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Atrophic Rhinitis 
Rhinosporidiosis 
Rhinoscleroma.
Atrophic Rhinitis 
Chronic nasal disease characterized by 
progressive atrophy of the mucosa and 
underlying turbinates forming dry crust and 
viscid secretions with characteristic foul 
odour, Ozaena.
Aetiology: 
 Primary: cause unknown 
 Secondary: due to specific aetiological factor
Primary: 
 Infection 
Klebsiella ozaenae 
Diptheroid bacilli 
Cocccobacillus foetidus ozaena 
 Hormonal imbalance 
at puberty 
more common in females 
 Nutritional 
common in poor socioeconomic status 
In Vit A / D and iron-deficiency 
 Heredity 
 Autoimmune 
Altered cellular reactivity 
Release of nasal mucosal antigen into systemic circulation
Secondary: 
 Chronic Rhinosinusitis 
 Chronic granulomatous lesions 
Tuberculosis 
Syphilis 
Leprosy 
 Surgery 
Excessive destruction nasal tissues
Pathology: 
 Epithelium: 
Patches of metaplasia 
Transition from ciliated columnar to non kerainized 
or keratinized squamous epithelium 
 Lamina propria: 
chronic cellular infiltration, granulation tissue and 
fibrosis. 
 Mucous glands: 
decreased in size and number 
 Vascular: 
decreased vascularity, periarteritis and endarteritis 
of terminal arterioles
Clinical Features: 
 Merciful anosmia 
because of atrophy of nerve elements (responsible for the 
perception of smell). 
 Nasal obstruction 
 Bleeding from the nose when the dried discharge 
(crusts) are removed. 
 Nasal cavities: 
roomy, filled with dry foul smelling black or dark green crusts 
 Septal perforation and dermatitis of nasal vestibule 
 Nose may show a saddly nose deformity. 
 Associated with similar atrophic changes in the 
pharynx, larynx producing symptoms pertaining to 
these structures. 
 Hearing impairment due to Eustachian tube blockage 
causing middle ear effusion. 
 Permanent loss of smell and impairement of taste
Treatment 
 medical 
 surgical. 
Medical measures include: 
 Nasal irrigation using normal saline 
 Nasal irrigation and removal of crusts using alkaline 
nasal douches (280ml of water, 28.4g of Sod 
bicarbonate, 28.4 g of Sod diborate, 56.7g of 
Sod.Chloride.) 
 25% glucose in glycerine, 
 Local antibiotics like Kemicetine antiozaena solution 
(Chloramphenicol + Ostradiol + Vit D2 ) 
 Ostradiol spray 
 Systemic streptomycin / rifampicin 
 Oral potassium iodide 
 Human placental extract : systemic 
injected in the submucosa
Surgical Interventions include: 
 Young's operation 
 Modified Young's operation 
 Narrowing of nasal cavities, 
submucosal injection of Teflon paste, 
section and medial displacement of lateral wall of 
nose 
 Transposition of parotid duct to maxillary 
sinus or nasal mucosa.
Rhinosporidiosis 
Endemic in southern India and Sri Lanka. 
In Nepal: Rajbiraj and Janakpur. 
Chronic infection of the upper respiratory tract – 
most commonly in the inferior turbinate of the 
nasal cavity. 
Causative agent: 
 the ? fungus Rhinosporidium seeberi 
 the waterborne organism Cyanobacterium microcystis 
aeruginosa 
Other sites of involvement include: 
 ears, larynx, esophagus, conjunctiva, and 
tracheobronchial tree, any part of body
Rhinosporidiosis 
Causative agent present in water and dust, 
readily infects the nasal mucosa. 
matures into a sporangium 
subsequently bursts to release multiple 
endospores, 
infects surrounding tissues.
Rhinosporidiosis 
Clinical Presentation: 
 Patients with nasal involvement present with 
nasal obstruction, 
epistaxis, and 
rhinorrhea. 
 Systemic dissemination rare 
 On Examination: 
Unilateral beefy-red granulomatous lesion with 
white spots. (Strawberry appearance)
Rhinosporidiosis 
Treatment: 
 Medical therapy with antibiotics or anti-fungal 
(not proven to be helpful) 
 Treatment of choice : 
Wide excision with electrocauterization of the 
lesional base. 
surgical excision of the lesion, (recurrence ~10%) 
 Dapsone
Rhinoscleroma 
Progressive granulomatous disease commencing in 
nose and extending into other areas of airway 
occurs in regions of poor standard of domestic hygiene. 
Causative organism: 
 K. rhinoscleromatis (Gm –ve bacillus) 
Histology: 
marked cellular infiltrates consisting of lymphocytes and plasma cells. There 
are many macrophages with clear to foamy cytoplasm (Mikulicz cells) Plasma 
cells eccentric nucleus with deep eosin-staining cytoplasm (Russel Bodies.)
Rhinoscleroma 
Clinical stages: 
 1) rhinitic (Atrophic) 
 2) florid (Granulation) 
 3) fibrotic (Cicatrizing). 
Symptoms : 
 vary with the location of the infection. 
 nasal cavity (septum): most common site, 
 other sites of infection include: 
paranasal sinuses, orbit, larynx, tracheobronchial tree, and middle 
ear. 
