx, sphenoid sinus, cribriform
plate or pterygopalatine fossa

Recent classification of maxillary antral malignancy is TNM

classification.
T- indicates primary tumor
N- Nodal status
M- distant metastasis
T1 Tumor limited to antral mucosa with no evidence of bone
destruction
T2 Tumor with evidence of bone destruction. In this stage the
posterior wall of maxilla is spared. There may also be extension
through the hard palate and middle meatus
T3 In this stage tumor involves the posterior wall of maxilla,
subcutaneous tissues,skin over the cheek and orbital floor
T4 Tumor involving the orbit / cribriform plate / Skull base /
Nasopharynx / Sphenoidsinus / Frontal sinus
N Nodal status
N1 Metastasis in a single ipsilateral lymph node measuring 3
cms or less in its greatest dimension
N2 Metastasis in a single ipsilateral node measuring 3cms 6
cms in its greatestdimension / multiple ipsilateral nodes not
exceeding 6cms in their greatest dimension /bilateral or
contralateral nodes not exceeding 6cms in their greatest
dimension
.Substages of N2:
N2a Single ipsilateral node which is more than 3 cms but less
than 6 cms in itsgreatest dimension
N2b Metastasis to multiple ipsilateral nodes which measure
more than 3 cms butless than 6 cms in their greatest dimension
N2c Metastasis to bilateral / contralateral nodes with none of
them measuring morethan 6 cms in their largest dimension
N3 Metastasis to regional nodes measuring more than 6 cms in
their greatestdimension
Tumor spread: Antral tumors spread in to:
1.Nasal cavity
2.Ethmoid
3.Orbit via the infra orbital fissure
4.Soft tissues over the cheek by eroding the anterior wall
5.Palate / alveolar ridge by dental foramina

6.Buccal sulcus
7.Infratemporal fossa by erosion of posterior wall of antrum
Management:Of malignant tumors of maxillary antrum is
dependent on tissue diagnosis and extent of the lesion. Tissue
biopsy is a must. All these patients should under go tissue
biopsy procedures like endoscopic antrostomy / caldwell luc
surgery to obtain tissue sample for histopathological diagnosis.
Role of imaging: Imaging plays a vital role in the assessment of
anatomical site of the lesion,extensions if any can also be clearly
seen. CT scanning and MRI scanning performed before surgery
assists in staging of the disease and in planning the optimal
surgical treatment modality.CT scans are highly accurate in
identifying bony erosion / remodelling. Bony remodelling is
commonly seen in malignant tumors involving salivary glands,
large cell lymphoma and melanoma. It is also very accurate in
accessing orbital involvement as it shows clear delineation of
the lamina papyracea. It is more accurate than MRI scanning in
identifying orbital invasion / invasion of anterior skull base.
MRI scans are pretty useful in the study of perineural invasion
of tumors like adenocystic carcinoma
.Surgical management:The following are the various surgical
modalities:1.Total maxillectomy
2.Medial maxillectomy
3.Lateral rhinotomy (limited malignancies)
4.Anterior craniofacial resection
5.Anterior midfacial degloving
Irradiation:Patients with stage I antral malignancies can be
subjected to full curative dose of radiotherapy. Pre operative /
post operative radiation can be followed according to the
prevailing portocol of the institution.
Sandwich therapy:In this type of therapy these patients receive
half the dose of curative radiotherapy and surgery is performed
after 6 weeks. Six weeks following surgery these patients
receive the remaining half of the curative dose of radiotherapy.
The advantage of this treatment modality is the tumor gets down
staged following radiotherapy making the process of surgery
that much easier. Post operative radiotherapy helps in the

completion of treatment. Nodal metastasis if any (occult) will be

sterilized by post op irradiation in these patients.
. Nasal polyp: Polyp is a Latin word meaning polypous (many
footed).
Definition:Polyp is defined as simple oedematous hypertrophied
mucosa of the nasal cavity. It can be unilateral / bilateral. Causes
of nasal polyp:1. Infections
2. Allergy
3. Polyp due to mucovisidosis
Classification:Nasal polyp can be classified as
:1. Simple polyp. Ethmoidal polypi. Antrochoanal polyp
2. Fungal polyp
3. Malignant polyp

Differences between antrochoanal polyp and ethmoidal polypi

Age
causes
numbers
site

Ethmoidal polypi
adults
Allergy
mutiple
Arises from
ethmoidal labyrinth
Seen easily on
anterior rhinoscopy
Mostly bilateral

Antrochoanal polyp
Children and
adolescents
Infection
solitary
Seen commonly in
post nasal exam
Usually unilateral

Recurrence is
common

Recurrence is
uncommon
Polypectomy Caldwel
luc surgery in
recurrent cases

Nasal polyp is a surgical condition. All these polypi should be

removed from the nasalcavity. It is usually performed under
direct vision using a nasal endoscope. After removal these
patients should be ideally placed under topical steroids. Steroids
not only helps in reducing the inflammation but also shrinks the
polypoidal mucosa. The polypoidal material removed during the
surgical procedure should be sent for biopsy

being the next common site of involvement. Anteriorly situated

congenital cholesteatomas areknown to affect the eustachean tube
function causing conductive deafness due to middle ear effusion,
where as posterior congenital cholesteatoma is known to cause
conductive deafness due toimpairment of ossicular chain
mobility.Staging of congenital cholesteatoma:Staging as suggested by
Derlacki and Clemis: They were the first to stage congenital
cholesteatoma.They classified congenital cholesteatoma into
1. Petrous pyramid cholesteatoma
2. Cholesteatoma involving the mastoid cavity
3. Cholesteatoma involving the middle ear cavity
.Potsic suggested the following staging mechanism:
Stage I : Single quadrant involvement with no ossicular / mastoid
involvement.
Stage II : Multiple quadrant involvement with no ossicular / mastoid
involvementStage
III : Ossicular involvement without mastoid involvementStage
IV : Mastoid extension
Nelson's staging:
Type I : Involvement of mesotympanum without involvement of incus
/ stapes

