Atrophic rhinitis

khem02 15,828 views 17 slides Sep 05, 2014
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AtrophicRhinitis
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, larynxproducing symptoms pertaining to
these structures.
Hearing impairment due to Eustachian tubeblockage
causing middle eareffusion.
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.

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