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SECTION II — Diseases of Nose and Paranasal Sinuses
TABLE 28.1 GRANULOMATOUS DISEASE OF NOSE
Bacterial Fungal Unspecified cause
Rhinoscleroma Rhinosporidiosis Wegener’s
granulomatosis
Syphilis Aspergillosis Nonhealing midline
granuloma
Tuberculosis Mucormycosis
Lupus Candidiasis Sarcoidosis
Leprosy Histoplasmosis
Blastomycosis
Figure 28.1. Rhinoscleroma nose.
Rare
TUBERCULOSIS
Primary tuberculosis of nose is rare. More often it is secondary to lung tuberculosis. Anterior part of nasal septum
and anterior end of inferior turbinate are the sites commonly involved. First, there is nodular infiltration followed later by ulceration and perforation of nasal septum
in its cartilaginous part.
Diagnosis can be made on biopsy and special staining
of sections for acid fast bacilli and culture of organisms.
Treatment is antitubercular drugs.
LUPUS VULGARIS
It is a low-grade tuberculous infection commonly affecting nasal vestibule or the skin of nose and face. The skin
lesions manifest characteristically as brown, gelatinous
nodules called “apple-jelly” nodules. In the vestibule, it
presents as chronic vestibulitis. Perforation may occur in
the cartilaginous part of nasal septum.
It is difficult to isolate tubercle bacilli by culture, how-
ever, biopsy of the lesion is useful to make the diagnosis.
Treatment is the same as for tuberculosis of nose.
LEPROSY
Leprosy is very common in the tropics and is widely prevalent in India. It is caused by Mycobacterium leprae. The
nose is involved as a part of systemic disease, more often in the lepromatous than tuberculoid or dimorphous
forms of disease.
Infection starts in the anterior part of nasal septum and
anterior end of inferior turbinate. Initially, there is excessive nasal discharge with red and swollen mucosa. Later,
crusting and bleeding supervene. Nodular lesions on the
septum may ulcerate and cause perforation. Late sequelae
of disease are atrophic rhinitis, depression of bridge of
nose and destruction of anterior nasal spine with retrusion of the columella (Figure 28.3).
Diagnosis can be made from the scrapings of nasal mucosa and biopsy. Acid-fast lepra bacilli can be seen in the
foamy appearing histiocytes called lepra cells.
Treatment is with dapsone, rifampin and isoniazid.
Reconstruction procedures are required when disease is
inactive.
Figure 28.2. Rhinoscleroma showing foamy Mikulicz cells (arrow)
and lymphocytic infiltration (arrowheads) (H&E, x400). Mikulicz cells
contain Gram-negative bacteria which can be better appreciated in sections stained with Giemsa stain and examined under oil immersion lens.
Scan to play Granulomatous Diseases of Nose I.
irrigation with alkaline solution. Bony and cartilaginous
sequestra should also be removed. Cosmetic deformity is
corrected after disease becomes inactive.
Complications
Syphilis can lead to vestibular stenosis, perforations of
nasal septum and hard palate, secondary atrophic rhinitis
and saddle nose deformity.
Figure 28.3. Leprosy nose.
Chapter 28 — Granulomatous Diseases of Nose
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FUNGAL INFECTIONS
RHINOSPORIDIOSIS (Figure 28.4 )
It is a chronic granulomatous disease caused by Rhinosporidium seeberi and affects both man and animals.
Epidemiology
Most of the cases come from India, Sri Lanka and Pakistan
though cases have been reported from Africa (Kenya, Tanzania, Rwanda, Burkina Faso, Chad and Egypt), South
America (Argentina, Brazil), North America, Europe and
Canada. No case is reported from Australia.
In India, disease is more common in the southern
states. It is prevalent in the states of Tamil Nadu, Kerala,
Madhya Pradesh, Chhattisgarh, Puducherry and Andhra
Pradesh. A few cases are also reported from Punjab and
Haryana.
Disease is also seen to involve animals such as cows,
bulls, horses, mules and dogs where men and animals
share the same infected ponds.
Aetiologic Agent (Figure 28.5)
It has long been considered to be a fungus but it has
been difficult to classify this organism. It has not been
cultured so far. However, some consider it to be a protozoan or a fish parasite belonging to the DRIP clade
(Dermocystidium, Rosette agent, Ichthyophonus and
Psorospermum).