Type II : Involvement of mesotympanum / attic along with erosion of

ossicles without extensioninto the mastoid cavity
Type III : Involvement of mesotympanum with mastoid
extensionStaging this disease will help in deciding the modality of
treatment and in predicting the long term prognosis.
Acquired Cholesteatoma: can be divided into two types,
primary acquired and secondary acquiredcholesteatomas.
Primay acquired cholesteatoma: In this condition there is no history of
pre-existing or previous episodes of otitis media or perforation.
Lesions just arise from the attic region of the middle ear.
Secondary acquired cholesteatoma: always follows active middle ear
infection which manages to destroy the ear drum along with the
annulus. This type of destruction is common in acute necrotising otitis
media following exanthematous fevers like measles etc.
Theories to explain pathogenesis of cholesteatoma:Various theories
have been postulated to explain the pathogenesis of cholesteatoma.
They are:
1. Cawthrone theory: This theory suggested by cawthrone in 1963
suggested that cholesteatoma always originated from congential
embryonic cell rests present in various areas of the temporal bone
.2. Theory of immigration: This theory was suggested by Tumarkin.
He was of the view that cholesteatoma was derived by immigration of
squamous epithelium from the deep portion of the external auditory
canal into the middle ear cleft through a marginal perforation or a
total perforationof the ear drum as seen in acute necrotising otitis
media
.3. Theory of invagination: This theory was suggested by Toss. He
theorised that persistent negative pressure in the attic region causes
invagination of pars flaccida causing a retraction pocket. This
retraction pocket becomes later filled with desquamted epithelial
debris which forms a nidus for the infection to occur later. Common
organisms known to infect this keratin debris are Psuedomonas,
E.coli, B. Proteus etc.
Toss also classified attic retraction pockets into 4 grades:1.
Grade I: The retracted pars flaccida is not in contact with the neck of
the malleus.

2. Grade II: The retracted pars flaccida is in contact with the neck of
the malleus to such an extentthat it seems to clothe the neck of the
malleus.
3. Grade III: Here in addition to the retracted pars flaccida being in
contact with the neck of the malleus there is also a limited erosion of
the outer attic wall or scutum
.4. Grade IV: In this grade in addition to all the above said changes
there is severe erosion of the outer attic wall or scutum.
4. Metaplastic theory: This theory was first suggested by Wendt in
1873. He took into considerationthe histological changes seen in
various portions of the middle ear cavity. The attic area of the
middle ear cavity is lined by pavement type of epithelium. This
epithelium undergoes metaplastic changes in response to
subclinical infection. This metaplastic mucosa is squamous in
nature thereby forming a nidus for cholesteatoma formation in
the attic region.Of all the above mentioned theories, the theory
of invagination appears to be the most plausible one currently
explaining the various pathologic features of cholesteatoma.
Clinical features of acquired cholesteatoma:Ear discharge: is
scanty and foul smelling. Infact the odur is best described as
musty in nature. This is due to the presence of saprophytic
infection and osteitis.Hearing loss: is commonly conductive in
nature. Some patients may even surprisingly have a normal
hearing despite the presence of a huge cholesteatoma. This
normal hearing could be attributed to the bridging effects of
cholesteatomatous mass.Sensorineural hearing loss if present
could be attributed to the absorption of toxins through the round
window membrane, or may be due to use of ototoxic antibiotics
topically on a long termbasis.
Ear ache: if present could be attributed to the presence of co
existing otitis externa, or presence of extradural abscess.Tinnitus
if present may indicate imminent sensorineural hearing
loss.Vertigo may be present if there is erosion of lateral
semicircular canal by the cholesteatomatous matrix. Fistula test
if performed is positive in these patient.
Fistula test: This test is positive if there is a third window is
present in the laryrinth due to the erosion of the labyrinthine

bone. This commonly occurs in the lateral semicircular canal

area. Thistest is performed using a snugly fitting siegles
pneumatic speculum and slowly applying pressure by
compressing the pneumatic bulb. If labyrinthine fistula is
present the patient will feel giddy and will have nystagmus.
Facial palsy may indicate erosion of facial nerve canal with
involvement of facial nerve.
On examiantion:There is destruction of the outer attic wall, with
presence of attic perforation. Cholesteatomatous flakes may be
seen through the perforation like cotton wool.There is associated
sagging of the posterior superior meatal wall.
Hearing tests indicate conductive deafness commonly if
labyrinth is uninvolved. It may turn out to be sensorineural
hearing loss if there is associated erosion of the labyrinth.X ray
mastoids may show slcerosis with presence of cavity.
Management:Since this is a surgical problem modified radical
mastoidectomy is advocated in almost all of thesepatients.The
aims of the surgical procedure is as follows:
1. To exteriorise the disease
2. To create adequate ventilation to the middle ear cavity
3. To create a permanent skin lined cavity exposed to the
exterior.
Meningitis is one of the important intracranial complications of acute
frontal sinusitis. Signs and symptoms of meningitis include:
1. High fever
2. Photophobia
3. Neck pain
4. Neck stiffness
5. Severe headache
6. Altered mental status
Osteomyelitis is one of the complications of acute frontal sinusitis.
This is caused by direct extension of infection or by thrombophlebitis
involving the diploic veins. In patients with osteomyelitis of anterior
table of frontal bone may lead to formation of subperiosteal abscess
whichpresent as swelling over the forehead. This is also known as the
Potts puffy tumor.

