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SECTION II — Diseases of Nose and Paranasal Sinuses
Figure 26.3. DNS associated with high-arched palate.
Figure 26.1. Anatomy of nasal septum.
often overlooked. Even the history may not be forthcoming. Trauma may also be inflicted at birth during difficult
labour 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 palate 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 (Figure 26.3).
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
black Americans.
4. hereditary Factors. Several members of the same
family may have deviated nasal septum.
TYPES OF DNS (FIGURE 26.4)
Deviation may involve only the cartilage, bone or both
the cartilage and bone.
Figure 26.2. Septal fracture showing: (A) Jarjaway type. (B) Chevallet
type.
AETIOLOGY
Trauma and errors of development form the two important factors in the causation of deviated septum.
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
1. anterior dislocation. Septal cartilage may be dislocated into one of the nasal chambers. This is better appreciated by looking at the base of nose when patient’s head
is tilted backwards (Figure 26.5).
2. c-shaped deFormity. Septum is deviated in a simple
curve to one side. Nasal chamber on the concave side of
the nasal septum will be wider and may show compensatory hypertrophy of turbinates.
3. s-shaped deFormity. 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 cartilage. A spur may press on
the lateral wall and gives rise to headache. It may also
Figure 26.4. Types of deviated nasal septum.
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Chapter 26 — Nasal Septum and Its Diseases
Figure 26.6. Cottle test: On pulling the cheek away from the midline, the nasal valve opens, increasing the airflow from that side of the
nasal cavity.
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Figure 26.5. Anterior dislocation. Caudal border of septal cartilage
projects into right naris.
predispose to repeated epistaxis from the vessels stretched
on its convex surface.
5. thickening. It may be due to organized haematoma
or overriding of dislocated septal fragments.
CLINICAL FEATURES
DNS can involve any age and sex. Males are affected more
than females.
1. nasal obstruction. Depending on the type of septal
deformity, obstruction may be unilateral or bilateral. Respiratory currents pass through upper part of nasal cavity,
therefore, high septal deviations cause nasal 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 (i) vestibular (caudal septal dislocation, synechiae or stenosis), (ii) at the nasal valve (synechiae, usually
postrhinoplasty), (iii) attic (along the upper part of nasal septum due to high septal deviation, (iv) turbinal (hypertrophic turbinates or concha bullosa) and (v) choanal
(choanal atresia or a choanal polyp). Unilateral choanal
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 nasal valve. In this test, cheek is drawn laterally while the patient breathes quietly. If the nasal airway
improves on the test side, the test is positive and indicates
abnormality of the vestibular component of nasal valve
(Figure 26.6).
2. headache. Deviated septum, especially a spur, may
press on the lateral wall of nose giving rise to pressure
headache.
3. sinusitis. Deviated septum may obstruct sinus ostia
resulting in poor ventilation of the sinuses. Therefore, it
forms an important cause to predispose or perpetuate sinus infections.
4. epistaxis. Mucosa over the deviated part of septum
is exposed to the drying effects of air currents leading to
formation of crusts, which when removed cause bleeding.
Bleeding may also occur from vessels over a septal spur.
5. anosmia. Failure of the inspired air to reach the olfactory region may result in total or partial loss of sense of
smell.
6. external deFormity. Septal deformities may be associated with deviation of the cartilaginous or both the
bony and cartilaginous dorsum of nose, deformities of
the nasal tip or columella.
7. middle ear inFection. DNS also predisposes to middle ear infection.
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SECTION II — Diseases of Nose and Paranasal Sinuses
TREATMENT
Minor degrees of septal deviation with no symptoms 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 adults under local anaesthesia. It
consists of elevating the mucoperichondrial and mucoperiosteal flaps on either side of the septal framework by a
single incision made on one side of the septum, removing
the deflected parts of the bony and cartilaginous septum,
and then repositioning the flaps (see section on Operative
Surgery for details).
Septoplasty
It is a conservative approach to septal 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 (see Chapter 88).
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.
