Endoscopic Sinus Surgery

Endoscopic surgery has made a great contribution towards
management of sinus disease. Indications for conventional
operations like those of Caldwell-Luc, frontal sinus operations,
external ethmoidectomy have greatly reduced.
Endoscopic surgery is minimally invasive surgery and does
not require skin incisions or removal of intervening bone
to acces, the disease. In the sinuses, ventilation and
drainage of the sinuses is established preserving the nasal
and sinus mucosa and its function of mucociliary clearance.
Advances in endoscopic surgery have been possible due to;
1. Development of better optics.
2. Improved brighter illumination.
3. Development of microsurgical instruments to work
with the endoscopes and precise removal of tissue
with sharp cuts without stripping the mucosa.
4. Concomitant developments in imaging techniques
like CT and MRI to precise ly define the area of
pathology.
5. Introduction of powered instrumentation in the form
of sofr-t i ~s ue shavers also called micro-debriders (to
remove n asa l polyps, soft-tissue masses or mucosa)
help reduce bleeding to a great extent while bonecutting
drills help endoscopic surgery of frontal sinus,
hcrimal sac , etc. to remove bony obstruction.
6. The lar ' t advancement has been the computerassisted
image-guided navigational surgery in difficult
cases or revisional surgery when landmarks are
not easy to identify.
Indications
1. Chronic bacterial sinusitis unresponsive to adequate
medical treatment.
2. Recurrent acute bacterial sinusitis.
3 . Polypo id rhinosinusitis (diffuse nasal polypos is) .
4. Fungal sinusitis with fung<11 ball or nasal polypi.
5. Antrochnanal p()lyp.
6. Mucoce le 0 frontoethmo id or sph enoid sinus.
7. Con trol oi epistclx is by endoscopic cautery.
8. Remova l of foreign body from the nose or sinus.
9. Endoscopic se ptoplasty.
Advanced Nasal Endoscopic Techniques
1. Removal of benign tumours, e.g. in ert d papillomas
or angiufibromas.
2. Orbital abscess or cellulitis management.
3. Dacryocystorhinostomy.
4 Repair of CSF leak.
5. Pituitary surgery.
6. Optic nerve decompress ion.
7. Orbital decompression for Graves disease.
8. Control of posterior epistaxis (endoscopic clipping
of sphenopalatine artery).
9. Choanal atresia.
Contra i nd icati ons
1. Inexperience and lack of proper instrumentation.
2. Disease inaccess ible by endoscopic procedures, e.g.
lateral front al sinus disease and stenosis of internal
opening of frontal sinus.
3. Osteomyelitis.
4. Threatened intracranial or intraorbital complication.
Anaesthesia
General anaesthesia is preferred by most of the surgeons.
Local anaesthesia with i.v. sedation can be used in
when limited work is to be done.
Position
Patient lies flat in supine position with head rest ing ,m a
ring or head rest. Some also prefer to raise it by IS°
Techniques
Two surgical techniques are followed;
(a) Anterior to posterior (Stammberger's technique ); In
this technique surgery proceeds from uncinate
process backward to sphenoid sinus. Advantage of
this technique is to tailor the extent of surge ry to
the extent of disease.
(b) Posterior to anterior (Wigand's techniq ue ); Surgery
starts at the sphenoid sinus and proceecls anteriorly
along the base of skull and medial orbital wall. This
is mostly done in extensive polyposis or in revisional
sinus surgery.
Steps of Operation
1. Remove the pledgees of cotton kept for nasal decongestion
and topical anaesthesia.
2. Inspect the nose with 4 m.m 0° endoscope or do
complete nasal endoscopy if not a lready done.
3 . Inj ect submucosa lly 1 % lignocaine with 1:100, 00
adrenaline under endoscopic control (Fig. 861):
(a) On the lateral wall, near the upper end of midelk
turbinate.
(b) On the la teral wall, just below the first
inj ect ion.
(c) On the la teral \vall, just above the inferior
turbinate.
(d) In the middle turbinate, posterior aspec t.
(e) Posterior aspect of nasal septum.
4. Replace cotton pledgets and repe at injections on
the opposite side if bilateral FESS is to be done.Medialise the middle turbinate and identify the unc inate
process and bulla ethmoida lis. If middle turbinate is large ,
partial or total turbinectomy is performed . In case of concha
bullosa, lateral lamella is removed. Definitive surgical
steps include:
1. Uncinectomy. Uncinate process is incised with
sickle knife and remo ved with Blakesley forceps.
2. Identification and enlargement of maxillary
ostium. Maxillary ostium lies above the inferior
turbinate and posterior to lower third of uncinate
process. Once localised, it is enlarged anteriorly with
a back-biting forceps or pos teriorly with a through
cut-s tra ight forceps.
3. Bullectomy. Bulla ethmoidal is is penetrated with
curette or Blakesley forceps and removed. Avoid
injury to medial orbital wa ll, skull base or anterior
ethmoidal artery.
4. Penetration of basal lamella and removal of posterior
ethmoid cells. Basa l lame lla is the dividing thin
bony septum between anterior and posterior ethmoid
cells. It is penetrated in the lower and medial part
with a sma ll curette and then removed with Blakesley
forceps. Posterior ethmoid cells are exenterated. Optic
nerve is at risk if Onodi cell is present. Onodi ce ll is
a pos terior ethmoid cell which extends into the sphenoid
bone late ral and superior to the sphenoid sinus.
5. Clearance of frontal recess and frontal sinusotomy.
Iffrontal sinus is clear on CT scan and patient
also does not suffer from fremea I h eCldaches, nothing
need to be done. In the event of fron tal sinus disease
, front al recess is cleared and frontal sinus
drainage established.
Opening of frontal sinus is situated lateral to
attachment of middle turbinate, medial to medial
orbital wa ll, anterior to anterior ethmoidal artery
and posterior to agger nasi cell{s). Surgery in the area
of frontal recess is challenging as any d isrespect to
the mucosa in this area would lead to stenosis of
frontal sinus opening with mucocele formation o r
recurrent frontal sinusitis6. Sphenoidotomy. This step is done after clearance of
pos terior ethmo id cells or Clfter frontal sinuso tomy.
It is omitted if sinus is hea lthy. In this procedure
ante rior wall of sphe noid sinus is removed, and pus
and inspi ssa ted mat erial from wit hin the sinus
removed. There are two ways to remove the anterior
sinus wa ll:
(a ) By entering the sphenoid s inus anterior and
inferior to the ethmo id cavity created by the
above steps.
(b) By enlarging the opening of sphenoid sinus with
Bla kesley forceps or J -curette. Sinus opening is
identified after removal of the posterior-inferior
portion of superior turbinate near the nasal septum
and about 1.0 cm above the upper border of
posterior choana.
7. Nasal packs. Fina lly the nasal packs are aprlied, if
septal surge ry has also been done with FESS o r to
stop any bleed ing from the nasa l cavity.
Post-operative Care
It is individua lised according to the exten t of surgery
done.
I. Removal of nasal packs. Nasa l packs, if kept, are
removed at the time of discharge 24 hours
operation.
2. Antibiotics. An intraopera tive intravenous antibi otic
(amoxyclav, cephalosporin or quinolone) is
administered and then continued for 7-10 days by
oral ro ute.
3. Antihistaminics. For a llergic patients.
4 . Analgesics. For re lief of post-opera ti ve pa in.Nasal irrigations. Saline irrigations are started after 1
week post-operatively to remove blood clots, crusts and
secretions and continued once or twice a day for 1 week.
Steroid nasal sprays. Required in cases of nasal
allergy or those operated fo r nasa l polyps.
Endoscopic toilet. Blood clots, crusts and debris are
removed by suction and forceps from the ethmoid area lateral
to middle turbinate. Any adhesion fonl1ation in the
nose is di vided with suction. Healthy mucosa should not
be disturbed. Suction can be done from within the maxillary
sinus wirh a curved cannula. Since the endoscopic
clearance is a painful process, topical nasal anaesthetic
with a decongestant is sprayed before the procedure.
Patient pays weekly visits for inspection of the cavity
for 4 weeks and there after as required till mucosalisation
of the cavity is complete.
Complications
They are similar to conventional surgery of ethmoid complex
and can be divided into major and minor. Mostly they
involve orbit or skull base, or are of general nature
Major
1. Orbital haemorrhage
2. Loss of vision/ blindness
3. Diplopia
4. (SF leak
5. Meningitis rhinitis or sinusitis
6. Brain abscess
7. Massive haemorrhage
8. Intracranial haemorrhage
and direct brain trauma
9. Anosmia
10. Injury to internal carotid
artery in sphenoid sinus
11. Injury to nasolacrimal
duct and epiphora
12. Death

Minor:
1. Periorbital ecchymosis2. Periorbital emphysema 3. Post-operative epistaxis4. Post-operative infection:5. Adhesions6. Stenosis of maxilla ry 0r frontal sinus
requiring blood transfusion7. Exacerbation of asthma8. Hyposmia9. Dental pain