Cavernous sinus thrombosis is a complication of acute frontal

sinusitis. Thrombophlebitis involvesthe diploic veins which are
valveless. The infection spreads to cavernous sinus causing
thrombophlebitis. Patients with cavernous sinus thrombosis present
with ophthalmoplegia, proptosis, visual loss, trigeminal nerve
deficits. Surgery is indicated in recalcitrant cases.
It includes frontal sinus trephening and endoscopic decompression.A
Agger nasi cellI Type I frontal cell (a single air cell above agger
nasi)
II Type II frontal cell (a series of air cells above agger nasi but
below the orbital roof)
III Type III frontal cell (this cell extends into the frontal sinus but is
contiguous with agger nasicell)
IV Type IV frontal cell lies completely within the frontal sinus
Diagnosis:Acute frontal sinusitis is a clinical diagnosis depending on
the duration of symptoms, i.e. lasting for less than 4 weeks.
CT scans may show false positive results. Major diagnostic criteria
include: Pain / tenderness over frontal sinus (tenderness can be
elicited by applying pressure in the floor of the frontal sinus.Head
ache showing classic periodicity (More during early morning hours
and gets better as the dayprogresses). This is due to the gravitational
effects of frontal sinus drainage.Nasal obstruction Purulent
rhinorrhoea Fever Hyposmia / anosmia
Unless complications are suspected imaging is not a must in the
diagnosis of acute frontal sinusitis.
Microbiology: Organisms causing acute infections of frontal sinus
include S. Pneumoniae, H.Influenza, and Moraxella Catarrhalis.
Aims of treatment: To control infections using antibiotics
To reduce oedema and remove obstruction to sinus ostium facilitating
drainage
Medical treatment will suffice. Surgery is not needed. Antibiotics
chosen should be able to manage the infecting spectrum of
organism. Complications of acute frontal sinusitis: Should be
suspected in patients with: Protracted symptoms with increasing
severityPeriorbital oedema due to preseptal cellulitisPainful and
restricted eye movements (orbital cellulitis) Neurological signs and
symptoms indicate intracranial complications Meningitis is one of the

important intracranial complications of acute frontal sinusitis. Signs

andsymptoms of meningitis include: High fever Photophobia Neck
pain.Neck stiffnessSevere headache Altered mental status
Write briefly on:
a. Malignant otitis externa:Definition: Malignant otitis externa is a
inflammatory disorder involving the external auditorycanal caused by
pseudomonas organism. Majority of these patients are elderly
diabetics. Thiscondition is termed as malignant otitis externa bec
ause of its propensity to cause complications.Hence the term
malignant must not be construed in a histological sense.History:1838
- Toulmousch reported the first case of otitis externa1959 - Meltzer
reported a case of pseudomonas osteomyelitis of temporal bone1968 Chandler discussed the various clinical features and described it as a
distinct clinical entityThe effectiveness of present day antibiotics in
the management of this condition should provoke thephysicians to
abandon the term malignant while describing this
condition.Epidemiology:The typical patient with malignant otitis
externa is an elderly diabetic, with males outnumberingfemales by
twice the number. This could be due to the possibility of males being
more prone tosecrete wax which are more acidic in nature. Malignant
otitis externa is very rare in children; if present it will be associated
with malnutrition or HIV infection.Pathophysiology
Malignant otitis externa is known to affect the external auditory canal
and temporal bone. The causative organism being pseudomonas
aeruginosa. These patients are invariably elderly diabetics.This
disorder usually begins as otitis externa and progresses to involve the
temporal bone. Spreadof this disease occurs through the fissures of
Santorini and osteo cartilagenous junction. Thisdisorder could be
caused by a combination of poor immune response and peculiar
characteristics of the offending microbe.Immunity is reduced in
patients with :1. Diabetes mellitus2. Blood cancer 3. HIV infections4.
Patients on anticancer drugsIt should also be remembered that
diabetic patients have impaired phagocytosis, poor
leukocyticresponse, and impaired intracellular digestion of bacteria.
Diabetic patients secrete wax which hasless lysozyme content than
normal thereby reducing the effectiveness of wax as an
antimicrobialagent.Pseudomonas aeruginosa is a gram negative