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 sterile needle. Larger haematomas are incised and drained
by a small anteroposterior 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 organize into fibrous tissue leading to a permanently thickened septum.
If secondary infection supervenes, it results in septal abscess with necrosis of cartilage and depression of nasal
dorsum.
SEPTAL ABSCESS
AETIOLOGY
Mostly, it results from secondary infection of septal haematoma. Occasionally, it follows furuncle of the nose or
upper lip. It may also follow acute infection such as typhoid or measles.
SEPTAL HAEMATOMA
AETIOLOGY
It is collection of blood under the perichondrium or periosteum of the nasal septum (Figure 26.7). It often results
from nasal trauma or septal surgery. In bleeding disorders,
it may occur spontaneously.
CLINICAL FEATURES
Bilateral nasal obstruction is the commonest presenting
symptom. This may be associated with frontal headache
and a sense of pressure over the nasal bridge.
CLINICAL FEATURES
There is severe bilateral nasal obstruction with pain and
tenderness over the bridge of nose. Patient may also complain of fever with chills and frontal headache. Skin over
the nose may be red and swollen. Internal examination of
nose reveals smooth bilateral swelling of the nasal septum
(Figure 26.8). Fluctuation can be elicited in this swelling.
Septal mucosa is often congested. Submandibular lymph
nodes may also be enlarged and tender.
Figure 26.7. Septal haematoma. Figure 26.8. Septal abscess.
Chapter 26 — Nasal Septum and Its Diseases
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169
Figure 26.9. Septal perforation.
TREATMENT
Abscess should be drained as early as possible. Incision
is made in the most dependent part of the abscess and a
piece of septal mucosa excised. Pus and necrosed pieces
of cartilage are removed by suction. Incision may require
to be reopened daily for 2–3 days to drain any pus or to
remove any necrosed pieces of cartilage. Systemic antibiotics are started as soon as diagnosis has been made and
continued at least for a period of 10 days.
COMPLICATIONS
Necrosis of septal cartilage often results in depression of
the cartilaginous dorsum in the supratip area and may
require augmentation rhinoplasty 2–3 months later.
Necrosis of septal flaps may lead to septal perforation.
Meningitis and cavernous sinus thrombosis following
septal abscess, though rare these days, can be serious
complications.
PERFORATION OF NASAL SEPTUM
(FIGURE 26.9)
AETIOLOGY
1. traumatic perForations. Trauma is the most common cause. Injury to mucosal flaps during SMR, cauterization of septum with chemicals or galvanocautery for
epistaxis and habitual nose picking are the common
forms of trauma. Occasionally, septum is deliberately perforated to put ornaments.
2. pathological perForations. They can be caused by:
1. Septal abscess.
2. Nasal myiasis.
3. Rhinolith or neglected foreign body causing pressure
necrosis.
Figure 26.10. Septal button for closure of perforation.
4. Chronic granulomatous conditions like lupus, tuberculosis and leprosy cause perforation in the cartilaginous part while syphilis involves the bony part. In
these cases, evidence of the causative disease may also
be seen in other systems of the body.
5. Wegener’s granuloma is a midline destructive lesion
which may cause total septal destruction.
3. drugs and chemicals
1. Prolonged use of steroid sprays in nasal allergy.
2. Cocaine addicts.
3. Workers in certain occupations, e.g. chromium
plating, dichromate or soda ash (sodium carbonate)
manufacture or those exposed to arsenic or its
compounds.
4. idiopathic. In many cases, there is no history of
trauma or previous disease and the patient may even be
unaware of the existence of a perforation.
CLINICAL FEATURES
Small anterior perforations cause whistling sound during inspiration or expiration. Larger perforations develop
crusts which obstruct the nose or cause severe epistaxis
when removed.
An attempt should always be made to find out the cause
before treatment of perforation. This may require biopsy
from the granulations or biopsy of the edge of the perforation. Inactive small perforations can be surgically
closed by plastic flaps. Larger perforations are difficult to
close. Their treatment is aimed to keep the nose crust-free
by alkaline nasal douches and application of a bland ointment. Sometimes, a thin silastic button can be worn to
get relief from the symptoms (Figure 26.10).