Life Cycle
Three stages have been recognized in the life cycle of the
organism: trophic stage, development of sporangia and
production of endospores (Figure 28.6).
(a) Trophic stage. The endospore is oval or rounded,
6–8 µm in size, clear cytoplasm, vesicular nucleus with
a nucleolus and a covering of chitin. It gradually increases in size, begins to divide cytoplasm and nucleus
forming small endospores by several divisions. Trophocyte becomes large filled with young endospores.
(a) Development of sporangium. The mature tropho-
cyte then develops into sporangium. A sporangium
Figure 28.4. Rhinosporidiosis presenting as (A) a polypoidal mass protruding through the naris and (B) multiple sites of involvement, viz. nose,
conjunctiva and tongue.
Scan to play Granulomatous Diseases of Nose II.
Figure 28.5. (A) Histologic section showing rhinosporidiosis (blue arrow) evoking mixed inflammatory response (H&E, x40). (B) Histologic
section showing sporangium (blue arrow) which is fully packed with immature sporoblasts at the periphery and mature ones at the centre
(H&E, x200).
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(b) Production of endospores. Sporangia filled with en-
SECTION II — Diseases of Nose and Paranasal Sinuses
Figure 28.6. Life cycle of rhinosporidiosis.
is 200–250 µm in diameter, contains 12,000–16,000
endospores. It has a thick wall consisting of two layers:
outer chitinous and inner cellulose layer.
Endospores mature with the formation of mucoid
and chitinous wall. Sporangium filled with thousands
of endospores develops a germinal pore ready to burst
and liberate the endospores.
dospores develop a high internal pressure and rupture,
liberating endospores into the surrounding tissue.
If internal pressure is not high, spores are liberated
one by one without breaking the wall. After liberation endospores start their life as trophic stage. Some
endospores are carried by lymphatic channels to the
blood stream to cause disseminated form of disease
(Figure 28.4B).
Clinical Features
The disease mostly affects nose and nasopharynx; other
sites such as lip, palate, conjunctiva, epiglottis, larynx,
trachea, bronchi, skin, vulva and 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.
In early stages, the patient may complain of nasal
discharge which is often blood tinged and nasal stuffiness. Sometimes, frank epistaxis is the only presenting
complaint.
Diagnosis
This 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
Complete excision of the mass with diathermy knife
and cauterization of its base. Recurrence may occur
after surgical excision. Not many drugs are effective
against the disease. Dapsone has been tried with some
success.
ASPERGILLOSIS
The usual causative organisms are Aspergillus niger, A. fumigatus or A. flavus. They invade nasal tissues when host’s
defence mechanisms are compromised due to immunosuppressive drugs.
Clinical Features
Clinical features are those of acute or subacute rhinitis or
sinusitis. A black or greyish membrane is seen in the nasal
mucosa. Exploration of maxillary sinus reveals a fungus
ball containing semisolid cheesy-white or blackish material. The organisms can be seen on special staining for
fungus.
Treatment
Surgical debridement of the involved tissues and antifungal drugs, e.g. Amphotericin B. Repeated irrigation of the
involved area with application of 1% solution of gentian
violet is also useful.
MUCORMYCOSIS
It is fungal infection of nose and paranasal sinuses which
may prove rapidly fatal. It is seen in uncontrolled diabetics or in those taking immunosuppressive drugs. From
the nose and sinuses, infection can spread to orbit, cribriform plate, meninges and brain. The rapid destruction
associated with the disease is due to affinity of the fungus
to invade the arteries and cause endothelial damage and
thrombosis. Typical finding is the presence of a black necrotic mass filling the nasal cavity and eroding the septum and hard palate. Special stains help to identify the
fungus in tissue sections.
Treatment is by amphotericin B and surgical debridement of the affected tissues and control of underlying
predisposing cause.
OTHER FUNGAL INFECTIONS
Other fungal infections of nose such as candidiasis, histoplasmosis, blastomycosis, etc. are rare.
GRANULOMAS OF UNSPECIFIED
AETIOLOGY
WEGENER’S GRANULOMATOSIS
Aetiology
It is a systemic disorder of unknown aetiology involving
mainly the upper airways, lungs, kidneys and the skin.
Chapter 28 — Granulomatous Diseases of Nose
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It should be differentiated from nonhealing midline
granuloma because the treatment of the two is quite
different.