aerobe with polar flagella. It is found on the skin. Itinvariably

behaves like an opportunistic pathogen. The pathogenicity of this
organism is due toability to secrete exotoxin and various enzymes like
lecithinase, lipase, esterase, protease etc. Sincethis organism is
clothed by a mucoid layer it is resistant to digestion by
macrophages.Clinical features:The patient gives history of trivial
trauma to the ear often by ear buds, followed by pain andswelling
involving the external auditory canal. Pain is often the common
initial presentation. It isoften severe, throbbing and worse during
nights. It needs increasing doses of analgesics. Onexamination
granulation tissue may be seen occupying the external canal. It often
begins at the bonycartilaginous junction of the external canal.
Discharge emanating from the external canal is scantyand foul
smelling in nature. When the discharge is foul smelling it indicates
the onset of osteomyelitis. Ironically the patient does not have fever
or other constitutional symptoms.Otoscopy: Reveals granulation
tissue at the bony cartilaginous junction. The ear drum is
usuallynormal. The external auditory canal skin is soggy and
edematous.Cranial nerve palsies are common when the disease affects
the skull base. The facial nerve is themost common nerve affected.
As the disease progresses the lower three cranial nerves are
affectedclose to the jugular foramen.Intracranial complications like
meningitis and brain abscess are also known to occur.Spread of
infection:1. Inferiorly through the stylomastoid foramen to involve the
facial nerve.2. Anteriorly to the parotid3. Posteriorly to the mastoid
and sigmoid sinus4. Superiorly to the meninges and brain5. Medially
to the sphenoid6. Spread through vascular channels are also
commonRole of imaging:
* Conventional radiology is of no use.** CT scan is useful in
assessing bone destruction.** MRI is useful in assessing soft tissue
involvement.
** Radionucleotide scans with Technetium 99 helps in assessing bone
involvementImaging algorithm in these patients are:1. TC99 scan to
seek evidence of bone involvement2. If this is positive CT scan and
MRI scan is a must to rule out bone and soft tissue involvement3.

Serial Ga 67 scans to assess the efficacy of treatment

modality.Levenson's criteria for diagnosis of malignant otitis externa:
* Refractory otitis externa** Severe nocturnal otalgia** Purulent
otorrhoea** Granulation tissue in the external canal** Growth of
Pseudomonas aeruginosa from external canal** Presence of diabetes
and and other immunocompromised state
Treatment:
Extensive surgical procedures have failed miserably to cure this
condition. The role of surgery isconfined to only exclusion of
malignancy by biopsy. Wound debridement is a possibility
inadvanced cases.Medical management:Carbenicillin, Pipercillin,
Ticarcillin can be used. Third and forth generation cephalosporins
can beused.Ciprofloxacillin in doses of 1.5 g - 2.5 g /day in divided
doses can be administered for a period of 2weeks.Gentamycin can
also be administered parenterally in doses of 80 mg iv two times a day
in adults.
. Cerumen:This is also known as ear wax. This is a yellowish waxy
substance secreted in the external auditorycanal of humans. It
protects the skin lining of the external auditory canal from excessive
moisture.It also protects the external canal from bacteria, fungi and
insects.Humans are known to secrete two types of cerumen:1. Soft
and moist2. Firm and dryPersons secreting soft and moist type of ear
wax have no problem due to its accumulation. It caneasily be
extruded by the normal cleansing mechanism of the external auditory
canal. Thisdifference in wax secretion has been traced to alterations in
C11 gene. Persons secreting frim anddry wax are more prone for
impaction of cerumen. Impaction of cerumen causes
conductivehearing loss.Cerumen is usually produced in the outer third
of the cartilagenous portion of the external auditorycanal. It is
composed of:1. Viscous secretions from sebaceous glands2. Less
viscous secretions from modified apocrine sweat glands3. Shed layers
of skinCerumen has been found to have bacterostatic effect.
Excessive occlusion of the external canal dueto accumulation of
cerumen and desquamated epithelial cells associated with migration
defect of the lining epithelium can cause keratosis obturans. This is a
painful condition which needs to betreated by removing the mass

under anesthesia.Removal of cerumen can be performed using

probes / curettes if the consistency is soft. If cerumenis excessively
soft then cotton buds can be used for removal.Firm cerumen should
be lubricated by using ceruminolytics / liquid paraffin to soften it up
beforeattempted removal.Aural syringing is one of the painless way
of removing accumulated cerumen
Septoplasty:
Septoplasty: is defined as a conservative surgical procedure designed
to correct anterior septaldeviations. (i.e. Deviations anterior to the
Cottle's line.Septoplasty is performed in deviations anterior to this
line.
Procedure: This involves 6 phases:
1. Gaining access to the septum
2. Correction of the pathology
3. Removal of the pathology
4. Shaping removed cartilage and bone
5. Reconstruction of septum
6. Stabilizing the septumIncision:
Freer's Hemitransfixation incision is used to gain access to the nasal
septum. This incisionis sited 2 mm posterior to the caudal edge of
cartilagenous septum.Anterior tunnel is created between the cartilage
and the perichondrium. This anterior tunnel iscreated on both sides.
Sometimes to gain adequate exposure to nasal septum, inferior
tunnels needto be created.In making the inferior tunnels, there is a
posterior and anterior approach. The posterior approach isalso known
as the maxilla - premaxilla approach.

Figure showing the various tunnels which are created during septal
surgery Correction of septal pathology: If the deviation of the septum
is caused by excessive tension to the septal cartilage, it can be
corrected by removing an inferior cartilagenous strip. Dislocations
due tofractures can be corrected intraseptally by mobilizing or
resection of parts of nasal septum.Removal of septal pathology:
Severe deformities involving the nasal septum may rarely require
complete removal of septal cartilage. The resected area is
reconstructed using the cartilaginous elements removed from the
septum.Indications for resection include duplications, spines, crests
and convexities present in the septum.All the cartilagenous material
removed should be saved for reconstruction. The parts of nasalseptum
that are straight are preserved to support the dorsum, tip and
columella of the nose.Reshaping cartilage and bone: Reshaping of
nasal septal cartilage should be done with as littletrauma as possible,
with maximum preservation of straight portions of nasal septum.