Diagnostic Nasal Endoscopy

Like anterior and posterior rhinoscopy, endoscopy of nose
and nasopharynx helps in the diagnosis of diseases of
nose, paranasal sinuses (PNS) and the nasopharynx.
Because of the brighter illumination, magnification and
angled view provided by the endoscopes, it is possible to
examine all clefts and crevices of the nose and nasopharynx.
It is an important part of examination of nose and
nasopharynx.
Indications
1. To diagnose any disease of the nose and PNS.
2. To diagnose source of bleeding in epistaxis.
3. To assess response to medical or surgical treatment
of the nose and PNS disease.
4. To take a precise biopsy from nose and nasopharynx.
Anaesthesia
Topical anaesthesia with 4% xylocaine and a vasoconstrictor
(oxymetazoline), first as a nasal spray and then
nasal packs.
Position
Sitting or supine.
Instruments
1. 4 mm 30° endoscope
2.7 mm 30° endoscope } Required when nasal
2.7 mm 70° endoscope passages are narrow
2. Freer's elevator or elevator with a suction channel
3. Suction tips
4. Biopsy forceps
5. Antifog solution or savlon to prevent fogging of the
endoscopic lens.
Technique
After nasal packs are removed, endoscopy is performed by
three passes:
First Pass (Examination of nasopharynx and
inferior meatus)
1. First obtain a general view of the nasal cavity. Look
for any septal deviation or spurs and their size,
mucous or purulent discharge in the nasal cavity and
colour of the nasal mucous membrane.
2. Pass the endoscope along the floor of nose into the
nasopharynx and examine: (i) opening of eustachian
tube, (ii) walls of nasopharynx, (iii) upper surface of
soft palate and uvula, and (iv) opening of eustachian
tube of opposite side. To see these structures endoscope
is rotated.
3. Withdraw the endoscope slightly and examine the
margins of choana and posterior ends of turbinates.
4. Withdraw endoscope slowly and at the same time
examine inferior meatus for opening of nasolacrimal
duct and Hasner's valve. Slight pressure over the
lacrimal sac may express a drop or two of lacrimal
fluid through the nasolacrimal opening.
Second Pass (Examination of the
sphenoethmoidal recess, superior meatus
and openings of sphenoid sinus and
posterior ethmoidal cells)
Endoscope is passed medial to middle turbinate to examine
posterior part of middle turbinate, sphenoethmoidal
recess, superior turbinate and meatus, opening of posterior
ethmoid cells (in the superior meatus) and opening of
sphenoid sinus in the posterior wall of sphenoethmoidal
recess between the nasal septum and superior turbinate.
Third Pass (Examination of the
middle meatus in detail)
Endoscope is passed from the front into the middle meatus.
Sometimes middle turbinate needs to be displaced medially
or 2.7 mm 30° endoscope have to be used. Examine
uncinate process, bulla ethmoidalis, hiatus semilunaris,
sinus of the turbinate (cavity on lateral side of middle
turbinate) and the frontal recess.
Sometimes middle meatus is better entered from
behind where the space is wider than from the front and
structures are seen from behind forward, e.g. basal lamina,
bulla ethmoidalis, hiatus semilunaris, sinus of the turbinate
and uncinate process and the frontal recess.
Complications
Sometimes bleeding can occur due to suction or manipulation
of instruments. It is usually mild and easily controlled
by vasoconstrictor nasal drops.

Submucous Resection of Nasal Septum And Septoplasty

Indications
1. Deviated nasal septum (DNS) causing symptoms of
nasal obstruction and recurrent headaches.
Z. DNS causing obstruction to ventilation of paranasal
sinuses and middle ear, resulting in recurrent sinusitis
and otitis media.
3. Recurrent epistaxis from septal spur.
4. As a part of septorhinoplasty for cosmetic correction
of external nasal deformities.
5. As a preliminary step in hypophysectomy (trans-septal
trans-sphenoidal approach) or vidian neurectomy
(trans-septal approach).
Contraindications
1. Patients below 17 years of age. In such cases, a conservative
surgery (septoplasty) should be done.
Z. Acute episode of respiratory infection.
3. Bleeding diathesis.
4. Untreated diabetes or hypertension.Anaesthesia
Local anaesthesia is preferred. General anaesthesia is
used in children and apprehensive adults.
Position
Reclining position with head-end of the table raised.
Steps of Operation
1. Infiltration of nasal septum. It is done in its subperichondrial
planes with 2% xylocaine and 1:50,000
adrenaline.
2. Incision. A curvilinear incision with forward
convexity is made at the mucocutaneous junction on the
left side of the septum. It cuts only through the mucosa
and perichondrium.
3. Elevation of mucoperichondrial and periosteal
flap. Plane of dissection is important. It should be
beneath the perichondrium and periosteum (Fig. 83.1A).
4. Incision of the cartilage. Cartilage is incised just
posterior to the first incision. Avoid cutting the opposite
mucoperichondrium, otherwise, it will result in perforation.
5. Elevation of opposite mucoperichondrium and
periosteum. With the elevator passed through the cartilage
incision, mucoperichondrial and periosteal flap is
raised from the opposite side of the septum (Fig. 83.1 B).
6. Removal of cartilage and bone. Now working
between the two flaps, cartilage and bone are removed.
Cartilage can be removed with Ballenger swivel knife
and bone with Luc's forceps. Bony spur or ridge can be
removed with gouge and hammer. Preserve a strip of cartilage
about 1 cm wide along the dorsal and caudal border
of the septum to prevent collapse of the bridge of
nose or retraction columella (Fig. 83.2).
7. Stitching. One or two catgut or silk stitches are
applied in the initial mucoperichondrial incision.
S. Packing. Ribbon gauze, smeared with an antibiotic
ointment or liquid paraffin, is packed in each nasal cavity
to prevent collection of blood between the flaps. Nasal
dressing is applied.
Post-operative Care
1. Patient is placed in semi-sitting position to prevent
oozing of blood. Outer nasal dressing is changed if
soaked in blood.
Z. A soft diet should be taken in the first two postoperative
days to minimise active mastication
which causes bleeding.
3. Pain, if any, should be controlled with analgesics.
4. Antibiotic cover is given for 5-6 days.
5. Nasal packs are gently removed after 24 hours and
thereafter, decongestant nasal drops and steam
inhalations are given daily for 5-6 days.
6. Silk stitch, if any, is removed on 5th or 6th day.
7. Patient should avoid trauma to the nose for
several days.
Compl ications
1. Bleeding. It may require repacking, if severe.
2. Septal haemawma. Evacuate the haematoma and
given intranasal packing on both sides of septum for
equal pressure.
3. Septal abscess. This can follow infection of septal
haematoma.
4. Perforation. When tears occur on opposing side of
mucous membrane.
5. Depression of bridge. Usually occurs in supratip area
due to too much removal of cartilage along the dorsal
border.
6. Retraction of columella. Often seen when caudal strip
of cartilage is not preserved.
7. Persistence of deviation. It usually occurs due to inadequate
surgery and may require revision operation.
8. Flapping of nasal septum. Rarely seen, when too much
of septal framework has been removed. Septum,
which now consists of two mucoperichondrial flaps,
moves to the right or left with respiration.
9. Toxic shock syndrome. It is rare after septal surgery. It
can follow staphylococcal (sometimes streptococcal)
infection and is characterised by nausea, vomiting,
purulent secretions, hypotension and rash. It should
be diagnosed early. It is treated by removal of packing,
hydrating the patient, maintaining blood pressure and
administering proper antibiotics.

SEPTOPLASTY:
Septoplasty is a conservative approach to septal surgery; as
much of the septal framework as possible is retained.
Mucoperichondrial/periosteal flap is generally ra ised
only on one side. This operation has almost replaced the
SMR operation.
Indications
1. Symptomatic deviated septum.
2. As a part of septorhinoplasty for cosmetic reasons.
3. As an approach to hypophysectomy.
4. Recurrent epistaxis due to septal spur.
Contraindications
1. Acute nasal or sinus infection.
2. Untreated diabetes.
3 . Hypertension.
4. Bleeding diathesis.
Anaesthesia
Local or general.
Position
Same as for SMR operation.Technique
1. Infiltrate the septum with 1 % lignocaine with ad renaline,
1:100,000.
2. In cases of deviated septum, make a slightly curvilinear
incision, 2-3 mm above the caudal end of septal
cartilage on the concave side (Killian's incision).
In case of caudal dislocation, a transfix ion or hemitransfixion
(Freer's) incision is made.
3. Raise mucoperichondrial/mucoperiosteal flap on
one side only.
4. Separate septal cartilage from the vomer and ethmoid
plate and raise mucoperiosteal flap on the opposite
side of septum.
5. Remove maxillary crest to realign the septal cartilage.
6. Correct the bony septum by removing the deformed
parts. Deformed septal cartilage is corrected by various
methods, such as:
(i) Scoring on the concave side (Fig. 84.1).
(ii) Cross-hatching or morcelizing.
(iii) Shaving.
(iv) Wedge excision.
Further manipulations like realignment of nasal spine,
separation of septal cartilage from upper lateral cartilages,
implantation of cartilage strip in the columella
or the dorsum of nose may be required.
7. Trans-septal sutures are put to coapt mucoperichondrial
flaps.
8. Nasal pack.
Post-operative Complications
Same as for SMR operation.
1. Bleeding.
2. Septal haernatorna and abscess.
3. Septal perforation.
4. Persistence of septal deviation, or external nasal
deformity.

Septal Haematoma

Aetiology
It is collection of blood under the perichondrium or
periosteum of the nasal septum . It often
results from nasal trauma or septal surgery. III bleeding
disorders, it may occur spontaneously.
Clinical Features
Bilateral nasal obstruction is the commonest presenting
symptom. This may be assoc iated with frontal headache
and a sense of pressure over the nasal bridge.
Examination reveals smooth rounded swelling of the
septum in both the nasal fossae. Palpation may show the
mass to be soft and fluctuant.
Treatment
Small haematomas can be aspirated with a wide bore
steriie needle. Large r haematomas are incised ai1d
drained by a small antero-posterior incision parallel to
the nasal floor. Excision of a small piece of mucosa from the
edge of incision gives better drainage. Following drainage,
nose is packed on both sides to prevent reaccumulation .
systemic antibiotics should be given to prevent septal abscess.
Complications
Septal haematoma, if not drained, may organise into
fibrous tissue leading to a permanently thickened septum.
If second::!ry infection supervenes, it results in septal
abscess with necrosis of cartilage and depression of
nasal dorsum.

