Progressive atrophy of nasal mucosa and underlying turbinate bones resulting in abnormal patency of the nasal passages, along with thick viscid secretions which, when dry, emit a characteristic foul smell.
Etiology
The condition is predominantly seen in young and middle-aged adults, especially females.
Specific infections:
Infection causes ciliostasis leading to epithelial destruction and progressive mucosal changes.
- Klebsiella ozaenae (M/C)
- Other infectious agents: Coccobacillus foetidus ozaenae, Bacillus mucosus, Diphtheroids bacillus, Bacillus pertussis, Haemophilus influenzae, Pseudomonas aeruginosa, and Proteus species
Nutritional deficiencies:
Disease is more common in lower socioeconomic classes and those living in poor hygienic conditions
- Iron deficiency anemia (M/C)
- Fat-soluble vitamin deficiency
- Proteins energy malnutrition
Secondary causes:
Disease develops secondary to other disease
- Granulomatous infections: Syphilis, lupus, rhinoscleroma, leprosy
- Long-standing purulent sinusitis
- Radiotherapy to nose
- Excessive surgical excision of turbinates
Pathology
Anatomical involvement:
- Ciliated columnar epithelium lost and replaced by stratified squamous epithelium
- Atrophy of seromucinous glands, venous blood sunusoids, and nerve emements
- Bone turbinate resorption
- Arrested development of paranasal sinuses
Vascular involvement:
- Type I (common, 50–80%): Endarteritis obliterans, periarteritis, and periarterial, fibrosis of the terminal arterioles. These patients benefit from the oestrogen therapy
- Type II (less common, 20–50%): Capillary vasodilation
Clinical features
Majority present with long duration of illness along with sequelae and complications of atrophic rhinitis.
Clinical triad:
Such a full blown clinical picture is usually seen during later stages and the early course of disease may consist of cacosmia only, with the presence of thick nasal crusts.
- Foetor: Patient does not get the smell himself/herself (merciful anosmia)
- Greenish crusts
- Roomy nasal cavities: Despite this, nasal obstruction ensues due to excessive crust formation
Long-term sequelae/complications:
- Nasal septal perforation
- Saddle nose deformity
- Nasal myiasis
- Chronic dacryocystitis
- Atrophic pharyngitis
Diagnosis
Tissue biopsy:
- Early loss of ciliary columnar epithelium
- Chronic inflammatory change followed by thickening and fibrosis of underlying structures
- Characteristic squamous cell metaplasia (despite its chronicity and squamous transformation, nothing is known about the occurrence of malignancy in AR)
Management
Complete cure not yet possible.
Nasal irrigation and removal of cysts
Alkaline solution used which looses the crust for easier removal
- 25% glucose in glycerine
- Oestradiol spray
- Local antibiotics
- Placental extract
- Systemic use of streptomycin
- Potassium iodide
- Kemicetine anti-ozaena solution: Chloramphenicol, oestradiol and vitamin D2
Surgical management:
- Young’s operation: Both nostrils closed completely by raising flaps. Reopened after 6 months or later.
- Modified Young’s operation: Closure of nostrils is partial instead of complete