Cartilage doesnot heal. Fractures and defects of the septal cartilage

will be filled with connective tissue.Retraction of connective tissue
can alter a good surgical result during the course of healing
process.The dynamics of healing process of septal cartilage should be
clearly understood before embarkingon this step.Reconstruction of
nasal septum: The patients septal cartilage is the most ideal one for
nasal septalreconstruction. Other materials like ear cartilage or rib
cartilage should be used only as a secondchoice. Use of septal
cartilages from tissue bank can be avoided if possible due to the risk
of infections. A strong strip of cartilage under the cartilagenous
dorsum of the nose should prevent theformation of saddle nose. Tip
projection is preserved by placing a strip of cartilage in the caudalpart
of nasal septum. This step will also prevent columella retraction in
these patients. Small bits of cartilage pieces can be used to fill up a
defect in the cartilagenous septum to prevent retraction of nasal soft
tissues due to scar formation.Stabilizing the septum after surgery:
This can be achieved by judicious use of splints, sutures andby
packing the nasal cavity with roller gauze. This not only helps to
stabilize the septum, but alsoDrtbalu's otolaryngology online

keeps the mucoperichondrium in contact withe the nasal septum. This

is important for the viabilityof nasal septum
Diagram showing evolution of brain abscess
Stages of formation of brain abscess:
Stage of cerebral oedema: This is infact the first stage of brain abscess
formation. It starts with anarea of cerebral oedema and encephalitis.
This oedema increases in size with spreading encephalitis.Walling off
of infection by formation of capsule: Brain attempts to wall off the

infected area withthe formation of fibrous capsule. This formation of

fibrous tissue is dependent on microglial and blood vessel
mesodermal response to the inflammatory process. This stage is
highly variable.Normally it takes 2 to 3 weeks for this process to be
completed.Liquefaction necrosis: Infected brain within the capsule
undergoes liquefactive necrosis witheventual formation of pus.
Accumulation of pus cause enlargement of the abscess.Stage of
rupture: Enlargement of the abscess eventually leads to rupture of the
capsule containingthe abscess and this material finds its way into the
cerebrospinal fluid as shown in the abovediagram.

Cerebellar abscess which occupy the posterior fossa cause raised intra
cranial tension earlier thanthose above the tentorium. This rapidly
raising intra cranial pressure cause coning or impaction of the

flocculus or brain stem into the foramen magnum. Coning produces

impending death. If thewalling off process (development of capsule)
is slow, softening of brain around the developingabscess may allow
spread of infection into relatively avascular white matter, leading to
theformation of seconday abscesses separate from the original or
connected to the original by acommon stalk. This is how multilocular
abscesses are formed. Eventually the abscess may ruptureinto the
ventricular system or subarachnoid space, causing meningitis and
death.The mortality rate of brain abscess is around 40%, early
diagnosis after the advent of CT scan hasimproved the prognosis of
this disease considerably..The bacteriological flora is usually a
mixture of aerobes and obligate anaerobes. Anaerobicstreptococci are
the commonest organisms involved. Pyogenic staphylococci is
common inchildren. Gram negative organims like proteus, E coli and
Pseudomonas have also been isolated.Clinical features:The earliest
stage where the brain tissue is invaded (stage of encephalitis) is
marked by the presenceof headache, fever, malaise and vomiting.
Drowsiness eventually follow. These early features maybe masked by
the complications such as meningitis or lateral sinus thrombosis. If
this stageprogresses rapidly to generalised encephalitis before it could
be contained by the formation of thecapsule, drowsiness may progress
to stupor and coma followed by death.. Usually the period of local
encephalitis is followed by a latent period during which the pus
becomes contained within thedeveloping fibrous capsule. During this
latent phase the patient may be asymptomatic.During the next state
(stage of expansion) the enlarging abscess first cause clinical features
due tothe alteration of CSF dynamics, and site specific features may
also be seen due to focal neurologicalimpairement. The pulse rate
slows with rising intracranial pressure, the temperature may fall
tosubnormal levels. Drowsiness may alternate with periods of
irritability. Papilloedema is also founddue to elevated CSF
pressure.Clinical features also vary according to the site of
involvement. Hence the differences that are seenbetween the cerebral
and cerebellar abscess.Cerebral (Temporo sphenoidal abscess):A
cerebral abscess in the dominant hemisphere often cause nominal
aphasia, where in the patienthas difficulty in naming the objects
which are in day to day use. He clearly knows the function of these

objects. Visual field defects arise from the involvement of optic

radiations. Commonly there isquadrantic homonymous hemianopia,
affecting the upper part of the temporal visual fields, morerarely it
may also involve the lower quadrants. The visual field loss are on the
side opposite to thatof the lesion. This can be assessed by
confrontation method. Upward development affects facialmovements
on the opposite side, and then progressively paralysis of the upper and
lower limbs. If the expansion occur in inward direction then paralysis
first affects the leg, then arm and finally theface.Cerebellar
abscess:The focal features associated with cerebellar abscess is
weakness and muscle incoordination on thesame side of the lesion.
Ataxia causes the patient to fall towards the side of the lesion. Patient
mayalso manifest intention tremors which may become manifest by
the finger nose test. This test isDrtbalu's otolaryngology online
performed by asking the patient to touch the tip of the nose with the
index finger first with the eyesopen and then with the eyes closed.
The patient may often overshoot the mark when attempted withthe
eyes closed in case of cerebellar abscess. The patient may also have
spontaneous nystagmus.Dysdiadokinesis is also positive in these
patients.Investigations:CT scan and MRI scans are the present modes
of investigation. Scan is ideally performed usingcontrast media. These
scans not only reveal the position and size of the abscess, the presence
of localised encephalitis can be distinguished from that of an
encapsulated abscess. Associatedconditions such as subdural abscess,
and lateral sinus thrombosis can also be seen.Management:Surgical
drainage of the abscess, followed by mastoidectomy to clear the ear
disorder
Enumerate the causes of conductive hearing loss with intacttympanic
membrane. Discuss the clinical features andmanagement of otitis
media with effusion in a 4 year old child.(15
marks)Introduction:Conductive deafness is defined as deafness
caused due to defectsinvolving the conducting mechanism of the ear.
The componentsof conducting mechanism include:External ear
Pinna, external auditory canal, ear drumMiddle ear Medial wall of
ear drum, the three ossicles, air in themiddle ear cavity.Any
derangement in the above mentioned components responsiblefor the