Physiology Of Nose

Functions of the nose are classified as:

1. Respiration.
2. Air conditioning of inspired air.
3. Protection of lower airway.
4. Vocal resonance.
5. Nasal reflex functions.
6. Olfaction.
7. Respiration

Nse is the natural pathway for breathing. Mouth
breathing is acquired through learning. So natural is the
instinct to breath through the nose that a newborn
infant with choanal atresia may asphyxiate to death if
urgent measures are not taken to relieve it. The nose also
permits breathing and eating to go on simultaneously.
During quiet respiration, inspiratory air current passes
through middle part of nose between the turbinates and
nasal septum. Very little air passes through inferior meatus
or olfactory region of nose. Therefore, weak
odorous substances have to be sniffed before they can
reach olfactory area.
During expiration, air current follows the same course
as during inspiration, but the entire air current is not
expelled directly through the nares. Friction offered at
limen nasi converts it into eddies under cover of inferior
and middle turbinates and this ventilates the sinuses
through the ostia.
Anterior end of inferior turbinate undergoes swelling
and shrinkage thus regulating inflow of air.
Nasal cycle. Nasal mucosa undergoes rhythmic cyclical
congestion and decongestion, thus controlling the air
flow through nasal chambers. When one nasal chamber is
working, total nasal respiration, equal to that of both nasal
chambers, is carried out by it. Nasal cycle varies every
2.5-4 hours and may be characteristic of an individual.
Air-conditioning of Inspired Air
Nose is aptly called the "air-conditioner" for lungs. It filters
and purifies the inspired air and adjusts its temperature
and humidity before it passes it on to the lungs.
(a) Filtration and purification. Nasal vibrissae at the
entrance of nose act as filters to sift larger particles
like fluffs of cotton. Finer particles like dust, pollen
and bacteria adhere to the mucus which is spread
like a sheet all over the surface of the mucous membrane.
The front of the nose can filter particles up to
3 fLm, while nasal mucus traps particles 0.5-3.0 um.
Particles smaller than 0.5 um seem to pass through
the nose into lower airways without difficulty.
(b) Temperature control of the inspired air is regulated by
large surface of nasal mucosa which is structurally
adapted to pelform this function. This mucous
membrane, particularly in the region of middle and
inferior turbinates and adjacent parts of the septum
is highly vascular with cavernous venous spaces or
sinusoids which control the blood flow, and this
increases or decreases the size of turbinates. This
makes an efficient "radiator" mechanism to warm up
the cold air. Inspired air which may be at 20°C or
O°C or even at subzero temperature is heated to near
body temperature (37°C) in one-fourth of second
that the air takes to pass from the nostril to the
nasopharynx. Similarly, hot air is cooled to the body
temperature.
(c) Humidification. This function goes on simultaneously
with the temperature comrol of inspired air. Relative
humidity of atmospheric a ir varies depending on climatic
conditions. Air is dry in winter and satura ted
with moisture in summer momhs. Nasal mucous
membrane adjusts the relative humidity of the
inspired air to 75% or more. Water, to saturate the
inspired air, is provided by the nasal mucous membrane
which is rich in mucous and serous secreting
glands. About 1000 ml of water is evaporated from
the surface of nasal mucosa in 24 hours.
Moisture is essential for integrity and functi on of the
ciliary epithelium. At 50% relative humidity, ciliary function
stops in 8-10 minutes. Thus, dry air predisposes to
infections of the respiratory tract. Humidification also has
a significant effect on gas exchange in the lower airways.
[n nasal obstruction, gaseous exchange is affected in the
lungs, leading to rise in pCO2, causing apnoeic spells during
sleep; it also decreases pO2.
Protection of Lower Airway
(a) Mucociliary mechanism. Nasal mucosa is rich in goblet
cells, secretory glands both mucous and serous.
Their secretion forms a continuo us sheet called
mucous blanket spread over the normal mucosa.
Muco us blanket consists of a superficial mucus layer
and a deeper serous layer, floating on the top of cilia
which are constantly beating to carry it like a "conveyer
belt" towards the nasopharynx. It
moves at a speed of 5-10' mm per minute and the
complete sh eet of mucus is cleared into the pharynx
every 10 to 20 minutes. The inspired bacteria ,
viruses and dust particles are entrapped on the viscous
mucous blanket and then carried to the
nasopharynx to be swallowed. Presence of turbina tes
almost doubles the surface area to perform this function.
A bout 600-700 ml of nasa l secre tions are produced
in 24 hours.
In mammals, cilia beat 10-20 times per second at room
temperature. They have a rapid "effective stroke" and a
slow "recovery stroke". In the former, the extended cilia
reach mucus layer while in the recovery stroke, they bend
and travel slowly in the reverse direction in the thin
serous layer, thus moving the mucous blanket in only one
direction. In immotile cilia syndrome, cilia are defective
and cannot beat effectively, leading to stagnation of
mucus in the nose and sinuses and bronchi causing
chronic rhinosinusitis and bronchiectasis. Movements
of cil ia a re affected by drying, drugs (adrenaline), excessive
heat or cold, smoking, infections and noxious fumes
like sulphur dioxide and carbon dioxide.
(b) Enzymes and immunoglobulins. Nasal secretions also
contain an enzyme called muramidase (lysozyme)
which kills bacteria and viruses. ImmunoglobulInS
IgA and IgE, and interferon are also present in nasal
sec retions and provide immunity against upper respiratory
tract infections.
(c) Sneezing. It is a protective reflex. Foreign particles
which irritate nasal mucosa a re expelled by sneezing.
Copious flow of nasal secretions that foltows initation
by noxious substance helps to wash them out.
The pH of nasal sec retion is nearly constant at 7. The
cilia and the lysozyme act best at this pH. Alteration in
nasal pH, due to infections or nasal drops, seriously
impair the functions of cilia and lysozyme.
So efficient are the functio ns of nose th~lt 500 cubic
feet of air, that we breathe every 24 hours, is filtered,
humidified, adjusted to proper temperature and cleared
of all the dust, bacteria and viruses befo re reaching the
lungs.
Vocal Resonance
Nose forms a resonating chamber for certain consonants
in speech. In phonating nasal consonants (MINING),
sound passes through the nasopharyngeal isthmus and
is emitted through the nose. When nose (or nasopharynx)
is blocked, speech becomes denasal, i.e. MINING
are uttered as B/D/G respectively.
Nasal Reflexes
Several reflexes are initiated in the nasa l mucosa. Smell
of a palatable food cause reflex secretion of sa liva and
gastric juice. Irritation of nasal mucosa causes sneezing .
Nasal function is closely related to pulmonary functions
th ro ugh nasobronchial and nasopulmonary reflexes. It
has been observed tha t nasal obstruction leads to
increased pulmona ry resistance and is re versed when
nasa l obstruction is surgically treated. Nasal packing in
cases of epistaxis or after nasal surgery leads to lowering
of p02 which returns to norma l after remova l of the
pack. Pulmonary hypertension or cor pulmonale can
develop in children with longstanding nasal obstruction
due to tonsil and adenoid hypertrophy and can be reversed
after removal of the tonsils and adenoids.
Olfaction
Sense of smell is well developed in lower animals to give
warning of the environmental dangers but it is comparatively
less important in man, still it is important for
pleasure and for enjoying the taste of food. When nose is
blocked, food tastes bland and unpalatable. Vapours of
ammonia are never used to test the sense of smell as they
stimulate fibres of the trigeminal nerve and cause irritation
in the nose rather than stimulate the olfactory
receptors.
Olfactory pathways. Smell is perceived in the olfacrory
region of nose which is situated high up in the nasal
cavity. This area contains millions of olfactory, receptor
cells. Peripheral process of each olfactory cell reaches the
mucosal surface and is expanded into a ventricle with several
cilia on it. This acts as a sensory receptor to receive
odorous substances. Central processes of the olfactory cells
are grouped into olfactory nerves which pass through the
cribriform plate of ethmoid and end in the mitral cells of
the olfactory bulb. Axons of mitral cells form olfactory
tract and carry smell to the prepiriform cortex and the
amygdalOid nucleus where it reaches consciousness.
Olfactory system is also associated with autonomic system
at the hypothalamic level.
Disorders of smell: It is essential for the perception of
smell that the odorous substance be volatile and that it
should reach the olfactory area unimpeded. Also necessary
are the healthy state of olfactory mucosa and the
integrity of neural pathways, i.e . olfactory nerves, olfactory
bulb and tract and the cortical centre of olfaction.
Anosmia is total loss of sense of smell while hyposmia
is partial loss. They can result from nasal obstruction due
to nasal polyp i, enlarged turbinates or oedema of mucous
membrane as in common cold, allergic or vasomotor
rhinitis. Anosmia is also seen in atrophic rhinitis, a
degenerative disorder or nasa l mucosa; peripheral neuritis
(toxic or influenzal) ; injury to olfactory nerves or
olfactory bulb in fractu res of anterior cranial fossa; and
intracranial lesions lik e ahscess, tumour or meningitis
which cause pressure on olfactory tracts.
Parosmia is perversion of smell; the person interprets
the odours incorrectly. Often these persons complain of
disgusting odours. It is seen in the recovery phase of
postinfluenzal anosmi a and the probable explanation is
misdirected regeneration of nerve fibres. Intracranial
tumour should be excluded in all cases of parosmia.
Sense of smell can be tested by asking the patient to
smell common odours such as lemon, peppermint, rose,
garlic or cloves from each side of the nose separately,
with eyes closed. Quantitative estimation (quantitative
olfactometry) requires special equipment.