Clinical Features
Early symptoms of Wegener’s granulomatosis include
clear or blood-stained nasal discharge which later becomes purulent. The patient often complains of “persistent cold” or “sinus.” Nasal findings include crusting,
granulations, septal perforation and a saddle nose. Destruction may also involve eyes, orbit, palate, oral cavity
or oropharynx. Middle ear can also be involved.
General systemic symptoms include anaemia, fatigue,
night sweats and migratory arthralgias.
Involvement of lung is manifested by cough and
sometimes haemoptysis. X-ray chest may show a single
or multiple cavity lesions.
Sooner or later, kidneys are also involved. Urine examination will show red cells, casts and albumin. Serum
creatinine level is raised. Renal failure is the usual cause of
death in these patients.
Diagnosis
Biopsy from the nose is diagnostic. It shows necrosis
and ulceration of mucosa, epithelioid granuloma and
necrotizing vasculitis involving small arteries or veins.
Erythrocyte sedimentation rate is raised.
Treatment
It consists of systemic steroids and cytotoxic drugs. Cyclophosphamide and azathioprine, both are found effective.
T-CELL LYMPHOMA
Earlier terms used to describe this lesion were midline
malignant lesion and polymorphic reticulosis.
It is a destructive lesion usually starting on one side of
nose involving the upper lip, oral cavity, maxilla and sometimes even extending to orbit. Histologically polymorphic
lymphoid tissue with angiocentric and angioinvasive features is seen. There is no vasculitis—a feature typical of Wegener’s granulomatosis. Unlike Wegener’s granulomatosis,
it is rapidly destructive and usually devoid of systemic involvement; there is absence of involvement of lung and
kidneys. Immunohistochemical studies of biopsy material
are necessary to establish diagnosis of T-cell lymphoma.
Localized T-cell lymphoma is treated by radiation while a
disseminated disease requires chemotherapy.
SARCOIDOSIS
It is a granulomatous disease of unknown aetiology resembling tuberculosis on histology but with the absence of caseation. It is a systemic disorder and the symptoms may
refer to involvement of lungs, lymph nodes, eyes or skin.
In the nose, it presents with submucosal nodules involving septum or the inferior turbinate with nasal obstruction, nasal pain and sometimes epistaxis. Nodules
may also form in the nasal vestibule or skin of face.
X-ray chest shows diffuse pulmonary infiltrate with hilar
adenopathy. Serum and urinary calcium levels are raised.
Biopsy of the lesions helps to establish the diagnosis.
Treatment is with systemic steroids. For nasal symptoms, steroids can be used locally as nasal spray.
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Chapter 29
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Miscellaneous Disorders
of Nasal Cavity
FOREIGN BODIES
AETIOLOGY
They are mostly seen in children and may be organic or
inorganic. Pieces of paper, chalk, button, pebbles and
seeds are the common objects. Pledgets of cotton or swabs
may be accidentally left in the nose.
CLINICAL FEATURES
Patient may present immediately if the history of foreign
body is known. If overlooked, the child presents with
unilateral nasal discharge which is often foul smelling
and occasionally bloodstained. It is a dictum that “If a
child presents with unilateral, foul-smelling nasal discharge,
foreign body must be excluded.” Occasionally, a radiograph
of the nose is useful to confirm and localize a foreign
body if it is radio-opaque. In addition to overlooked foreign body in the nose, other important causes for unilateral blood-stained discharge in a child are rhinolith, nasal
diphtheria, nasal myiasis and acute or chronic unilateral
sinusitis.
TREATMENT
Pieces of paper or cotton swabs can be easily removed
with a pair of forceps. Rounded foreign bodies can be removed by passing a blunt hook (a eustachian catheter is a
good instrument) past the foreign body and gently dragging it forward along the floor. In babies and uncooperative children, general anaesthesia with cuffed endotracheal tube is used. Patient is placed in Rose’s position,
a pack is inserted into the nasopharynx and the foreign
body retrieved with a forceps or a hook. Foreign bodies
lodged far behind in the nose may need to be pushed
into the nasopharynx before removal. A nasal endoscope
is very useful to locate the foreign body and carefully
remove it.
COMPLICATIONS
A foreign body left in the nose may result in:
1. nasal infection and sinusitis.
2. rhinolith formation.
3. inhalation into the tracheobronchial tree.
