This document discusses three chronic nasal diseases: atrophic rhinitis, rhinosporidiosis, and rhinoscleroma. Atrophic rhinitis causes nasal atrophy and foul odors. It can be primary from infection or nutritional factors, or secondary from other conditions like sinusitis. Rhinosporidiosis is caused by Rhinosporidium seeberi and presents as red nasal lesions. Rhinoscleroma is caused by Klebsiella rhinoscleromatis and presents in stages from rhinitis to fibrosis, commonly affecting the nose and spreading to other areas. Treatment involves antibiotics, surgery, or other measures depending on the specific condition.
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.
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
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.