DEVIATED NASAL SEPTUM (DNS)

This is an important cause of nasal obstruction.
Aetiology
Trauma and errors of development form the two import
facto rs in the causation of deviated sepcum.
1. Trauma. A lateral blow on the nose may cause displacement
of septal cartilage from the vomerine groove
and maxillary crest, while a crushing blow from the front
may cause buckling, twisting, fractures and duplication of
nasal septum with telescoping of its fragments. Injuries to
the nose commonly occur in childhood but are often
overlooked. Even the history may not be forthcoming.
- Trauma may also be inflicted at birth during d
hour when nose is pressed during its passage through
the birth canal. Birth injuries should be immediately
attended to as they result in septal deviation later in life.
2. Developmental error. Nasal septum is formed by
the tectoseptal process which descends to meet the two
halves of the developing pa late in the midline. During
the primary and secondary dentition, further development
takes place in the palate, which descends and
widens to accommodate the teeth.
Unequal growth between the palate and the base of
skull may cause buckling of the nasal septum. In mouth
breathers, as in adenoid hypertrophy, the palate is often
highly arched and the septum is deviated
Similarly, DNS may be seen in cases of cleft lip and
palate and in those with dental abnormalities.
3. Racial factors. Caucasians are affected more than
Negroes.
4. Hereditary factors. Several members of the same
family may have deviated nasal septum.
Types of DNS
Deviation may involve only the cartilage, bone or both
the cartilage and bone .
1. Anterior dislocation. Septal cClrtiiage may be dislocated
into one of the nasal chambers. This is better
appreciated by looking at the base of nose when patient's
head is tilted backwards
2. C-shaped deform ity. Septum is deviated in a simple
curve to one side. Nasal chamber on the concave side
of the nasal septum will be wider and may show com pensmory
hypertrophy of turbinates.
3. S-shaped deformity. Septum may show as-shaped
curve either in vertical or anteroposterior plane. Such a
deformity may cause bilateral nasal obstruction.
4. Spurs. A spur is a shelf- like projection often found
at the junction of bone and carti lage. A spur may press on
the latera l wall and gives rise to headache. It may also predispose
to repeated epistaxis from the vessels stretched on
its convex sUlface.
5. Thickening. It may be due to organised haematoma
or over-riding of dislocated septal fragments.
Clinical features
DNS can involve any age and sex. Ma les are affected
more than females.
1. Nasal obstruction. Depending on the type of septal
deformity, obstruction may be unilateral or bilateral.
Respiratory c urrents pass through upper part of nasa l cavity,
therefore, high. septal deviation cause nasa l obstruction
more than lower ones.
When examining a case of nasal obstruction, one should
ascertain the site of obstruction in the nose. It could be (1)
vestibular (caudal septal dislocation, synechiae or stenosis),
(2) at the nasal valve (synechiae, Llsually post-rhino.plasty),
(3) attic (a long the upper part o.f nasal septum due to high
septal deviat ion; (4) turbinal (hypertrophic turbinates or
concha bullosa); and (5) choanal (choanal atresia or a
choanal polyp.) unilateral choana1 atresia maY be missed
in infancy and childhood. Choanal polyp may be missed
on the anterior rhinoscopy unless posterior rhinoscopy or
nasal endoscopy is done.
Cottle test. It is used in nasal obstruction due to abnormality
of the nasa l valve. In this test, cheek is drawn laterally
while the patient breathes quietl y. If the nasal
airway improves on the test side, the test is positive, am.!
indicates abnormality of the vestibular component ot'
nasal valve
2. Headache. Deviated septum, especially a spur.
may press on the latera l wall of nose giving rise to
pressure headache.
3. Sinusitis. Deviated septum may obstruct sinu,
ost ia resu lting in poor ventilation of the sinuses.
Therefore, it forms an important cause to predispose or
perpetuate sinus infec tions.
4. Epistaxis. Mucosa over the deviated part of septum
is exposed to the dryi ng effects o.f air cu rrents leading
to. formation of crusts which when removed, cause
bleed ing. Bleeding may a lso occur from vessels over a
septal spur.
5. Anosmia. Fa ilure of the inspired air to reach tht'
olfactory region may res ult in total or partial loss of sens
of smell
6. External deformity. Septal deformities may be
associated with deviation of the cartilaginous or both
the bony and cartilaginous dorsum of nose, deform itie
of the nasal tip or columella.
7. Middle ear infection. DNS also predisposes to middle ear infection.
Treatment
Minor degrees of septal deviation with no sympwms are
commonly seen in patients and require no treatment. It
is only when deviated septum produces mechanical nasal
obstruction or the symptoms given above, that an operation
is indicated.
Submucous resection (SMR) operation. It is generally
done in adu lts under local anaesthesia. It consists
of elevating the mucoperichondrial and mucoperi os teal
flaps on either side of the septal framework by a single
incision made on one side of the septum, removing the
deflected parts of the bony and cartilaginous septum, and
then repositioning the fl aps (see section on Operative
Surgery for details).
Septoplasty. It is a conservative approach to septa l
surgery. In this operation, much of the septal framework
is retained. Only the most deviated parts are removed.
Rest of the septal framework is corrected and repositioned
by plastic means. Mucoperichondrial/periosteal
flap is generally raised only on one side of the septum,
retaining the attachment and blood supply on the other.
Septoplasty has now almost replaced SMR operation.
Septal surgery is usually done after the age of 17 so as
not to interfere with the growth of nasal skeleton.
However, if a child has severe septal deviation causing
marked nasal obstruction, conservative septal surgery
(septoplasty) can be performed to provide a good airway.

ATROPHIC RHINITIS (OZAENA)

It is a chronic inflammation of nose characterised by
atrophy of nasal mucosa and turbinate bones. The nasal
cavities are roomy and full of foul -smelling crus ts.
Atrophic rhinitis is of two types: primary and secondary.
Primary Atrophic Rhinitis
Aetiology (Remember Mnemonic HERNIA)
The exact cause is not known. Various theories advanced
regarding its causation are:
(a) Hereditary factors. Disease is known to involve more
than one member in the same family.
(b) Endocrinal disturbance. Disease usually starts :Jt
puberty, involves females more th an males, the
crusting and foetor associated with disease tends to
cease after me nopause; these factors ha\'e r .Jl I::J the
possibility of disease being an endocrina l dl ~ orde r.
(c) Racial factors. White and ye llow rae s are more susceptible
than natives of equatorial Africd.
(d) Nutritional deficiency. Disease may be due to deficiency
of vitamin A, D or iron or some other dietary
factors. The fact that incidence of di:.ease is decreasing
in western countries and is rarely seen in well-to-
do families raises the possibility of some
nutritional deficiency.
(e) Infective. Various organisms have been cul tureJ from
cases of atrophic rhinitis such as Klebsiella ozaenae ,
(Perez bacillus), diphtheroids, P vulgaris, Esch. coli,
Staphylococci and Streptococci but th e ' are all considered
to be secondary invade rs responsible for fou I
smell rather than the primary ca usat ive organisms of
the disease.
(f) Autoimmune process. The body reacts by a destructive
process to the antigens released from the nasal
mucosa. Viral infection or some other unspecified
agents may trigger antigenicity of nasal mucosa.
Pathology
Ciliated columnar epithelium is lost and is replaced by
strat ified squamous type. There is atrophy of seromucinous
glands, ve nous blood sinusoid s and nerve elements.
Arteries in the mucosa, periosteum and bone show oblitt
rati ve endarteritis. The bone of turbinates undergoes
resorption causing widening of nasal chambers. Paranasal
sinuses are small due to their arrested development.
Clinical Features
Disease is commonly seen in females and starts around
puberty. There is foul smell from the nose making the
patient a social outcast though patient himself is unaware
of the smell due to marked anosmia (merciful anosmia)
which accompanies these degenerative changes. Patient
may complain of nasal obstruction in spite of unduly wide
nasal chambers. This is due to large crusts filling the
nose. EpistaxiS may occur when the crusts are removed.
Examina tion shows nasal cavi ty to be full of greenish or
greyish black dry crusts covering the turbinates and septum.
Attempts to remove them may cause bleeding. When
the crusts have been removed, nasal cavities appear roomy
with atrophy of turbinates so much so that the posterio r
wall of nasopharynx can be easily seen. Nasal turbinates
may be reduced to mere ridges. Nasal mucosa appears
pale. Septal perforation and dermatitis of nasal vestibule
may be present. Nose may show a saddle deformity.
Atrophic changes may also be seen in the pharyngeal
mucosa which may appear dry and gl8zed with crusts.
Similar changes may occur in the larynx with cough
and hoarseness of voice (atrophic laryngitis).
Hearing-impairment may be noticed because of
obstruction to eustachian tube and middle ear effusion.
Paranasal sinuses are usually small and underdeveloped
with thick walls. They appear opaque on X-ray.
Antral wash is difficult to perform due to thick walls of
the sinuses.
Prognosis
The disease persists for years but there is a tendency to
recover spontaneously in middle age.
Treatment
It may be medical or surgical.
1. Medical. Complete cure of the disease is not yet
possible. Treat ment aims a t maintaining n asa l hygiene by
removal of crusts and the associated putrefying smell,
and to further check crust format ion.
(a) Nasal irrigation and removal of crusts. Warm normal
saline or an alkaline solution made by dissolving a teaspoonful
of powder containing soda bicarbonate 1
part, Sodium biborate 1 part, Sodium chloride 2 parts
in 280 ml of water, is used to irrigate the nasal cavities.
The solution is run through one nostril and comes out
from the other. It loosens the crusts and removes thick
tenacious discharge Care should be taken to avoid
pushing the fluid into the sinuses and eus tachian tube.
Initially, irrigations are done 2 or 3 times a day but
later once every 2 or 3 days is sufficient. Hard crusts
may be difficult to remove by irrigation. They are first
loosened and then mechanically removed with forceps
or suction.
(b) 25% glucose in glycerine. After crusts are removed,
nose is painted wi th 25% glucose in glycerine. This
inhibits the growth of proteolytic organisms which
are responsible for foul smell.
(c) Local antibiotics. SpraYing or painting the nose with
appropriate antibiotics help to eliminate secondary
infection. Kemicetine antiozaena solution contains
chloromycetin, oestradiol and vitamin D2 and may
be found useful .
(d) Oestradiol spray. Helps to increase vascularity of nasal
mucosa and regeneration of seromucinous glands.
(e) Placental extract injected submucosally in the nose
may provide some relief.
(f) Systemic use of streptomycin. 1 gm/day for 10 days has
given good resu lts in reducing crusting and odour.
It is effective against Klebsiella organisms,
(g) Potassium iodide given by the mouth promotes and
liquefies nasal secretion.
2, Surgical. It includes:
(a) Young's operation. 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.
(b) 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.
Secondary Atrophic Rhinitis
Specific infections like 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
to 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.