Treatment : 
 Tetracycline Streptomycin x 6 weeks 
 Acriflavine solution ( in vitro killed K. rhinoscleromatis) 
 Significant airway obstruction requires surgical excision. 
 Radiotherapy 
 Laser treatment.
THANK YOU

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Atrophic Rhinitis, Rhinosporidiosis, and Rhinoscleroma

  • 2. Atrophic Rhinitis Chronic nasal disease characterized by progressive atrophy of the mucosa and underlying turbinates forming dry crust and viscid secretions with characteristic foul odour, Ozaena.
  • 3. Aetiology:  Primary: cause unknown  Secondary: due to specific aetiological factor
  • 4. Primary:  Infection Klebsiella ozaenae Diptheroid bacilli Cocccobacillus foetidus ozaena  Hormonal imbalance at puberty more common in females  Nutritional common in poor socioeconomic status In Vit A / D and iron-deficiency  Heredity  Autoimmune Altered cellular reactivity Release of nasal mucosal antigen into systemic circulation
  • 5. Secondary:  Chronic Rhinosinusitis  Chronic granulomatous lesions Tuberculosis Syphilis Leprosy  Surgery Excessive destruction nasal tissues
  • 6. Pathology:  Epithelium: Patches of metaplasia Transition from ciliated columnar to non kerainized or keratinized squamous epithelium  Lamina propria: chronic cellular infiltration, granulation tissue and fibrosis.  Mucous glands: decreased in size and number  Vascular: decreased vascularity, periarteritis and endarteritis of terminal arterioles
  • 7. Clinical Features:  Merciful anosmia because of atrophy of nerve elements (responsible for the perception of smell).  Nasal obstruction  Bleeding from the nose when the dried discharge (crusts) are removed.  Nasal cavities: roomy, filled with dry foul smelling black or dark green crusts  Septal perforation and dermatitis of nasal vestibule  Nose may show a saddly nose deformity.  Associated with similar atrophic changes in the pharynx, larynx producing symptoms pertaining to these structures.  Hearing impairment due to Eustachian tube blockage causing middle ear effusion.  Permanent loss of smell and impairement of taste
  • 8. Treatment  medical  surgical. Medical measures include:  Nasal irrigation using normal saline  Nasal irrigation and removal of crusts using alkaline nasal douches (280ml of water, 28.4g of Sod bicarbonate, 28.4 g of Sod diborate, 56.7g of Sod.Chloride.)  25% glucose in glycerine,  Local antibiotics like Kemicetine antiozaena solution (Chloramphenicol + Ostradiol + Vit D2 )  Ostradiol spray  Systemic streptomycin / rifampicin  Oral potassium iodide  Human placental extract : systemic injected in the submucosa
  • 9. Surgical Interventions include:  Young's operation  Modified Young's operation  Narrowing of nasal cavities, submucosal injection of Teflon paste, section and medial displacement of lateral wall of nose  Transposition of parotid duct to maxillary sinus or nasal mucosa.
  • 10.
  • 11. Rhinosporidiosis Endemic in southern India and Sri Lanka. In Nepal: Rajbiraj and Janakpur. Chronic infection of the upper respiratory tract – most commonly in the inferior turbinate of the nasal cavity. Causative agent:  the ? fungus Rhinosporidium seeberi  the waterborne organism Cyanobacterium microcystis aeruginosa Other sites of involvement include:  ears, larynx, esophagus, conjunctiva, and tracheobronchial tree, any part of body
  • 12. Rhinosporidiosis Causative agent present in water and dust, readily infects the nasal mucosa. matures into a sporangium subsequently bursts to release multiple endospores, infects surrounding tissues.
  • 13. Rhinosporidiosis Clinical Presentation:  Patients with nasal involvement present with nasal obstruction, epistaxis, and rhinorrhea.  Systemic dissemination rare  On Examination: Unilateral beefy-red granulomatous lesion with white spots. (Strawberry appearance)
  • 14. Rhinosporidiosis Treatment:  Medical therapy with antibiotics or anti-fungal (not proven to be helpful)  Treatment of choice : Wide excision with electrocauterization of the lesional base. surgical excision of the lesion, (recurrence ~10%)  Dapsone
  • 15. Rhinoscleroma Progressive granulomatous disease commencing in nose and extending into other areas of airway occurs in regions of poor standard of domestic hygiene. Causative organism:  K. rhinoscleromatis (Gm –ve bacillus) Histology: marked cellular infiltrates consisting of lymphocytes and plasma cells. There are many macrophages with clear to foamy cytoplasm (Mikulicz cells) Plasma cells eccentric nucleus with deep eosin-staining cytoplasm (Russel Bodies.)
  • 16. Rhinoscleroma Clinical stages:  1) rhinitic (Atrophic)  2) florid (Granulation)  3) fibrotic (Cicatrizing). Symptoms :  vary with the location of the infection.  nasal cavity (septum): most common site,  other sites of infection include: paranasal sinuses, orbit, larynx, tracheobronchial tree, and middle ear. Treatment :  Tetracycline Streptomycin x 6 weeks  Acriflavine solution ( in vitro killed K. rhinoscleromatis)  Significant airway obstruction requires surgical excision.  Radiotherapy  Laser treatment.