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 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:
(a) Hereditary factors. Disease is known to involve more than one member in the same family. (b) 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 endcrinal disorder (c) Racial factors. White and yellow races are more susceptible than natives of equatorial of Africa. d) Nutritional defzciency

diseae may be due to deficiency of vit. 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. (e) Infective. Various organisms have been culture from cases of atrophic rhinitis such as Klebsiella ozaenae, (Perez bacillus), diphtheroids, P vulgaris, Esch. coli, Staphylococci and Streptococci but they are all considered to be secondary invaders responsible for fouI smell rather than the primary causative organisms of the disease. (f) Autoimmune process. The body reacts by a destructive process to the antigens released from the nasal mucoso. 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 seromuci- nous glands, venous blood sinusoids and nerve elements. Arteries in the mucosa, periosteum and bone show oblit- t rative 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 8 social outcast though patient himself is unaware of the smel.l 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 sep- tum. 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 mall show a saddle deformity Atrophic changes may also be seen in the pharyngeal mucosa which may appear dry and glazed with crusts (atrophic pharyngitis, page 238). 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 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.

Treatment

It may be medical or surgical.

1. Medical. Complete cure of the disease is not yet possible. Treatment aims at maintaining nasal hygiene by removal of crusts and the associated putrefYll1g 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 tea- spoonful of powder containing soda bicarbonate 1 part, Sodium biborate 1 part, Sod ium chloride 2 parts in 280 ml of water, is used to irrigate the nasal cavities. The soiution 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 2 or 3 times a day but later once every 2 or 3 days is sufficient. Hard crusts may be diffkult to

remove by iITigation. They are first loosened and then mechanically removed with forceps or sliction. . (b) 25% glucose in gl),cerine. 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'l'~1 antiozaena solution contains chloromycetin, oestradiol and vitamin l)2 and may be found useful. . (d) Oestradiolspray.Helpstoincreasevascularityofnasal mucosa and regeneration of seromucinous glands. . (e) Placental extract injected submucosally in the nose may provide some relief. . (f) Sys temic use of streptomycin. 1 glday for 10 days has given good results in reducing crusting and odour. It is effecLive 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 to teflon paste. (iil Insertion of fat, cartilage, bone or teflon strips under the mucoperiosteum of the floor and lat- eral 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 rhino- scleroma 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.