Rhinosporidiosis

It is a fungal granuloma caused by Rhinosporidium seeberi.
It is seen in India, Pakistan and Sri Lanka. In India, most
of the cases are seen in southern states though several
cases have also been reported from other parts of the
country.
Clinical features. The disease mostly affects nose and
nasopharynx; other sites such as lip, palate, conjunctiva,
epiglottis, larynx, trachea, bronchi, skin, vulva, vagina may
also be affected.
The disease is acquired through contaminated water
of ponds also frequented by animals. In the nose, the disease
presents as a leafy, polypoidal mass, pink to purple in
colour and attached to nasal septum or lateral wall.
Sometimes, it extends into the nasopharynx and may
hang behind the soft palate. The mass is very vascular
and bleeds easily on touch. Its surface is studded with
white dots representing the sporangia of fungus.
In early stages, the patient may complain of nasal discharge
which is often blood-tinged, or nasal stuffiness.
Sometimes, frank epistaxis is the only presenting complaint.
Diagnosis is made on biopsy. It shows several sporangia,
oval or round in shape and filled with spores which may be
seen bursting through its chitinous wall. It has not been
possible to culture the organism or transfer the disease to
experimental animals.
Treatment is complete excision of the mass with
diathermy knife and cauterisation of its base. Recurrence
may occur after surgical excision. Not many drugs are
effective against the disease. Dapsone has been tried with
some success.

CSF Rhinorrhoea

CSF rhinorrhoea presents as flow of clear fluid from the
nose.
Aetiology.
(i) Traumatic: Head injuries, surgery of frontal, ethmoid
or sphenoid sinus or hypophysectomy. It may
follow as a complication of endoscopic sinus surgery.
It may be immediate or delayed in onset.
(ii) Tumours: Large osteomas of frontoethmoid region,
tumours of the pituitary or the olfactory bulb.
(iii) Congenital defects in skull associated with
encephalocele.
(iv) Spontaneous type.
Sites of leakage. CSF from anterior cranial fossa
reaches the nose by way of cribriform plate, ethmoid air
cells or frontal sinus. CSF from middle cranial fossa
reaches the nose via sphenoid sinus. Sometimes, injuries
of temporal bone result in leakage of CSF into the middle
ear and thence via the eustachian tube into the nose
(otorhinorrhoea) .
Diagnosis. There is history of dribbling of clear fluid
from the nose on bending or straining. CSF rhinorrhoea
should be differentiated from nasal discharge of allergic
or vasomotor rhinitis. Discharge in CSF rhinorrhoea is
clear and watery, appears suddenly in a gush of drops
when bending forward or straining, is uncontrollable and
cannot be sniffed back. There is no associated sneezing,
nasal congestion or lacrimation. When collected into a
test-tube and allowed to stand, it remains clear in contradistinction
to nasal discharge that leaves a sediment
because of mucus and other proteins. This is also the reason
that a nasal discharge stiffens the handkerchief. CSF
contains glucose which can be demonstrated by oxidaseperoxidase
paper strip or biochemical tests. f32 transferrin
is specific for CSF. Itis absent in nasal secretions or tears.
Its presence confirms the diagnosis of CSF leak.
Localisation of CSF leak. It is done by intrathecal
injection of a dye (fluorescein 5%, 1 ml) or a radioisotope
and placing pledgets of cotton in the olfactory slit,
middle meatus, sphenoethmoidal recess and near the
eustachian tube and examining the pledgets for dye or
rad ioactivity.
Olfactory slit--> Cribriform plate
Middle meatus--> Frontal or ethmoid sinuses
Sphenoethmoidal recess --> Sphenoid sinus
Inferior meatus near the --> Temporal bone
eustachian tube

Common Causes of Bilateral Nasal Obstruction

Vestibule
Bilateral vestibulitis
Collapsing nasal alae
Stenosis of nares
Congenital atresia of nares
Nasal cavity
Acute rhinitis (viral, bacterial)
Chronic rhinitis & sinusitis
Rhinitis medicamentosa
Allergic rhinitis
Hypertrophic turbinates
DNS
Nasal polypi
Atrophic rhinitis
Rhinitis sicca
Septal haematoma
Septal abscess
Bilateral choanal atresia
Nasopharynx
Adenoid hyperplasia
Large choanal polyp
Thornwaldt's cyst
Adhesions between soft palate and posterior pharyngeal
wall
Large benign and malignant tumours

Common Causes of Unilateral Nasal Obstruction

Vestibule
Furuncle
Vestibulitis
Stenosis of nares
Atresia
Nasoalveolar cyst
Papilloma
Squamous cell carcinoma
Nasal cavity
Foreign body
DNS
Hypertrophic turbinates
Concha bullosa
Antrochoanal polyp
Synechia
Rhinolith
Bleeding polypus of septum
Benign and malignant tumours of nose and paranasal
sinuses
Sinusitis, unilateral
Nasopharynx
Unilateral choanal atresia

Antrochoanal Polyp

This polyp arises from the mucosa of max illary antrum
near its accessory ostium, comes out of it and grows in
the choana and nasal cavity. Thus it has three parts.
(a) Antral: which is a thin stalk.
(b) Choanal: which is round and globular.
(c) Nasal: which is flat from side to side.
Aetiology. Exact cause is unknown. Nasal allergy coupled
with sinus infection is incriminated. Antrochoanal
polypi are seen in children and young adults. Usually
they are single and unilateral.
Symptoms. Unilateral nasal obstruction is the presenting
symptom. Obstruction may become bilateral when
polyp grows into the nasopharynx and starts obstructing
the opposite choana. Voice may become thick and dull
due to hyponasality. Nasal discharge, mostly mucoid,
may be seen on one or both sid es.
Signs. As the antrochoanal polyp grows posteriorly,
it may be missed on anterior rhinoscopy. When large, a
smooth greyish mass covered with nasal discharge may be
seen. It is soft and can be moved up and down with a
probe. A large polyp may protrude from the nostril and
show a pink congested look on its exposed part. Posterior rhinoscopy
may reveal a globular mass filling the choana or the nasopharynx.
A large polyp may hang down behind the soft palate and present in the oropharynx.
Differential diagnosis
1. A blob of mucus often looks like a polypi but it would
disappear on blowing the nose.
2. Hypertrophied middle turbinate is differentiated by
its pink appearance and hard feel of bone on probe
testing.
3. Angiofibroma has history of profuse recurrent epistaxis.
It is firm in consistency and easily bleeds on probing.
4. Other neoplasms may be differentiated by theIr fleshy
pink appearance, friable nature and their tendency to
bleed.
X-rays of paranasal sinuses may show opacity of the
involved antrum. X-ray, (lateral view) soft tissue nasopharynx,
reveals a globular swelling in the postnasal space.
It is differentiated from angiofibroma by the presence of a
column of air behind the polyp.
Treatment. An antrochoanal polyp is easily removed
by avulsion either through the nasal or oral route. Recurrence
is uncommon after complete removal. In cases
which do recur, Caldwell-Luc operation may be required
to remove the polyp completely from the site of its origin
and to deal with co-existent maxillary sinusitis. These
days, endoscopic sinus surgery has superceded other modes
of polyp removal. Caldwell-Luc operation is avoided .