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Chapter 27
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Acute and Chronic Rhinitis
ACUTE RHINITIS
Acute rhinitis can be viral, bacterial or irritative type.
VIRAL RHINITIS
1. common cold (coryZa)
• Aetiology. It is caused by a virus. The infection is usu-
ally contracted through airborne droplets. Several
viruses (adenovirus, picornavirus and its subgroups
such as rhinovirus, coxsackie virus and enteric cytopathic human orphan virus) are responsible. Incubation period is 1–4 days and illness lasts for 2–3 weeks.
• Clinical features. To begin with, there is burning sensa-
tion at the back of nose soon followed by nasal stuffiness, rhinorrhoea and sneezing. Patient feels chilly
and there is low-grade fever. Initially, nasal discharge
is watery and profuse but may become mucopurulent due to secondary bacterial invasion. Secondary
invaders include Streptococcus haemolyticus, pneumococcus, Staphylococcus, Haemophilus influenzae, Kleb-
siella pneumoniae and Moraxella catarrhalis.
• Treatment. Bed rest is essential to cut down the
course of illness. Plenty of fluids are encouraged.
Symptoms can be easily controlled with antihistaminics and nasal decongestants. Analgesics are useful to relieve headache, fever and myalgia. Nonaspirin containing analgesics are preferable as aspirin
causes increased shedding of virus. Antibiotics are
required when secondary infection supervenes.
• Complications. The disease is usually self-limiting
and resolves spontaneously after 2–3 weeks, but occasionally, complications such as sinusitis, pharyngitis, tonsillitis, bronchitis, pneumonia and otitis
media may result.
2. inFluenZal rhinitis. Influenza viruses A, B or C are
responsible. Symptoms and signs are similar to those of
common cold. Complications due to bacterial invasion
are common.
membrane may form in the nose, which with attempted
removal causes bleeding.
Secondary bacterial rhinitis is the result of bacterial in-
fection supervening acute viral rhinitis.
diphtheritic rhinitis. Diphtheria of nose is rare these
days. It may be primary or secondary to faucial diphtheria
and may occur in acute or chronic form. A greyish membrane is seen covering the inferior turbinate and the floor
of nose; membrane is tenacious and its removal causes
bleeding. Excoriation of anterior nares and upper lip may
be seen. Treatment is isolation of the patient, systemic
penicillin and diphtheria antitoxin.
IRRITATIVE RHINITIS
This form of acute rhinitis is caused by exposure to dust,
smoke or irritating gases such as ammonia, formaline,
acid fumes, etc. or it may result from trauma inflicted on
the nasal mucosa during intranasal manipulation, e.g. removal of a foreign body. There is an immediate catarrhal
reaction with sneezing, rhinorrhoea and nasal congestion.
The symptoms may pass off rapidly with removal of the
offending agent or may persist for some days if nasal epithelium has been damaged. Recovery will depend on the
amount of epithelial damage and the infection that supervenes.
CHRONIC RHINITIS
Chronic nonspecific inflammations of nose include:
1. Chronic simple rhinitis.
2. Hypertrophic rhinitis.
3. Atrophic rhinitis.
4. Rhinitis sicca.
5. Rhinitis caseosa.
CHRONIC SIMPLE RHINITIS
3. rhinitis associated with exanthemas. Measles,
rubella and chickenpox are often associated with rhinitis
which precedes exanthemas by 2–3 days. Secondary infection and complications are more frequent and severe.
BACTERIAL RHINITIS
nonspeciFic inFections. It may be primary or secondary. Primary bacterial rhinitis is seen in children and is
usually the result of infection with pneumococcus, streptococcus or staphylococcus. A greyish white tenacious
Aetiology
Recurrent attacks of acute rhinitis in the presence of predisposing factors leads to chronicity. The predisposing
factors are:
1. Persistence of nasal infection due to sinusitis, tonsillitis and adenoids.
2. Chronic irritation from dust, smoke, cigarette smoking, snuff, etc.
3. Nasal obstruction due to deviated nasal septum, synechia leading to persistence of discharge in the nose.
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4. Vasomotor rhinitis.