RHINOLITH
AETIOLOGY
It is stone formation in the nasal cavity. A rhinolith usually forms around the nucleus of a small exogenous foreign
body, blood clot or inspissated secretions by slow deposition of calcium and magnesium salts. Over a period of
time, it grows into a large, irregular mass which fills the
nasal cavity and then may cause pressure necrosis of the
septum and/or lateral wall of nose.
CLINICAL FEATURES
Rhinoliths are more common in adults. Its common presentation is unilateral nasal obstruction and foul-smelling discharge which is very often bloodstained. Frank
epistaxis and neuralgic pain may result from ulceration
of the surrounding mucosa.
On examination, a grey brown or greenish-black
mass with irregular surface and stony hard feel is seen
in the nasal cavity between the septum and turbinates. It is often brittle and a portion of it may break
off while manipulating. Sometimes it is surrounded by
granulations.
TREATMENT
They are removed under general anaesthesia. Most of
them can be removed through anterior nares. Large
ones need to be broken into pieces before removal.
Some particularly hard and irregular ones require lateral
rhinotomy.
NASAL MYIASIS (MAGGOTS IN NOSE)
Maggots are larval forms of flies. They are seen to infest
nose, nasopharynx and paranasal sinuses causing extensive destruction (Figures 29.1 A, B, C and 29.2). Flies,
particularly of the genus Chrysomyia, are attracted by the
foul-smelling discharge emanating from cases of atrophic
rhinitis, syphilis, leprosy or infected wounds and lay eggs,
about 200 at a time, which within 24 h hatch into larvae.
In India, they are mostly seen from the month of August
to October.
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Figure 29.1. Maggot nose. (A) Swelling of the nose and puffy eyelids with serosanguinous nasal discharge. (B) Maggots have practically destroyed
the cheek and eye in this old and neglected lady. (C) Perforation of the palate (arrow).
SECTION II — Diseases of Nose and Paranasal Sinuses
CLINICAL FEATURES
In the first 3 or 4 days maggots produce intense irritation,
sneezing, lacrimation and headache. Thin blood-stained
discharge oozes from the nostrils. The eyelids and lips become puffy. Till this time patient is not aware of maggots.
He may present simply as a case of epistaxis. It is only
on the third or fourth day that the maggots may crawl
out of the nose. Patient has foul smell surrounding him.
Maggots cause extensive destruction to nose, sinuses, soft
tissue of face, palate and the eyeball. Fistulae may form
in the palate or around the nose. Death may occur from
meningitis.
TREATMENT
All visible maggots should be picked up with forceps.
Many of them try to retreat into darker cavities when
light falls on them. Instillation of chloroform water and
oil kills them. Nasal douche with warm saline is used to
Figure 29.2. (A) The maggot. (B) The fly responsible for maggots.
remove slough, crusts and dead maggots. A patient with
maggots should be isolated with a mosquito net to avoid
contact with flies which can perpetuate this cycle. All patients should receive instruction for nasal hygiene before
leaving the hospital.
NASAL SYNECHIA
Adhesion formation between the nasal septum and turbinates by scar tissue is often the result of injury to opposing surfaces of nasal mucosa. It can result from intranasal
operations such as septal surgery, polypectomy, removal
of foreign bodies, reduction of nasal fractures, endoscopic sinus surgery or even intranasal packing. Severe infections which cause ulcerative lesions in the nose can also
lead to synechia formation.
Nasal synechia (Figure 29.3) often cause nasal obstruction or may impede drainage from the sinuses resulting in
sinusitis, headache and nasal discharge.
Figure 29.3. Nasal synechia left.
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Chapter 29 — Miscellaneous Disorders of Nasal Cavity
PHYSIOLOGY
CSF forms a jacket of fluid round the brain and spinal
cord acting as a buffer against sudden jerks. It is secreted
by choroid plexuses in the lateral, third and fourth ventricles and is absorbed into the dural venous sinuses by
arachnoid villi. Villi have one-way valve mechanism allowing CSF of the subarachnoid space to be absorbed into
the blood but not vice versa. Total volume of CSF varies from 90 to 150 mL. It is secreted at the rate of about
20 mL/h (350-500 mL/day). Thus total CSF is replaced
three to five times every day. Normal CSF pressure at lumbar puncture is 50-150 mm H2O. CSF pressure rises on
coughing, sneezing, nose blowing, straining on stools or
lifting heavy weight–activities which should be avoided
in cases of CSF leak or after its repair.
