Dr. T. Balasubramanian M.S. D.L.O.
Atrophic rhinitis is defined as a chronic nasal disease characterised
by progressive atrophy of the nasal mucosa along with the underlying
bones of turbinates. There is also associated presence of viscid
secretion which rapidly dries up forming foul smelling crusts.
This fetid odor is also known as ozaena. The nasal cavity is also
abnormally patent. The patient is fortunately unaware of the
stench emitting from the nose as this disorder is associated with
Aetiology: The etiology of this problem still remains obscure.
Numerous pathogens have been associated with this condition, the most
important of them are 1. Coccobacillus, 2. Bacillus mucosus,
3. Coccobacillus foetidus ozaenae, 4. Diptheroid bacilli and 5.
Klebsiella ozaenae. These organisms despite being isolated
from the nose of diseased patients have not categorically been proved
as the cause for the same.
Other possible factors which could predispose to this disease are:
1. Chronic sinusitis
2. Excessive surgical destruction of the nasal mucosa and
3. Nutritional deficiencies
5. Endocrine imbalances (Disease is known to worsen with pregnancy /
6. Heredity (Autosomal dominent pattern of inheritance identified)
7. Autoimmune disease
The triad of atrophic rhinitis as described by Dr. Bernhard
Fraenkel are 1. Fetor, 2. crusting and
Age of onset: Usually commences at puberty.
Females are commonly affected than males. Heredity is known to be
an important factor as there appears to be increased
susceptibility among yellow races, latin races and American negro
races. Poor nurtrition could also be a factor. Bernat
(1965) postulated iron deficiency could be a cause of this disorder.
Recently immunologists have considered atrophic rhinitis to be an
autoimmune disorder. Fouad confirmed that there was altered
cellular reactivity, loss of tolerance to nasal tissues. This
according to him could be caused / precipitated by virus infection,
1. Metaplasia of ciliated columnar nasal epithelium into
2. There is a decrease in the number and size of compound alveolar
3. Dilated capillaries are also seen
Pathologically atrophic rhinitis has been divided into two types:
Type I: is characterised by the presence of endarteritis and
periarteritis of the terminal arterioles. This could be
caused by chronic infections. These patients benefit from the
vasodilator effects of oestrogen therapy.
Type II: is characterised by vasodilatation of the capillaries,
these patients may worsen with estrogen therapy. The endothelial cells
lining the dilated capillaries have been demonstrated to contain more
cytoplasm than those of normal capillaries and they also showed
a positive reaction for alkaline phosphatase suggesting the
presence of active bone resorption. It has also been
demonstrated that a majority of patients with atrophic rhinitis belong
to type I category.
Once the diagnosis of atrophic rhinitis is made then the etiology
should be sought. Atrophic rhinitis can be divided in to two
1. Primary atrophic rhinitis - the classic form which is supposed to
arise denovo. This diagnosis is made by a process
of exclusion. This type of disease is still common in middle
east and India. All the known causes of atrophic rhinitis
must be excluded before coming to this diagnosis. Causative
organisms in these patients have always be Klebsiella ozenae.
2. Secondary atrophic rhinitis: Is the most common form seen in
developed countries. The most common causes for this problem
1. Extensive destruction of nasal mucosa and turbinates during nasal
2. Following irradiation
3. Granulomatous infections like leprosy, syphilis,
The presenting symptoms are commonly nasal obstruction and
epistaxis. Anosmia i.e. merciful may be present making the
patient unaware of the smell emanating from the nose. These
patients may also have pharyngitis sicca. Choking attacks may
also be seen due to slippage of detached crusts from the nasopharynx
into the oropharynx. These patients also appear to be dejected
and depressed psychologically.
Clinical examination of these patients show that their nasal cavities
filled with foul smelling greenish, yellow or black crusts, the nasal
cavity appear to be enormously roomy. When these crusts are
removed bleeding starts to occur.
Pic showing greenish yellow crusts of atrophic rhinitis
Why nasal obstruction even in the presence of roomy nasal cavity?
This interesting question must be answered. The nasal
cavity is filled with sensory nerve endings close to the
nasal valve area. These receptors sense the flow of air
through this area thus giving a sense of freeness in the nasal
cavity. These nerve endings are destroyed in patients with
atrophic rhinitis thus depriving the patient of this
sensation. In the absence of these sensation the nose feels
Are more or less the same in both primary and secondary atrophic
rhinitis. Plain xrays show lateral bowing of nasal walls,
thin or absent turbinates and hypoplastic maxillary sinuses.
CT scan findings:
1. Mucoperiosteal thickening of paranasal sinuses
2. Loss of definition of osteomeatal complex due to resorption of
ethmoidal bulla and uncinate process
3. Hypoplastic maxillary sinuses
4. Enlargement of nasal cavity with erosion of the lateral nasal
5. Atrophy of inferior and middle turbinates
Nasal douching - The patient must be asked to douche the nose atleast
twice a day with a solution prepared with:
Sodium bicarbonate - 28.4 g
Sodium diborate - 28.4 g
Sodium chloride - 56.7 g
mixed in 280 ml of luke warm water.
The crusts may be removed by forceps or suction. 25% glucose in
glycerin drops can be applied to the nose thus inhibiting the growth of
In patients with histological type I atrophic rhinitis oestradiol in
arachis oil 10,000 units/ml can be used as nasal drops.
Kemecetine antiozaena solution - is prepared with chloramphenicol 90mg,
oestradiol dipropionate 0.64mg, vitamin D2 900 IU and propylene glycol
in 1 ml of saline.
Potassium iodide can be prescribed orally to the patient in an attempt
to increase the nasal secretion.
Systemic use of placental extracts have been attempted with varying
degrees of success.
1. Submucous injections of paraffin, and operations aimed at displacing
the lateral nasal wall medially. This surgical procedure is known
as Lautenslauger's operation.
2. Recently teflon strips, and autogenous cartilages have been inserted
along the floor and lateral nasal wall after elevation of flaps.
3. Wilson's operation - Submucosal injection of 50% Teflon in
4. Repeated stellate ganglion blocks have also been employed with some
5. Young's operation - This surgery aims at closure of one or both
nasal cavities by plastic surgery. Young's method is to raise
folds of skin inside the nostril and suturing these folds together thus
closing the nasal cavities. After a period of 6 to 9 months when
these flaps are opened up the mucosa of the nasal cavities have found
to be healed. This can be verified by postnasal examination
before revision surgery is performed. Modifications of this
procedure has been suggested (modified Young's operation) where a
3mm hole is left while closing the flaps in the nasal vestibule.
This enables the patient to breath through the nasal cavities. It
is better if these surgical procedures are done in a staged manner,
while waiting for one nose to heal before attempting on the other side.
Atrophic changes seen postoperatively
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