5. Endocrinal or metabolic factors, e.g. hypothyroidism,
excessive intake of carbohydrates and lack of exercise.
Pathology
Simple chronic rhinitis is an early stage of hypertrophic rhinitis. There is hyperaemia and oedema of mucous
membrane with hypertrophy of seromucinous glands
and increase in goblet cells. Blood sinusoids particularly
those over the turbinates are distended.
Clinical Features
1. Nasal obstruction. Usually worse on lying and affects
the dependent side of nose.
2. Nasal discharge. It may be mucoid or mucopurulent,
thick and viscid and often trickles into the throat as
postnasal drip. Patient has a constant desire to blow
the nose or clear the throat.
3. Headache. It is due to swollen turbinates impinging
on the nasal septum.
4. Swollen turbinates. Nasal mucosa is dull red in colour. Turbinates are swollen; they pit on pressure and
shrink with application of vasoconstrictor drops (this
differentiates the condition from hypertrophic rhinitis). Middle turbinate may also be swollen and impinge
on the septum.
5. Postnasal discharge. Mucoid or mucopurulent discharge is seen on the posterior pharyngeal wall.
Treatment
1. Treat the cause with particular attention to sinuses,
tonsils, adenoids, allergy, personal habits (smoking or
alcohol indulgence), environment or work situation
(smoky or dusty surroundings).
2. Nasal irrigations with alkaline solution help to keep
the nose free from viscid secretions and also remove
superficial infection.
3. Nasal decongestants help to relieve nasal obstruction
and improve sinus ventilation. Excessive use of nasal
drops and sprays should be avoided because it may
lead to rhinitis medicamentosa. A short course of systemic steroids helps to wean the patients already addicted to excessive use of decongestant drops or sprays.
4. Antibiotics help to clear nasal infection and concomitant sinusitis.
HYPERTROPHIC RHINITIS
It is characterized by thickening of mucosa, submucosa,
seromucinous glands, periosteum and bone. Changes are
more marked on the turbinates.
Aetiology
Common causes are recurrent nasal infections, chronic
sinusitis, chronic irritation of nasal mucosa due to smoking, industrial irritants, prolonged use of nasal drops and
vasomotor and allergic rhinitis.
Symptoms
Nasal obstruction is the predominant symptom. Nasal
discharge is thick and sticky. Some complain of headache,
heaviness of head or transient anosmia.
Signs
Examination shows hypertrophy of turbinates. Turbinal
mucosa is thick and does not pit on pressure. It shows little shrinkage with vasoconstrictor drugs due to presence
of underlying fibrosis.
Maximum changes are seen in the inferior turbinate. It
may be hypertrophied in its entirety or only at the anterior end, posterior end or along the inferior border giving
it a mulberry appearance.
Treatment
Attempt should be made to discover the cause and remove it. Nasal obstruction can be relieved by reduction in
size of turbinates. The various methods are:
1. Linear cauterization.
2. Submucosal diathermy.
3. Cryosurgery of turbinates.
4. Partial or total turbinectomy. Hypertrophied inferior
turbinate can be partially removed at its anterior end,
inferior border or posterior end. Middle turbinate, if
hypertrophied, can also be removed partially or totally.
Excessive removal of turbinates should be avoided as it
leads to persistent crusting.
5. Submucous resection of turbinate bone. This removes
bony obstruction but preserves turbinal mucosa for its
function.
6. Lasers have also been used to reduce the size of
turbinates.
Compensatory Hypertrophic Rhinitis
This is seen in cases of marked deviation of septum to
one side. The roomier side of the nose shows hypertrophy
of inferior and middle turbinates. This is an attempt on
the part of nature to reduce the wide space to overcome
the ill effects of drying and crusting that always attend
wider nasal space. Hypertrophic changes in these cases
are not reversible with the correction of nasal septum and
often require reduction of turbinates at the time of septal
surgery.
