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.