Bilateral Ethmoidal Polypi

Aetiology. Aetiology of nasal polypi is very complex
and not well-understood. They may arise in inflammarory
conditions of nasal mucosa (rhinosinusitis), disorders of
ciliary motility or abnormal composition of nasal mucus
(cystic fibrosis). Various diseases associated with the formation
of nasal polypi are:
(i) Chronic rhinosinusitis. Po lypi are seen in chronic
rhinosinusitis of both allergic and non-allergic origin.
Non-allergic rhinitis with eosinophilia syndrome
(NARES) is a form of chronic rhinitis
associated with polypi.
(ii) Asthma. 7% of the patients with asthma of atopic
or non-atopic origin show nasal polypi.
(iii) Aspirin intolerance. 36% of the patients with aspirin
intolerance may show polypi. Sampter's triad consists
of nasal polypi, asthma and aspirin intolerance.
(iv) Cystic fibrosis. 20% of patients with cystic fibrosis
form polypi. It is due to abnormal mucus.
(v) Allergic fungal sinusitis. Almost all cases of fungal
sinusitis form nasal polypi.
(vi) Kartagener's syndrome. This consists of bronchiectasis
sinusitis, situs inversus and ciliary dyskinesis.
(vii) Young's syndrome. It consists of sinopulmonary disease
and azoospermia.
(viii) Churg-Strauss syndrome. Consists of asthma, fever,
eosinophilia, vasculitis and granuloma.
(ix) Nasal mastocytosis. It is a form of chronic rhinitis
in which nasal mucosa is infiltrated with mast cells
but few eosinophils. Skin tests for allergy and IgE
levels are normal.
Pathogenesis. Nasal mucosa, particularly in the
region of middle meatus and turbinate becomes oedematous
due to collection of extracellular fluid causing polypoidal
change. Polypi which are sessile in the beginning
become pedunculated due to gravity and the excessive
sneezing.
Pathology. In early stages, surface of nasal polypi is
covered by ciliated columnar epithelium like that of normal
nasal mucosa but later it undergoes a metaplastic change
to transitional and squamous type on exposure to atmospheric
irritation. Submucosa shows large intercellular
spaces filled with serous fluid. There is a(so intlItration
with eosinophils and round cells.
Site of origin. Multiple nasal polypi always arise from
the lateral wall of nose, usually from the middle meatus.
Common sites are uncinate process, bulla ethmoidalis, ostia
of sinuses, medial surface and edge of middle turbinate.
Allergic nasal polypi almost never arise from the septum
or the floor of nose.
Symptoms
1. Multiple polypi can occur at any age but are mostly
seen in adults.
2. Nasal stuffiness leading ro total nasal obstruction may
be the presenting symptom.
3. Partial or total loss of sense of smell.
4. Headache due to associated sinusitis.
5. Sneezing and watery nasal discharge due to associated
allergy.
6. Mass protruding from the nostril.
Signs. On anterior rhinoscopy, polypi appear as smooth,
glistening, grape-like masses often pale in colour. They
may be sessile or pedunculated, insensitive to probing
and do not bleed on touch. Often they are multiple and
bilateral. Long-standing cases present with broadening of
nose and increased intercanthal distance. A polyp may
protrude from the nostril and appear pink and vascular
simulating neoplasm . Nasal cavity may show
purulent discharge due to associated sinusitis.
Probing of a solitary ethmoidal polyp may be necessary
to differentiate it from hypertrophy of the turbinate
or cystic middle turbinate.
Diagnosis. Diagnosis can be easily made on clinical
examination. CT scan of paranasal sinuses is essential to
exclude the bony erosion and expansion suggestive of neoplasia.
Simple nasal polypi may sometimes be associated
Fig. 32.1 A polyp protruding from the left nostril in a
patient with bilateral ethmoidal polypi.
with malignancy underneath, especially in people .lbove
40 years and this must be excluded by histol gical examination
of the suspected tissue. CT scan also helps to
plan surgery.
Treatment
Conservative
1. Early polypoidal changes with oedematous mucosa
may revert to normal with antihistaminics and control
of allergy.
A short course of steroids may prove useful in case of
people who cannot tolerate antihistaminics and/or
in those with asthma and polypoidal nasal mucosa.
They may also be used to prevent recurrence after
surgery. Contra indications to use of steroids, e.g.
hypertension, peptic ulcer, diabetes, pregnancy and
tuberculosis should be excluded.
Surgical
1. Polypectomy. One or two polyps which are pedunculated
can be removed . with snare. Multiple and
sess ile polypi require special forceps.
2. Intranasal ethmoidectomy. When polypi are multiple
and sess ile they require uncapping of the ethmoidal
air cells by intranasal route, a procedure called
intranasal ethmoidectomy.
3. Extranasal ethmoidectomy. This is indicated when
polypi recur after intranasal procedures and surgical
landmarks are ill-defined due to previous surgery.
Approach is through the medial wall of the orbit by
an external incision, medial to medial canthus.
4. Transantral ethmoU:l.ectomy. This is indicated when
infection and polypoidal changes are also seen in the
maxillary antrum. In this case, antrum is opened by
Caldwell-Luc approach and the ethmoid air cell
approached through the medial wall of the antrum.
This procedure is also superceded by endoscopic sinus
surgery.
5. Endoscopic sinus surgery. These days, ethmoidal
polypi are removed by endoscopic sinus surgery more
popularly called FESS (functional endoscopic sinus
surgery). It is done with various endoscopes 0(00 ,300
and 70° angulation. Polypi can be removed more accurately
when ethmoid cells are removed, and drainage
and ventilation provided to the other involved sinuses
such as maxillary, sphenoidal or frontal.

Epistaxis: Causes And Management

They may be divided into:
A. Local, in the nose or nasopharynx.
B. General.
C. Idiopathic.
A. Local Causes
Nose
1. Trauma. Finger nail trauma, injuries of nose, intranasal
surgery, fractures of middle third of face and base of
skull, hard-blowing of nose, violent sneeze.
2. Infections.
Acute: Viral rhinitis, nasal diphtheria, acute sinusitis.
Chronic: All crust-forming diseases, e.g. atrophic
rhinitis, rhinitis sicca, tuberculosis, syphilis septal
perforation, granulomatous lesion of the nose, e.g.
rhinosporidiosis.
3. Foreign bodies.
Non-living: Any neglected foreign body, rhinolith.
Living: Maggots leeches.
4. Neoplasms of nose and paranasal sinuses.
Benign: Haemangioma, papilloma.
Malignant: Carcinoma or sarcoma.
5. Atmospheric changes. High altitudes, sudden decompression
(Caisson's disease).
6. Deviated nasal septum.
Nasopharynx
1. Adenoiditis
2. Juvenile angiofibroma
3. Malignant tumours
B. General Causes
1. Cardiovascular system. Hypertension, arteriosclerosis,
mitral stenosis, pregnancy (hypertension and
hormonal).
2. Disorders of blood and blood vessels. Aplastic anaemia,
leukaemia, thrombocytopenic and vascular purpura,
haemophilia, Christmas disease, scurvy, vitamin K
deficiency, hereditary haemorrhagic telangectasia.
3. Liver disease. Hepatic cirrhosis (deficiency of factor
II, VII, IX & X).
4. Kidney disease. Chronic nephritis.5. Drugs. Excessive use of salicylates and other analgesics
(as for joint pains or headaches), anticoagulant
therapy (for heart disease).
6. Mediastinal compression. Tumours of mediastinum
(raised venous pressure in the nose).
7. Acute general infection. Influenza, measles, chickenpox,
whooping cough, rheumatic fever, infectious
mononucleosis, typhoid, pneumonia, malaria, dengue
fever .
8.Vicarious Menstruation
C. Idiopathic
Many times the cause of epistaxis is not clear.
SITES OF EPISTAXIS
1. Little's area. In 90% cases of epistaxis, bleeding
occurs from this site.
2. Above the level of middle turbinate. Bleeding from
above the middle turbinate and corresponding area
on the septum is often from the anterior and posterior
ethmoidal vessels (internal carotid system).
3. Below the level of middle turbinate. Here bleeding is from
the branches of sphenopalatine artery. It may be
hidden, lying lateral to middle or inferior turbinate
and may require infrastructure of these turbinates
for localisation of the bleeding site and placement of
packing to control it.
4. Posterior part of nasal cavity. Here blood flows
directly into the pharynx.
5. Diffuse. Both from septum and lateral nasal wall.
This is often seen in general systemic disorders and
blood dyscrasias.
6. Nasopharynx.
CLASSIFICATION OF EPISTAXIS
Anterior Epistaxis
When blood flows out from the front of nose with the
patient in sitting position.
Posterior Epistaxis
Mainly the blood flows back into the throat. Patient may
swallow it and later have a "coffee coloured" vomitus.
This may erroneously be diagnosed as haematemesis.
Management
In any case of epistaxis, it is important to know:
1. Mode of onset. Spontaneous or finger nail trauma.
2. Duration and frequency of bleeding.
3. Amount of blood loss.
4. Side of nose from where bleeding is occurring.
5. Whether bleeding is of anterior or posterior type.
6. Any known bleeding tendency in the patient or
family.
7. History of known medical ailment (hypertension,
leukaemias, mitral valve disease, cirrhosis, nephritis).
8. History of drug intake (analgesics, anticoagulants,
etc.). .
First Aid
Most of the time, bleeding occurs from the Little's area
and can be easily controlled by pinching the nose with
thumb and index finger for about 5 minutes. This compresses
the vessels of the Little's area. In Trotter's method
patient is made to sit, leaning a little forward over a basin
to sp it any blood, and breathe quietly from the mouth.
Cold compresses should be applied to the nose to cause
reflex vasoconstriction.
Cauterisation
ThiS IS useful ll1 anterior epistaxIs when bleedll1g point
has been located. The area is first anaesthetised and the
bleeding point cauterised with a bead of silver nitrate or
coagulated with electrocautery.
Anterior Nasal Packing
In cases of active anterior epistaxis, nos~ is cleared of blood
clots by suction and attempt is made to localise the bleeding
site. In minor bleeds, from the accessible sites, cauterisation
of the bleeding area can be done. If bleeding is
profuse and/or the site of bleeding is difficult to localise,
anterior packing should be done. For this, use a ribbon
gauze soaked with liquid paraffin. About 1 metre gauze
(2.5 cm wide in adults and 12 mm in children) is required
for each nasal cavity. First, few centimetres of gauze are
folded upon itself and inserted along the floor, and then
the whole nasal cavity is packed tightly by layering the
gauze from floor to the roof and from before backwards.
Packing can also be done in vertical layers from back to
the front. One or both cavities may need to
be packed. Pack can be removed after 24 hours if bleeding
has stopped. Sometimes, it has to be kept for 2 to 3 days;
in that case, systemic antibiotics should be given to prevent
sinus infection and toxic shock syndrome.
Posterior Nasal Packing
It is required for patients bleeding posteriorly into the
throat. A postnasal pack is first prepared by tying three
silk ties to a piece of gauze rolled into the shape of a
cone. A rubber catheter is passed through the nose and
its end brought out from the mouth (Fig. 33.4). Ends of
the silk threads are tied to it and catheter withdrawn
from nose. Pack, which follows the silk thread, is now
guided into the nasopharynx with the index finger.
Anterior nasal cavity is now packed and silk threads tied
over a dental roll. The third silk thread is cut short and
allowed to hang in the oropharynx. It helps in easy
removal of the pack later. Patients requiring postnasal
pack should always be hospitalised. Instead of postnasal
pack, a Foley's catheter can also be used . The bulb is
inflated with saline and pulled forward so that choana
is blocked and then an anterior nasal pack is kept in the
usual manner. These days nasal balloons are also available.
A nasal balloon has two bulbs, one for
the postnasal space and the other for nasal cavity.
Endoscopic Cautery
Posterior bleeding point can sometimes be better located
with an endoscope. It can be coagulated with suction
cautery. Local anaesthesia with sedation may be required.
Elevation of Mucoperichondrial Flap and
SMR Operation
In case of persistent or recurrent bleeds from the septum,
just elevation of mucoperichondrial flap and then repositioning
it back helps to cause fibrosis and constrict
blood vessels. SMR operation can be done to achieve the
same result or remove any septal spur which is sometimes
the cause of epistaxis.
Ligation of Vessels
(a) External carOM. When bleeding is from the external
carotid system and the conservative measures have
failed, ligation of external carotid artery above the
origin of superior thyroid artery should be done. It is
avoided these days in favour of embolisation or
ligation of more peripheral branches.
(b) Maxilla?")' arte?")'. Ligation of this artery is done in
uncontrollable posterior epistaxis. Approach is via
Caldwell-Luc operation. Posterior wall of maxillary
sinus is removed and the maxillary artery or its
branches are blocked by applying clips.
Endoscopic ligation of the maxillary artery can
a lso be done through nose.
(c) Ethmoidal arteries. In anterosuperior bleeding above
the middle turbinate, not controlled by packing,
anterior and posterior ethmoidal arteries which supply
this area, can be ligated. The vessels are exposed
in the medial wall of the orbit by an external ethmoid
incision.
General Measures in Epistaxis
1. Make the patient sit up with a back rest and record any
blood loss taking place through sp itting or vomiting.
2. Reassure the patient. Mild sedation should be given.
3. Keep check on pulse, BP and respiration.
4. Maintain haemodynamics. Blood transfusion may
be required.
S. Antibiotics may be given to prevent sinusitis, if
pack is to be kept beyond 24 hours.
6. Intermittent oxygen may be required in patients
with bilateral packs because of increased pulmonary
resistance from nasopulmonary reflex.
7. Investigate and treat the patient for any underlying
local or general cause.

