Definition: Atrophicrhinitis is defined as a chronic nasal disease characterised by progressiveatrophy of the nasal mucosa along with the underlying bones ofturbinates. There is also associated presence of viscid secretion which rapidlydries up forming foul smelling crusts. This fetid odor is also known asozaena. The nasal cavity is also abnormally patent. The patient isfortunately unaware of the stench emitting from the nose as this disorder isassociated with merciful anosmia. Aetiology: The etiology of this problem still remains obscure. Numerous pathogens have been associated with this condition, the most importantof them are 1. Coccobacillus, 2. Bacillus mucosus, 3. Coccobacillus foetidus ozaenae, 4. Diptheroid bacilli and 5.Klebsiella ozaenae. These organisms despite being isolated from thenose of diseased patients have not categorically been proved as the cause forthe same. Other possible factors which could predispose to this disease are:1. Chronic sinusitis2. Excessive surgical destruction of the nasal mucosa andturbiantes 3. Nutritional deficiencies 4. Syphilis.5. Endocrine imbalances (Disease is known to worsen with pregnancy /menstruation)6. Heredity (Autosomal dominent pattern of inheritance identified)7. Autoimmune diseaseThe triad of atrophic rhinitis as described by Dr. Bernhard Fraenkel are 1. Fetor, 2.crusting and 3. atrophy. Age of onset: Usually commences at puberty.Females are commonly affected than males. Heredity is known to bean important factor as there appears to be increased susceptibility amongyellow races, latin races and American negro races. Poor nurtritioncould 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 toleranceto nasal tissues. This according to him could be caused / precipitated byvirus infection, malnutrition, immunodeficiency. Pathology:1. Metaplasia of ciliated columnar nasal epithelium intosquamous epithelium.2. There is a decrease in the number and size of compound alveolar glands3. Dilated capillaries are also seenPathologically atrophic rhinitis has been divided into two types:Type I: is characterised by the presence of endarteritis andperiarteritis of the terminal arterioles. This could be caused bychronic infections. These patients benefit from the vasodilator effectsof oestrogen therapy.Type II: is characterised by vasodilatation of the capillaries,these patients may worsen with estrogen therapy. The endothelial cells liningthe dilated capillaries have been demonstrated to contain more cytoplasm thanthose of normal capillaries and they also showed a positive reaction foralkaline phosphatase suggesting the presence of active bone resorption. It has also been demonstrated that a majority of patients with atrophicrhinitis belong to type I category. Once the diagnosis of atrophic rhinitis is made then the etiologyshould be sought. Atrophic rhinitis can be divided in to two typesclinically:1. Primary atrophic rhinitis - the classic form which is supposed toarise denovo. This diagnosis is made by a processof exclusion. This type of disease is still common in middle eastand India. All the known causes of atrophic rhinitis must beexcluded before coming to this diagnosis. Causative organisms in thesepatients have always be Klebsiella ozenae.2. Secondary atrophic rhinitis: Is the most common form seen indeveloped countries. The most common causes forthis problem could be:1. Extensive destruction of nasal mucosa and turbinates during nasalsurgery2. Following irradiation3. Granulomatous infections like leprosy, syphilis,tuberculosis etcClinical features:The presenting symptoms are commonly nasal obstruction andepistaxis. Anosmia i.e. merciful may be present making the patientunaware of the smell emanating from the nose. These patients may alsohave pharyngitis sicca. Choking attacks may also be seen due to slippageof detached crusts from the nasopharynx into theoropharynx. These patients also appear to be dejectedand depressed psychologically. Clinical examination of these patients show that their nasal cavitiesfilled with foul smelling greenish, yellow or black crusts, the nasal cavityappear to be enormously roomy. When these crusts are removed bleeding starts tooccur.
Why nasalobstruction even in the presence of roomy nasal cavity?This interesting question must be answered. The nasalcavity is filled with sensory nerve endings close to the nasal valvearea. These receptors sense the flow of air through this area thus givinga sense of freeness in the nasal cavity. These nerve endings are destroyedin patients with atrophic rhinitis thus depriving the patient of thissensation. In the absence of these sensation the nose feelsblocked. Radiographic findings:Are more or less the same in both primary and secondary atrophicrhinitis. Plain xrays show lateral bowing of nasal walls, thin orabsent turbinates and hypoplastic maxillary sinuses.CT scan findings:1. Mucoperiosteal thickening of paranasal sinuses2. Loss of definition of osteomeatal complex due to resorption ofethmoidal bulla and uncinate process3. Hypoplastic maxillary sinuses4. Enlargement of nasal cavity with erosion of the lateral nasalwall5. Atrophy of inferior and middle turbinatesManagement:Conservative:Nasal douching - The patient must be asked to douche the nose atleasttwice a day with a solution prepared with:Sodium bicarbonate -28.4 gSodium diborate - 28.4 gSodium chloride - 56.7 g mixed in 280 ml of luke warm water.The crusts may be removed by forceps orsuction. 25% glucose in glycerin drops can be applied to the nose thusinhibiting the growth of proteolytic organism.In patients with histological type I atrophic rhinitis oestradiol inarachis 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 mlof saline.Potassium iodide can be prescribed orally to the patient in an attemptto increase the nasal secretion.Systemic use of placental extracts have been attempted with varyingdegrees of success.Surgical management:1. Submucous injections of paraffin, and operations aimed at displacingthe lateral nasal wall medially. This surgical procedure is known asLautenslauger's operation.2. Recently teflon strips, and autogenous cartilages have been inserted along thefloor and lateral nasal wall after elevation of flaps.3. Wilson's operation - Submucosal injection of 50% Teflon inglycerin paste.4. Repeated stellate ganglion blocks have also been employed with somesuccess5. Young's operation - This surgery aims at closure of one or bothnasal cavities by plastic surgery. Young's method is to raise folds ofskin inside the nostril and suturing these folds together thus closing thenasal cavities. After a period of 6 to 9 months when these flaps areopened up the mucosa of the nasal cavities have found to be healed. Thiscan be verified by postnasal examination before revision surgery isperformed. Modifications of this procedure has been suggested (modifiedYoung's operation) where a 3mm hole is left while closing the flaps in thenasal vestibule. This enables the patient to breath through the nasalcavities. It is better if these surgical procedures are done in a stagedmanner, while waiting for one nose to heal before attempting on the other side.