AETIOLOGY
183
Treatment is removal of synechia and prevention of
the opposing raw surfaces to come into contact with each
other by placing a thin silastic or a cellophane sheet between them. This is changed every two or three days till
healing is complete.
CHOANAL ATRESIA
It is due to persistence of bucconasal membrane and
may be unilateral or bilateral, complete or incomplete,
bony (90%) or membranous (10%). Unilateral atresia
is more common and may remain undiagnosed until
adult life. Bilateral atresia presents with respiratory obstruction as the newborn, being a natural nose breather, does not breathe from mouth. Diagnosis of choanal
atresia can be made by (i) presence of mucoid discharge
in the nose, (ii) absence of air bubbles in the nasal discharge, (iii) failure to pass a catheter from nose to pharynx, (iv) putting a few drops of a dye (methylene blue)
into the nose and seeing its passage into the pharynx,
or (v) flexible nasal endoscopy, (vi) installing radioopaque dye into the nose and taking a lateral film, and
(vii) computed tomography (CT) scan in axial plane is
more useful.
Emergency management may be required in bilateral
choanal atresia to provide an airway. A feeding nipple
with a large hole provides a good oral airway (McGovern’s technique) and obviates the need for tracheostomy.
Definitive treatment consists of correction of atresia by
transnasal or transpalatal approach. The latter is usually
done at one and a half years. Choanal atresia can be corrected by using nasal endoscopes and drill. Removal of
a part of posterior nasal septum transnasally is another
option to treat such cases.
• Trauma. Most of the cases follow trauma. It can be acci-
dental or surgical. Surgical trauma includes endoscopic
sinus surgery, trans-sphenoidal hypophysectomy, nasal polypectomy or skull base surgery. In endoscopic
sinus surgery, CSF leak may be immediate or delayed
in onset.
• Inflammations. Mucoceles of sinuses, sinunasal polypo-
sis, fungal infection of sinuses and osteomyelitis, can
all erode the bone and dura.
• Neoplasms. Tumours, both benign and malignant, in-
vading the skull base.
• Congenital lesions. Meningocele, meningoencephaloce-
les and gliomas can have associated skull base defect.
• Idiopathic. Where cause is unknown and patient has
spontaneous leak.
SITES OF LEAKAGE
CSF from anterior cranial fossa reaches the nose via (i) cribriform plate, (ii) roof of ethmoid air cells or (iii) frontal sinus. CSF from middle cranial fossa follows injuries to
sphenoid sinus. In fractures of temporal bone, CSF reaches
the middle ear and then escapes through the eustachian
tube into the nose (CSF otorhinorrhoea) (Figure 29.4).
CSF RHINORRHOEA
DEFINITION
Leakage of CSF into the nose is called CSF rhinorrhoea. It
may be clear fluid or mixed with blood as in acute head
injuries.
Figure 29.4. Sites of leakage: (a) frontal sinus, (b) ethmoid sinus,
(c) sphenoid sinus, and (d) eustachian tube (temporal bone fracture).
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SECTION II — Diseases of Nose and Paranasal Sinuses
TABLE 29.1 DIFFERENCES BETWEEN CSF AND NASAL SECRETIONS
Features CSF fluid Nasal secretion
History Nasal or sinus surgery, head injury or intracranial tumour Sneezing, nasal stuffiness, itching in the
nose or lacrimation
Flow of discharge A few drops or a stream of fluid gushes down when
bending forward or straining; cannot be sniffed back
Character of discharge Thin, watery and clear Slimy (mucus) or clear (tears)
Taste Sweet Salty
Sugar content More than 30 mg/dL (Compare with sugar in CSF after
lumbar puncture as sugar is less in CSF in meningitis.)
Presence of β2 transferrin
Always present. It is specific for CSF Always absent
Continuous, no effect of bending forward or
straining. Can be sniffed back
Less than 10 mg/dL
DIAGNOSIS
There is history of clear watery discharge from the nose
on bending the head or straining. It may be seen on rising in the morning when patient bends his head (reser-
voir sign-fluid which had collected in the sinuses, particularly sphenoid, empties into the nose). CSF rhinorrhoea
should be differentiated from nasal discharge of allergic
or vasomotor rhinitis as the former is sudden, gushes in
drops when bending and cannot be sniffed back. Nasal
discharge, because of its mucus content, also stiffens the
handkerchief (Table 29.1).