ATROPHIC RHINITIS (OZAENA)
It is a chronic inflammation of nose characterized by atrophy of nasal mucosa and turbinate bones. The nasal cavities are roomy and full of foul-smelling crusts. 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:
1. Hereditary factors. Disease is known to involve more
than one member in the same family.
2. Endocrinal disturbance. Disease usually starts at pu-
berty, involves females more than males, the crusting
and foetor associated with disease tends to cease after
menopause; these factors have raised the possibility of
disease being an endocrinal disorder.
3. Racial factors. White and yellow races are more sus-
ceptible than natives of equatorial Africa.
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4. Nutritional deficiency. Disease may be due to deficiency of vitamin A, D or iron or some other dietary factors. The fact that incidence of disease is decreasing in
western countries and is rarely seen in well-to-do families raises the possibility of some nutritional deficiency.
5. Infective. Various organisms have been cultured from
cases of atrophic rhinitis such as Klebsiella ozaenae,
(Perez bacillus), diphtheroids, Proteus vulgaris, Escheri-
chia coli, staphylococci and streptococci but they are
all considered to be secondary invaders responsible for
foul smell rather than the primary causative organisms
of the disease.
6. 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 stratified squamous type. There is atrophy of
seromucinous glands, venous blood sinusoids and nerve elements. Arteries in the mucosa, periosteum and bone show
obliterative 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.
Examination shows nasal cavity 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 posterior 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 glazed with crusts
(atrophic pharyngitis, p. 289).
Similar changes may occur in the larynx with cough
and hoarseness of voice (atrophic laryngitis).
Hearing impairment may be noticed because of ob-
struction to eustachian tube and middle ear effusion.
Paranasal sinuses are usually small and underdevel-
oped 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.
removal of crusts and the associated putrefying smell,
and to further check crust formation.
(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
eustachian tube. Initially, irrigations are done two or
three times a day but later once in 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 with 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 g/day for 10 days has
given good results 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 com-
pletely 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 bilateral nasal obstruction, modified Young’s operation aims to partially close the nostrils. It is also
claimed to give the same benefit as Young’s.
(b) Narrowing the nasal cavities. Nasal chambers are very
wide in atrophic rhinitis and air currents dry up secretions leading to crusting. Narrowing the size of the
nasal airway helps to relieve the symptoms. Among
the techniques followed, some are:
(i) Submucosal injection of teflon paste.
(ii) Insertion of fat, cartilage, bone or teflon strips
under the mucoperiosteum of the floor and lateral wall of nose and the mucoperichondrium
of the septum.
(iii) Section and medial displacement of lateral wall
of nose.
treatment. It may be medical or surgical.
1. medical. Complete cure of the disease is not yet pos-
sible. Treatment aims at maintaining nasal hygiene by
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
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SECTION II — Diseases of Nose and Paranasal Sinuses
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.
RHINITIS SICCA
It is also a crust-forming disease seen in patients who
work in hot, dry and dusty surroundings, e.g. bakers,
iron- and goldsmiths. Condition is confined to the anterior third of nose particularly of the nasal septum. Here,
the ciliated columnar epithelium undergoes squamous
metaplasia with atrophy of seromucinous glands. Crusts
form on the anterior part of septum and their removal
causes ulceration and epistaxis, and may lead to septal
perforation.
Treatment consists of correction of the occupational
surroundings and application of bland ointment or one
with an antibiotic and steroid to the affected part. Nose
pricking and forcible removal of crusts should be avoided.
Nasal douche, like the one used in cases of atrophic rhinitis, is useful.
RHINITIS CASEOSA
It is an uncommon condition, usually unilateral and
mostly affecting males.
Nose is filled with offensive purulent discharge and
cheesy material. The disease possibly arises from chronic
sinusitis with collection of inspissated cheesy material.
Sinus mucosa becomes granulomatous. Bony walls of sinus may be destroyed, requiring differentiation from malignancy. Treatment is removal of debris and granulation
tissue and free drainage of the affected sinus. Prognosis
is good.
