ATROPHIC RHINITIS pg 1465 (Scott Brown)

Definition
Atrophic rhinitis is a chronic nasal disease characterized by
progressive atrophy of the mucosa and the underlying bone of
the turbinates. It is associated with viscid secretions which dry
resulting in crust formation with a characteristic foul odour,
sometimes called ozaena.
Epid
Primary atrophic rhinitis has become less common in countries
where social conditions and health have generally improved. It
affects both sides of the nose, occurs after puberty, and is more
common in women. Because of this, an endocrine imbalance
has been postulated as a cause, whereas others believe it has
an autoimmune basis, possibly initiated by a virus or owing to
vitamin or iron deficiencies.
Rinitis atrofi primer telah menjadi semakin jarang di negaranegara dengan kondisi sosial dan kesehatan yang telah
meningkat secara umum. Penyakit ini mempengaruhi kedua
Aetiology (Remember Mnemonic HERNIA)
PRIMARY ATROPHIC RHINITIS
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 puberty,
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 susceptible
than natives of equatorial Africa.

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, Escherichia 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.
Secondary atrophic rhinitis
develops directly as a result of granulomatous nasal infections,
chronic rhinosinusitis, excessive nasal surgery, trauma and
irradiation.
Pathology
There are patches of metaplasia in the epithelium, with a
transition from the usual ciliated columnar epithelium to
nonkeratinized or keratinized squamous epithelium. The lamina
propria shows chronic cellular infiltration, granulation

tissue and fibrosis. 39 The mucous glands are decreased in size

and number. Vascular changes have been demonstrated in the
form of decreased vascularity, periarteritis and endarteritis of
the terminal arterioles. Taylor and Young 40 were, however,
unable to demonstrate such endarteritis and periarteritis of
terminal arterioles, and suggested a possible other type of
atrophic rhinitis in which there was vasodilatation of the
capillaries.
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. 256). 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.

INVESTIGATIONS
It is advisable to exclude the presence of sepsis in the
paranasal sinuses by radiology and, if necessary, by proof
puncture or sinus endoscopy. Swabs from nasal secretions may
be cultured, but the results are unlikely to be helpfuL
Serological tests to exclude syphilis are essential as syphilis is
the most likely condition to be confused with atrophic rhinitis.
The haemogram, serum proteins and iIon should also be
checked.

Treatment
MEDICAL TREATMENT
Regular nasal cleansing is the basis of conservative treatment
in atrophic rhinitis. The patient should be instructed to douche
the nose twice daily with a
hypertonic and alkaline solution which has traditionally been
prepared by dissolving a teaspoonful of a mixture of sodium
bicarbonate, sodium diborate and sodium chloride (in
proportions of 1:1:2) in half a pint (280 mL) of warm water.
Following the alkaline nasal douche, a solution of 25 percent
glucose in glycerine may be applied, so as to inhibit the
proteolytic organisms in the
nasal cavity. Injections of human placental extract have been
administered both systemically and locally (submucosal
intranasal) and have been noted to result in an improvement,
but are unlikely to be used currently due to the concerns of
virus transmission from such homologous sources. Rifampicin
600 mg orally once daily for 12 weeks has been used with
reportedly good results. [** /*]
SURGICAL TREATMENT
Numerous attempts to relieve the condition surgically have
been made in the past. These include submucous injections of

paraffin and procedures aimed at displacing the lateral nasal

walls medially. Various materials, such as teflon strips,
powdered teflon in glycerine, plastipore, bone and cartilage,
have been
inserted submucosally after raising flaps of mucoperichondrium
from the septum or mucoperiosteum from the floor and lateral
nasal wall. The most conunonly used operation, however,
remains the one described by Young.44 The procedure involves
raising flaps of skin from the medial and lateral walls of
the nasal vestibule and suturing them together so as to
completely close the nasal passages. The nasal cavities are
then re-opened after periods varying from several months to
several years, usually to reveal normal nasal mucosa
and absence of crusting. Presumably, the absence of the drying
effects of air flow results in regeneration of healthy nasal
mucosa. However, there are obvious disadvantages of
complete bilateral nasal closure, and a modified
operation with partial nostril closure leaving a 3 rom hole has
been found to give similar results and to be better tolerated.42
Ghosh45 described an alternative surgical technique of
vestibuloplasty, wherein a posteriorly based skin flap is raised
in the lateral wall of the nasal vestibule and sutured on itself,
thus decreasing the lateral flow of air into the nasal cavity.

Prognosis
The disease persists for years but there is a tendency to
recover spontaneously in middle age.