Acute Maxillary Sinusitis

Aetiology
1. Most commonly, it is viral rhinitis which spreads to
involve the sinus mucosa. This is followed by bacterial
invasion.
2. Diving and swimming in contaminated water.
3. Dental infections are important source of maxillary
sinusitis. Roots of premolar and molar teeth are related
to the floor of sinus and may be separated only by a
thin layer of mucosal covering. Periapical dental
abscess may burst into the sinus; or the root of a tooth,
during extraction, may be pushed into the sinus. In
case of oroantral fistula, following tooth extraction,
bacteria from oral cavity enter the maxillary sinus.
4. Trauma to the sinus such as compound fractures, penetrating
injuries or gun shot wounds may be followed
by sinusitis.
Predisposing factors. One or more of the predisposing
factors enumerated for sinusitis in general may be
responsible for acute or recurrent infection.
Clinical Features
Clinical features depend on (a) severity of inflammatory
process and (b) efficiency of ostium to drain the exudates.
Closed ostium sinusitis is of greater severity and leads
more often to complications.
1. Constitutional symptoms consist of fever, general malaise
and body ache. They are the result of toxaemia.
2. . Headache. Usually, this is confined to forehead and
may thus be confused with frontal sinusitis.
3. Pain. Typically, it is situated over the upper jaw, but
may be referred to the gums or teeth. For this reason
patient may primarily consult a dentist. Pain is aggravated
by stooping, coughing or chewing. Occasionally,
pain is referred to the ipsilateral supraorbital region
and thus may simulate frontal sinus infection.
4. Tenderness. Pressure or tapping over the anterior
wall of antrum produces pain.
5. Redness and oedema of cheek. Commonly seen in
children. The lower eyelid may become puffy.
6. Nasal discharge. Anterior rhinoscopy shows pus or
mucopus in the middle meatus. Mucosa of the middle
meatus and turbinate may appear red and
swollen.
Postural test. If no pus seen in the middle meatus, it is
decongested with a pledget of cotton soaked with a
vasoconstrictor and the patient is made to sit with
the affected sinus turned up. Examination after 10-15
minutes may show discharge in the middle meatus.
7. Post nasal discharge. Pus may be seen on the upper
soft palate on posterior rhinoscopy.
Diagnosis
Transillumination test. Affected sinus will be found
opaque.
X-rays. Waters' view will show either an opacity or a
fluid level in the involved sinus.
Treatment
Medical
1. Antimicrobial drugs. Ampicillin and amoxicillin are
quite effective and cover a wide range of organisms.
Erythromycin or doxycycline or cotrimoxazole are
equally effective and can be given to those who are
sensitive to penicillin. f3-lactamase-producing strains
of H. inf/uenzae and M. catarrhalis may necessitate
the use of amoxicillin/clavllianic acid or cefllroxime
axetil. Sparfloxacin is also effective, and has the
advantage of single daily dose.
2. Nasal decongestant drops. 1 % ephedrine or 0.1 % xylo or
oxymetazoline are used as nasal drops or sprays to
decongest sinus ostium and encourage drainage.
3. Steam inhalation. Steam alone or medicated with
menthol or Tr. Benzoin Co. provides symptomatic
relief and encourages sinus drainage. Inhalation
should be given 15 to 20 minutes after nasal decongestion
for better penetration.
4. Analgesics. Paracetamol or any other suitable analgesic
should be given for relief of pain and headache.
S. Hot fomentation. Local heat to the affected sinus is
often soothing and helps in the resolution of inflammation.
Surgical
Antral lavage. Most cases of acute maxillary sinusitis
respond to medical treatment. Lavage is rarely necessary.
It is done only when medical treatment has failed and
that too only under cover of antibodies.
Complications
1. Acute maxillary sinusitis may change to subacute or
chronic sinusitis.
2. Frontal sinusitis. Frontonasal duct which opens in middle
meatus is obstructed due to inflammatory oedema.
3. Osteitis or osteomyelitis of the maxilla.
4. Orbital cellulitis Or abscess. Infection spreads to the
orbit either directly, from the roof of maxillary sinus
or indirectly, after involvement of ethmoid sinuses.

Chronic Maxillary Sinusitis

Sinus infection lasting for months or years is called
chronic sinusitis. Most important cause of chronic sinusitis
is failure of acute infection to resolve.
Pathophysiology
Acute infection destroys normal ciliated epithelium
impairing drainage from the sinus. Pooling and stagnation
of secretions in the sinus invites infection.
Persistence of infection causes mucosal changes, such as
loss of cilia, oedema and polyp formation, thus continuing
the vicious cycle
Pathology
In chronic infections, process of destruction and
attempts at healing proceed simultaneously. Sinus
mucosa becomes thick and polypoidal (hypertrophic
sinusitis) or undergoes atrophy (atrophic sinusitis).
urface epithelium may show desquamation, regeneration
or metaplasia. Submucosa is infiltrated with lymphocytes
and plasma cells and may show microabscesses,
granulations, fibrosis or polyp formation.
Bacteriology
Mixed aerobic and anaerobic organisms are often
present.
Clinical Features
Clinical features are often vague and similar to those
of acute sinusitis but of lesser severity. Purulent nasal
discharge is the commonest complaint. Foul-smelling
discharge suggests anaerobic infection. Local pain and
headache are often not marked except in acute exacerbations.
Some patients complain of nasal stuffiness and
anosmia.
Diagnosis
1. X-ray of the involved sinus may show mucosal
thickening or opacity.
2. X-rays after injection of contrast material may show
soft tissue changes in the sinus mucosa.
3. CT scan is particularly useful in ethmoid and sphenoid
sinus infections and has replaced studies with
contrast materials.
4. Aspiration and irrigation: Finding of pus in the sinus
is confirmatory.
Treatment
It is essential to search for underlying aetiological factors
which obstruct sinus drainage and ventilation. A workup
for nasal allergy may be required. Culture and sensitivity
of sinus discharge helps in the proper selection of
an antibiotic.
Initial treatment of chronic sinusitis is conservative,
including antibiotics, decongestants, antihistaminics and
sinus irrigations. More often, some form of surgery is
required either to provide free drainage and ventilation
or radical surgery to remove all irreversible diseases so as
to provide wide drainage or to obliterate the sinus.
Recently, endoscopic sinus surgery is replacing radical
operations on the sinuses and provides good drainage
and ventilation. It also avoids external incisions.
Surgeries For Chronic Maxillary Sinusitis:
1. Antral puncture and irrigation. Sinus cavity is irrigated
with a cannula passed through the inferior
meatus. Removal of pus and exudates helps the sinus
mucosa to revert to normal.
2. Intranasal antrostomy. It is indicated if sinus irrigations
fail to resolve infection. A window is created
in the inferior meatus to provide aeration to the
sinus and its free drainage.
3. Caldwell-Luc operation. In this operation, antrum is
entered through its anterior wall by a sublabial incision.
All irreversible diseases are removed and a
window is created between the antrum and inferior
meatus.