conduction of sound could cause conductive deafness.Causes of

conductive hearing loss in a patient with intact ear drum:External ear
causes:Impacted cerumen. Impacted cerumen can cause
conductivehearing loss to the extent of 30%. The hearing loss is more
if thecerumen is closely adherent to the ear drum thereby preventing
itseffective vibration in response to sou
Osteomas involving bony portion of external canal. These are benign
lesions involving the bony portion of the external auditorycanal. This
is common in swimmers. Presence of these masses inthe external
canal prevents effective sound transmission to the ear drum.Ear drum
causes:
Tympanosclerosis (extensive) involving the ear drum can cause
ineffecive sound transmission to the middle ear ossicular
chain.Extensive tympanosclerosis can prevent ear drum from
vibrating normally in response to sound
.Middle ear causes:Ossicular chain defects:Fusion of head of the
malleus and incus.Disruption of incusFixation of foot plate of stapes
(otosclerosis)Accumulation of fluid in the middle ear cavity:Secretory
otitis media In this condition middle ear cavity isfilled with fluid.
This causes ineffective sound coupling betweenthe ear drum and the
ossicular chain. This condition is common inchildren and chronic
adenotonsillitis has been implicated as the potential cause for this
condition.Acute otitis media Purulent material gets accumulated in
themiddle ear cavity. These patients have intense ear ache in
additionof conductive deafness.Adhesive otitis media Eustachean
tube dysfunction may cause blockage in the communication between
the middle ear cavity and the nasopharynx. This in turn prevents
normal ventilation of themiddle ear. Absence of regular gas exchange
via the eustacheantube causes vacuum in the middle ear cavity. This
vacuum causesthe ear drum to prolapse into the middle ear cavity. It
may be soretracted that it could be in direct contact with the
promontory. Inthis condition there is ineffective sound coupling
between the ear drum and the ossicular chain
Clinical features and management of otitis media with effution ina 4
year old child:Age of occurrence: OME shows classically a bimodal
distribution.The first peak occurs around 2 years of age, and the

second peak occurs at about 5 years of age. This distribution occurs

roughlyaround the ages when the child goes to preschool and
primaryschool.Clinical features: A high index of suspicion is
necessary toidentify this condition. Every child with upper
respiratoryinfection must be otoscopically examined. These children
have atendency to keep fiddling with the ear using their fingers /
ear buds. This could be the direct result of conductive
deafness.Otoscopic findings: The tympanic membrane may be
bulging, or retracted with a distorted cone of light. The ear drum may
appear yellow, blue or simply clear white. Pneumatic otoscopy will
reveala ear drum which has a restricted mobility.Management:1.
Antibiotics: Amoxycillin is the drug of choice followed
bycephalosporins.2. Nasal decongestants like oxymetazoline /
xylometazoline mayhelp in some cases.3. Topical nasal steroids can
be used in resistant cases.4. Autoinflation of eustachean tube by
performing valsalvamaneuver. Balloon blowing may also
help. Surgical management:1. Adenotonsillectomy2. Myringotomy
and insertion of ventilation tubes This isusually performed in the
anteroinferior quadrant. It should be borne in mind that antero inferior
quadrant is closest to thetympanic end of the eustachean tube.
Insertion of ventilation tubein this area would ensure drainage of
middle ear contents andventilation via the external auditory canal.
Figure showing anterior nasal packingTo manage post nasal bleed a
post nasal pack is a must. Post nasal packing can be done in 2
ways:Post nasal packing (conventional): A gauze roll about the size
of the patient's naso pharynx is used here. Three silk threads must
betied to the gauze roll. One at each end and the other one at
themiddle. The patient should be in a recumbent position.
After anesthetising the nasal cavity with 4% xylocaine the mouth is
heldopen. Two nasal catheters are passed through the nasal cavities
tillthey reach just below the soft palate. These lower ends of
thecatheters are grasped with forceps and pulled out through
themouth. The silk tied to the ends of the gauze is tied to the
nasalcatheters. The post nasal pack is introduced through the mouth
andgradually pushed into the nasopharynx, at the same time the
nasalcatheters on both sides of the nose must be pulled out. When

the pack snugly sits inside the nasopharynx, the two silk threads tiedto
its end would have reached the anaterior nares along with thefree end
of the nasal suction catheter.
Drtbalu's otolaryngology online