CSF rhinorrhoea after head trauma is mixed with
blood and shows double target sign when collected on a
piece of filter paper. It shows central red spot (blood) and
peripheral lighter halo.
Nasal endoscopy can help to localize CSF leak in some
cases. Otoscopic/microscopic examination of the ear may
reveal fluid in the middle ear in cases of otorhinorrhoea.
LABORATORY TESTS
Beta-2 transferrin is a protein seen in CSF and not in the
nasal discharge. Its presence is a specific and sensitive test
and requires only a few drops of CSF. The specimen of
nasal discharge is tested for this protein. Perilymph and
aqueous humour are the only other fluids which contain
this protein.
Another protein called beta trace protein is also specific
for CSF and is widely used in Europe. It is secreted by
meninges and choroid plexus. Facilities to test these proteins are not easily available everywhere. Glucose testing
by oxidase peroxidase or biochemical estimation are no
longer used.
LOCALIZATION OF SITE
1. High-resolution CT scan. Cuts are taken at 1-2 mm.
Both coronal and axial cuts are important to see the
bony defects. Axial cuts show any defects of frontal or
sphenoid sinus.
2. MRI. T2-weighted image MRI is useful in depicting the
site of leak. It requires that CSF leak is active at the
time of scan. It is a noninvasive test. It is indicated also
if encephalocele or intracranial pathology is suspected.
3. Intrathecal fluorescein study. It can be done preop-
eratively to diagnose the site or intraoperatively at
the time of repair. It is an invasive procedure. Only
0.25-0.5 mL of 5% fluorescein diluted with 10 mL of
CSF is injected. Patient lies in 10° head down position for sometime. Dye can be detected intranasally
with the help of endoscope. Dye appears bright yellow
but when seen with a blue filter it appears fluorescent
green. One should examine olfactory cleft (cribriform
plate), middle meatus (frontal and ethmoidal sinuses),
sphenoethmoidal recess (sphenoid sinus) and area of
torus tubarius (temporal bone fracture) to localize the
lesion.
4. Use of intrathecal radioactive substances has been
abandoned.
5. CT cisternogram. It requires intrathecal injection
of iohexol and a CT scan to localize the site in cases
when beta-2 transferrin cannot be done. Now it is not
favoured by many.
TREATMENT
Early cases of post-traumatic CSF rhinorrhoea can be
managed by conservative measures such as bed rest, elevating the head of the bed, stool softeners, and avoidance
of nose blowing, sneezing and straining. Prophylactic
antibiotics can be used to prevent meningitis. Acetazolamide decreases CSF formation. These measures can be
combined with lumbar drain if indicated.
Surgical repair can be done by the following:
1. Neurosurgical intracranial approach.
2. Extradural approaches such as external ethmoidectomy for cribriform plate and ethmoid area, trans-septal sphenoidal approach for sphenoid and osteoplastic
flap approach for frontal sinus leak.
3. Transnasal endoscopic approach. With the advent
of endoscopic surgery for nose and sinuses, most of
the leaks from the anterior cranial fossa and sphenoid
sinus can be managed endoscopically with a success
rate of 90% with first attempt. Principles of repair
include:
(a) Defining the sites of bony defect (Figure 29.5). It
can be
(i) Cribriform plate
(ii) Lateral lamina close to anterior ethmoid artery
(iii) Roof of ethmoid
(iv) Frontal sinus leak
(v) Sphenoid sinus
(b) Preparation of graft site.
(c) Underlay grafting of the fascia extradurally fol-
lowed by placement of mucosa (as a free graft or
pedicled flap) (Figure 29.6).
Figure 29.5. Sites of bony defect: (a) cribriform plate and
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(b) ethmoid roof.
Chapter 29 — Miscellaneous Disorders of Nasal Cavity
Figure 29.6. Repair of CSF rhinorrhoea.
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(d) If bony defect is larger than 2 cm, it is repaired with
cartilage (from nasal septum or auricular concha)
followed by placement of mucosa.
(e) Placement of surgicel and gelfoam further strength-
ens the area. This is followed by a high antibiotic
smeared nasal pack.
Sometimes fat from the thigh or abdomen is used
to plug the defect in place of fascia graft.
(f) Lumbar drain if CSF pressure is high.
(g) Antibiotics
CSF leak from frontal sinus often requires osteoplastic
flap, operation and obliteration of the sinus with fat.
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