Complications Of Sinusitis

A. Local:

(i) Mucocele/Mucopyocele
(ii) Mucous retention cyst
(iii) Osteomyelitis
- Frontal bone
(more common)
- Maxilla

B. Orbital:

(i) Preseptal inflammatory
oedema of lids
(ii) Subperiosteal abscess
(iii) Orbital cellulitis
(iv) Orbital abscess
(v) Superior orbital fissure
syndrome
(vi) Orbital apex syndrome

C. Intracranial:

(i) Meningitis
(ii) Extradural abscess
(iii) Subdural abscess
(iv) Brain abscess
(v) Cavernous sinus
thrombosis

D. Descending infections(otitis media, pharyngitis, tonsillitis, Persistent laryngitis and tracheobronchitis)
E. Focal infections(polyarthritis, tenosynovitis, fibrositis)

Killian's Dehiscence, Waldeyer's Ring And Pharyngeal Spaces

Killian's Dehiscence

Inferior constrictor muscle has two parts; thyropharyngeus
with oblique fibres and cricopharyngeus with transverse
fibres. Between these two parts exists a potential
gap called Killian's dehiscence. It is also called the "gateway
of tears" as perforation can occur at this site during
oesophagoscopy. This is also the site for herniation of
pharyngeal mucosa in cases of pharyngeal pouch.

Waldeyer's Ring:

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

Pharyngeal Spaces

There are two potential spaces in relation to the pharynx
where abscesses can form.
1. Retropharyngeal space, situated behind the pharynx
and extending from the base of skull to the bifurcation
of trachea (see page 246).
2. Parapharyngeal space, situated on the side of pharynx.
It contains carotid vessels, jugular vein, last
four cranial nerves and cervical sympathetic chain

ADENOIDS

Anatomy and Physiology
The nasopharyngeal tonsils, commonly called "adenoids",
is situated at the junction of the roof and posterior wall of
the nasopharynx. It is composed of vertical ridges of lymphoid
tissue separated by deep clefts and covered by ciliated
columnar epithelium. Unlike palatine tonsils,
adenoids have no crypts and no capsule. Adenoid tissue is
present at birth, shows physiological enlargement up to the
age of six years, and then tends to atrophy at puberty and
almost completely disappears by the age of 20.
Adenoids receive their blood supply from :
(i) Ascending palatine branch of facial.
(ii) Ascending pharyngeal branch of external carotid.
(iii) Pharyngeal branch of the third part of maxillary
artery.
(i v) Ascending cervical branch of inferior thyroid
artery of thyrocervical trunk.
Lymphatics from the adenoid drain into upper jugular
nodes directly or indirectly via retropharyngeal and parapharyngeal
nodes.
Aetiology
Adenoids are subject to physiological enlargement in
childhood. Certain children have a tendency to generalised
lymphoid hyperplasia in which adenoids also take
part.
Recurrent attacks of rhinitis, sinusitis or chronic tonsillitis
may cause chronic adenoid infection and hyperplasia.
Allergy of the upper respiratory tract may also contribute
to the enlargement of adenoids.
Clinical Features
Symptoms and signs depend not merely on the absolute
size of the adenoid mass but are rel ative to the available
space in the nasopharynx.
Enlarged and infected adenoids may cause nasal, aural
or general symptoms.
A. Nasal Symptoms
1. . Nasal obstruction is the commonest symptom. This
leads to mouth breathing. Nasal obstruction also
interferes with feeding or suckling a child. As respiration
and feeding cannot take place simultaneously,
a child with adenoid enlargement fails to
thrive. .
2. Nasal discharge. It is partly due to choanal obstruction,
as the normal nasal secretions cannot drain into
nasopharynx and partly due to associated chronic
rhinitis. The child often has a wet bubbly nose.
3. Sinusitis. Chronic maxillary sinusitis is commonly
associated with adeno ids. It is due to persistence of
nasal discharge and infection. Reverse is also true that
a primary maxillary sinusitis may lead to infected and
enlarged adenoids.
4. Epistaxis. When adeno ids are acutely inflamed, epistaxis
can occur with nose blowing.
5. Voice change. Vo ice is tone less and loses nasal quality
due to nasal obstruction.
B. Aural Symptoms
1. Tubal obstruction . Adenoid mass blocks the
eustachian tube leading to retracted tympaniC membrane
and conductive hearing loss.
2. Recurrent attacks of acute otitis media may occur due
to spread of infection via the eustachian tube.
3. Chronic suppurative otitis media may fail to resolve in
the presence of infected adenoids.
4. Serous otitis media. Adenoids form an important cause
of serous otit is media in children. The waxing and
waning size of adeno ids causes intermittent eustachian
tube obstruction with fluctuating hearing loss.
c. General Symptoms
1. Adenoid facies: Chronic nasal obstruction and
mouth breathing lead to characteristic facia l appearance
called adenoid facies. The child has an elongated
face with dull expression, open mouth
prominent and crowded upper teeth, and hitched up
upper lip. Nose gives a pinched-in appearance due
to disuse atrophy of alae nasi. Hard palate in the;e
cases is highly arched as the moulding action of the
tongue on palate is lost.
2. Pulmonary hypertension. Long-stand ing nasal
obstruction due to adenoid hypertrophy can cause
pulmonary hypertension and cor pu lmonale.
Diagnosis
Examination of postnasal space is possible in some young
children and an adenoid mass can be seen with a mirror.
A rigid or a flexible nasopharyngoscope is also useful [
see details of the nasopharynx. Soft tissue lateral radiograph
of nasopharynx will reveal the size of adenoid
and also the extent to which nasopharyngeal air Sp8 C~
has been compromised. Detailed nasal exam·
ination shou ld always be conducted to exc lude otht'"
causes of nasal obstruction.
Treatment
When symptoms are not marked, breathing exercises,
decongestant nasal drops and antihistaminics for any coexistent
nasal allergy can cure the condition without
resort to surgery.
When symptoms are marked, adenoidectomy is done.

Nasal Septum: Anatomy

Nasal septum consists of three parts:
1. Columellar septum. It is formed of columella
containing the medial crura of alar cartilages united
together by fibrous tissue and covered on either side by
skin.
2. Membranous septum. It consists of double layer
of skin with no bony or cartilaginous support. It lies
between the columella and the caudal border of septal
cartilage. Both columellar and membranous parts are
freely movable from side to side.
3. Septum proper. It consists of osteocartilaginous
framework, covered with nasal mucous membrane.
Its principal constituents are:
(i) the perpendicular plate of ethmoid
(i i) the vomer, and
(iii) a large septal (quadrilateral) cartilage wedged
between the above two bones anteriorlv. Other
bones which make minor contribution- at the
periphery are: crest of nasal bones, nasal spine of
frontal bone, rostrum of sphenoid, crest of palatine
bones and the crest maxilla, and the anterior nasal
spine of maxilla.
Septal cartilage not only forms a partition between the
right and left nasal cavities but also provides support to the
tip and dorsum of cartilaginous part of nose. Its destruction,
e.g. in septal abscess, injuries, tuberculosis or excessive
removal during septal surgery, leads to depression of lower
part of nose and drooping of the nasal tip .
Septal cartilage lies in a groove in the anterior edge of
vomer and rests anteriorly on anterior nasal spine. During
trauma, it may get dislocated from anterior nasal spine or

vomerine groove causing caudal septal deviation or septa
spur respectively. This compromises the nasal airway.
Septal cartilage is also intimately related to the upper lateral
cartilages of nose and is in fact fused with them in the
upper third. For this reason septal deviation may be associated
with deviation of cartilaginous part of external nose.

Blood Supply:

Internal Carotid System
(a) Anterior ethmoidal artery} Branches of ophthalmic
(b) Posterior ethmoidal artery artery
External Carotid System
(a) Sphenopalatine artery (branch of maxillary artery)
gives nasopalatine and posterior medial nasal
branches.
(b) Septal branch of greater palatine artery (Br. of maxillary
artery).
(c) Septal branch of superior labial artery (Br. of facial
artery) .

Nerve supply:

Nasal septum is supplied by branches of sphenopalatine ganglion and the anterior ethmoidal nerve.

Little's area or Kiesselbach's plexus: This is the vascular
area in the antero-inferior part of nasal septum ju •
above the vestibule. Anterior ethmoidal, sphenopalatine
greater palatine and septal branch of superior labial arteries
and their corresponding veins form an anastomostis
here. This is the commonest site for epistaxis. This is also
the site for origin of the "bleeding polypus" (haemangioma)
of nasal septum.