Figure showing postnasal pack in situThe two silk threads tied to the
suction catheters are untied. Thecatheters are removed from the nose.
The silk thread is used tosecure the pack in place by tying both the
ends to the columella of the nose. The silk tied to the middle portion
of the gauze pack isdelivered out through the oral cavity and taped to
the angle of thecheek. This middle portion silk will help in removal of
the nasal pack. In addition to the postnasal pack anterior nasal
packing mustalso be done in these patients.Postnasal pack using
baloon catheters: Specially designed balooncatheters are available.
This can be used to perform the post nasal pack. Foleys catheter can
be used to pack the post nasal space.Foley's catheter is introduced
through the nose and slid up to thenasopharynx. The bulb of the
catheter is inflated using air throughthe side portal of the catheter. Air
is used to inflate the bulb because even if the bulb ruptures
accidentally there is absolutelyno danger of aspiration into the lungs.
After the foleys catheter isinflated the free end is knotted and
anchored at the level of theanterior nares.Problems of nasal packing:1.
Epiphora (watering of eyes) occur due to blocking of the nasalend of
the nasolacrimal duct.2. Heaviness /headache due to blocking of the
normal sinusostium.3. Prolonged post nasal pack can cause
eustachean tube block andsecretory otitis media.4. Prolonged nasal
packing can cause secondary sinusitis due to blockage of sinus

ostium. Newer packing materials: Newer packing materials made

of silicone are available. The advantages of these material are thatthey
are not irritating, patient can breath through the nose with the pack on
through the vent provided, these packs can be retainedinside the nasal
cavity for more than 2 weeks. They can beremoved and repositioned
if necessory. The only disadvantage isthat they are expensive.Surgical
management:Endoscopic cauterisation can be tried if the bleeders are
localisedand accessible. If not accessible, ligation of the internal
maxillaryartery can be done through caldwelluc approach.
Spenopalatineartery clipping can be done endoscopically. It is
accessible close tothe posterior end of the middle turbinate. In rare
cases externalcarotid artery ligation at the neck can be resorted to.
Externalcarotid artery is differentiated from the internal carotid in the
neck by the fact that internal carotid artery does not give rise
to branches in the neck, while the external carotid artery does
so.Ethmoidal artery ligation: If epistaxis occur high in the nasalvault,
anterior and posterior ethmoidal arteries may be ligatedusing
ligaclips. These arteries can be accessed using an
externalethmoidectomy incision. The anterior ethmoidal artery is
usuallyfound 22mm from the anterior lacrimal crest. If ligation of
theanterior ethmoidal artery does not stop bleeding then
posterior ethmoidal artery should also be ligated. The posterior
ethmoidalartery can be found 12mm posterior to the anterior
ethmoidalvessel.Epistaxis caused by the presence of tumors both
benign andmalignant calls for definitive treatment of the tumor perse.
Drtbalu's otolaryngology online
3. What are the causes of stridor in children? Discuss the
types, procedure and complications of Tracheostomy. (3 + 2 + 3 + 2
=10 marks)Causes of stridor in children can be classified according to
theanatomy of the lesion:1. Supralaryngeal causes:a. Nose - choanal
atresiaObstruction due to infection / truama / tubes b. Cranio facial
anamolies:These patients have narrowing of oropharynx, nasopharynx
andnasal cavities. The may also additionally manifest
withmacroglossia. The various anamolies associated with
respiratorydifficulties are:Pierre Robin syndromeTreacher collin
syndromeApert's syndromeCruzon's syndromeMobieus syndrome

c. Macroglossia :Beckwith Wiedemann syndromeDown's syndromed.

Tumors:Hemangioma Neuroblastoma
Drtbalu's otolaryngology online
3. Obturator 4. Suction tube5. A tape to anchor the
tubeCricothyrotomy: Is not performed commonly nowadays
becauseof high incidence of postoperative subglottic stenosis.
This procedure is indicated only under extremely
emergencyconditions.Cricothyroid membrane is incised through
vertical incision andtracheostomy tube is inserted through it. Ideally
these patientsmust be converted into a regular tracheostomy within 48
hours.Surgical procedure:Anaesthesia: Under emergency situations it
is performedunder local infiltration anaesthesia. Under elective
conditionsit is performed under general anaesthesia.Position: Supine
with neck hyperextended.Incision: Emergency tracheostomy is
performed with avertical incision extending from the lower border of
cricoidcartilage up to 2cm above supra sternal notch. This area is
alsoknown as the Burn's space and is devoid of deep
cervicalfascia.Elective tracheostomy is performed through a
horizontalincision at 2cm above the sternal notch.If performed under
emergency settings local anaesthesia is prefered. The drug used is 2 %
xylocaine with 1 in 100000adrenaline. 2 ml of this solution is
infiltrated in to the Burnsspace.
Drtbalu's otolaryngology online
Through a vertical incision extending from the lower border of cricoid
cartilage up to 2cm above the sternal notch theskin, platysma, and
cervical fascia are incised. Branches of anterior jugular vein if any
are ligated and divided. Sternohyoidand Sternothyroid muscles are
retracted using langenbachsretractors. The anterior wall of trachea is
exposed after splitting the pretracheal fascia. The tracheal rings are
clearlyidentified. Few drops of 2% xylocaine is instilled into
thetrachea through a syringe. This process serves to desensitisethe
tracheal mucosa while it is being incised. Incision over thetrachea is
sited between the second and the third trachealrings. If the