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Granulomatous Diseases of Nose
Various granulomatous lesions involving the nose are listed in Table 28.1. They are the result of bacterial or fungal
infections or due to causes not yet clear. Many of these
lesions may be manifestations of systemic diseases, which
should always be looked for while making the diagnosis.
Biopsy of the lesion is also essential, not only to establish
the correct diagnosis of granulomatous disease but also to
exclude a neoplasm, in which many of these diseases may
clinically simulate.
BACTERIAL INFECTIONS
RHINOSCLEROMA
It is a chronic granulomatous disease caused by Gramnegative bacillus called Klebsiella rhinoscleromatis or Frisch
bacillus. The disease is endemic in several parts of the
world. In India, it is seen more often in the northern than
in the southern parts.
Pathology
The disease starts in the nose and extends to nasopharynx, oropharynx, larynx (mostly subglottic region), trachea and bronchi. Mode of infection is unknown. Both
sexes of any age may be affected.
Clinical Features
The disease runs through the following stages:
(a) Atrophic stage. It resembles atrophic rhinitis and is
characterized by foul-smelling purulent nasal discharge and crusting.
(b) Granulomatous stage. Granulomatous nodules form in
nasal mucosa. There is also subdermal infiltration of lower part of external nose and upper lip giving a “woody”
feel (Figure 28.1). Nodules are painless and nonulcerative.
(c) Cicatricial stage. This causes stenosis of nares, distor-
tion of upper lip, adhesions in the nose, nasopharynx
and oropharynx. There may be subglottic stenosis with
respiratory distress.
Diagnosis
Biopsy shows infiltration of submucosa with plasma cells,
lymphocytes, eosinophils, Mikulicz cells and Russell bodies. The latter two are diagnostic features of the disease
(Figure 28.2 ). Mikulicz cells are large foam cells with
a central nucleus and vacuolated cytoplasm containing
causative bacilli. Russell bodies are homogenous eosinophilic inclusion bodies found in the plasma cells. They
occur due to accumulation of immunoglobulins secreted
by the plasma cells. The causative organisms can be cultured from the biopsy material.
Treatment
Both streptomycin (1 g/day) and tetracycline (2 g/day)
are given together for a minimum period of 4–6 weeks
and repeated, if necessary, after 1 month. Treatment is
stopped only when two consecutive cultures from the biopsy material are negative. Steroids can be combined to
reduce fibrosis.
Surgical treatment may be required to establish the air-
way and correct nasal deformity.
SYPHILIS
Nasal syphilis is of two types: acquired and congenital.
1. acquired. It occurs as:
(a) Primary. It manifests as primary chancre of the vesti-
bule of nose. It is rare.
(b) Secondary. Rarely recognized. It manifests as simple
rhinitis with crusting and fissuring in the nasal vestibule. Diagnosis is suggested by the presence of mucous patches in the pharynx, skin rash, fever and generalized lymphadenitis.
(c) Tertiary. This is the stage in which nose is commonly
involved. Typical manifestation is the formation of
a gumma on the nasal septum. Later, the septum is
destroyed both in its bony and cartilaginous parts.
Perforation may also appear in the hard palate. There
is offensive nasal discharge with crusts. Bony or cartilaginous sequestra may be seen. Bridge of the nose
collapses causing a saddle nose deformity.
2. congenital. It occurs in two forms: early and late.
(a) Early form. It is seen in the first 3 months of life and
manifests as “snuffles.” Soon the nasal discharge becomes purulent. This is associated with fissuring and
excoriation of the nasal vestibule and of the upper lip.
(b) Late form. Usually manifests around puberty. Clinical
picture is similar to that seen in tertiary stage of acquired
syphilis. Gummatous lesions destroy the nasal structures. Other stigmata of syphilis such as corneal opacities, deafness and Hutchinson’s teeth are also present.
Diagnosis
It is made on serological tests (VDRL) and biopsy of
the tissue with special stains to demonstrate Treponema
pallidum.
Treatment
Penicillin is the drug of choice: benzathine penicillin
2.4 million units i.m. every week for 3 weeks with a total dose of 7.2 million units. Nasal crusts are removed by
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