tracheostome is planned for a long duration then itis better to excise a

portion of the tracheal ring completely. If tracheostomy is planned for
a short duration of less than amonth then the cartilage is not
completely removed but partially excised creating a flap based either
superiorly or inferiorly. This is known as the Bjork flap. This flap can
besutured to the skin to keep the tracheostome open.Trahceostomy
tube is inserted into the opening and the woundis closed with silk.A
wet gauze is placed over the tracheostome in order tomoisturise the
inspired air.If the patient is to be connected to a ventilator, then a
portextube is used. If the tracheostomy is performed to releive
acuteairway obstruction then a metal tracheostomy tube like theFuller
or Jackson is preferred.Complications of tracheostomy:1. Injury to
thryoid isthumus causing troublesome bleeding2. Too lateral
dissection may cause extensive bleeding and possible injury to
recurrent laryngeal nerve.3. Injury to the apex of the lung (right)
Drtbalu's otolaryngology online
4. Sudden apnoea when the trachea is opened, due to loss of hypoxic
respiratory drive. This can be prevented by slowopening of the
trachea, or by subjecting the patient to inhagecarbogen a mixture of
carbondioxide and oxygen.5. Subcutaneous emphysema if pretracheal
fascia is notdissected properly, or too small a tube is introduced into
thetracheostome.6. Injury to great vessels. This can occur in children
In this stage neovascularisation of the area occur. This phaseis also
reversible, but takes a long time to become normal.Stage of fibrous
organisation:In this stage the transudate in the submucosal area is
replaced by fibrinous material. This stage is more or less resistant
toconservative line of management.These stages can be clearly
observed by laryngoscopy under stroboscopic light. Local
oedematous swelling of recent onsetvibrates in phase with the whole
vocal fold, whereas an older and more fibrous swelling can impede
the vibrations so muchthat only a part of the cord is seen to vibrate.
Theimprovement in the vibration pattern or signs of recovery
are picked up early during stroboscopic examination.Clinical
features:1. Change in voice2. Fatiguability of voice3. Decreased pitch
rangeManagement:1. Voice rest plays a sheetanchor role in the

management of vocal nodule. This may range from complete voice

rest to partial rest.2. Speech therapy will help patients with habitual
dysphoniafrom developing vocal nodule.3. Treatment of sinus
infections, tonsillitis and adenoiditismust not be ovelooked.4. If the
vocal nodule bceome permanent then microlaryngealremoval is
advocated.
Drtbalu's otolaryngology online
d. Rinne's test:is a tuning fork test used to clinically testhearing
deficiencies in patients. It is designed to compare air conduction with
bone conduction thresholds. Under normalcircumstances, air
conduction is better than bone conduction.Ideally 512 tuning fork is
used. It should be struck against theelbow or knee of the patient to
vibrate. While striking caremust be taken that the strike is made at the
junction of theupper 1/3 and lower 2/3 of the fork. This is the
maximumvibratory area of the tuning fork. It should not be
struck against metallic object because it can cause overtones. Assoon
as the fork starts to vibrate it is placed at the mastoid process of the
patient. The patient is advised to signal whenhe stops hearing the
sound. As soon as the patient signals thathe is unable to hear the fork
anymore the vibrating fork istransferred immediatly just close to the
external auditorycanal and is held in such a way that the vibratory
prongsvibrate parallel to the acoustic axis. In patients with
normalhearing he should be able to hear the fork as soon as it
istransferred to the front of the ear. This result is known asPositive
rinne test. (Air conduction is better than boneconduction). In case of
conductive deafness the patient willnot be able to hear the fork as
soon as it is transferred to thefront of the ear (Bone conduction is
better than air conduction). This is known as negative Rinne. It occurs
inconductive deafness. This test is performed in both the ears.If the
patient is suffering from profound unilateral deafness thenthe sound
will still be heard through the opposite ear this conditionleads to a
false positive rinne.e. Rhinoscleroma: This is a chronic
granulomatouscondition of the nose and upper airway. This condition
iscaused by infection by the bacilli Klebsiella rhinoscleromatis.
Drtbalu's otolaryngology online

It is also known as Firsch bacilli (as an honor to von Firshwho

described this organism).Pathophysiology: This condition is
contracted by directinhalation of droplets / contaminated material.
This infectionusually prefers transitional epithelial zones (like
vestibule of nose where the squamous epithelium changes in to
ciliatedcolumnar epithelium and supraglottic area of larynx).Clinical
features:1. Nasal obstruction2. Rhinorrhoea3. Epistaxis4. Nasal
deformity5. Anesthesia of palate6. AnosmiaClassically this condition
passes through three stages:Catarrhal stage: This initial stage begins
with non specificrhinitis progressing on to formation of foul smelling
thick discharge and crusting of the nasal mucosa.Granulomatous
stage: This stage is also known ashyperplastic stage. Nasal mucosa
shows rubbery nodules / polypoidal lesion. Epistaxis may be present.
The nasalcavity appears enlarged with destruction of nasal
cartilages.Involvement of maxillary antrum is common in this stage
andmay form the reservoir.The soft palate appears to be thickened at
its junction withthat of hard palate. If the lesion presents like a tumor
withevidence of tissue destruction it is known as
pseudotumerousrhinoscleroma.Sclerotic stage: This stage is
characterised by sclerosis andfibrosis. In this stage the nodules
present in the nasal mucosa
gets replaced by fibrous tissue.Management: Antibiotics. Tetracycline
happens to be thedrug of choice. Ciprofloxacillin and rifampicin have
alsofound to be effective.Steroids can be administered inorder to
prevent excessivescarring of tissues.Surgery is indicated in patients
with extensive scarring of thenose.(5 x 5 = 25 marks)