Atrophic rhinitis is a chronic nasal disease characterized by atrophy of the nasal mucosa and bone of the turbinates. It is associated with thick, foul-smelling secretions and crust formation. The cause is often unknown but may be due to infections, surfactant deficiency, or autonomic imbalances. Treatment involves regular nasal cleansing, topical medications to hydrate the nose, systemic antibiotics, and sometimes surgery to decrease nasal volume or improve vascularity.

1. ATROPHIC RHINITIS
Dr Grace Vandana
MS ENT (PG)

2. DEFINITION
 Atrophic rhinitis is a chronic nasal disease
characterized by progressive atrophy of the mucosa
and the underlying bone of the turbinates.
 It is associated with viscid secretions which dry
resulting in crust formation with a characteristic foul
odour,called ozaena.

3. HISTORY
 Dr Spencer Watson called it ozenae in 1875
 Dr Bernhard Fraenkel 1876 described triad
 Fetor
 Crustings and
 Atrophy of nasal structures

4. EPIDEMIOLOGY
 0.3-1% in countries with high prevalence
 More common in animals- swines and cattle
 Predominant in young and middle aged
 More common in females
 More common in tropical countries
 Most common in low socoeconomic classes living
in poor hygenic conditions.

5. AETIOLOGY
 The precise aetiology is still unknown.
 Cases wherein no specific aetiologic factor can be identified
are designated primary atrophic rhinitis.
 Cases wherein a specific aetiologic factor can be implicated
are designated secondary atrophic rhinitis.

6.  Developmental :
 Congenitally spacious nasal cavity
 Poor pneumatization of maxillary antrum

7. Infections:
 A wide range of bacterial flora have been reported from
the nasal secretions of these patients, namely,
 Coccobacillus foetidus ozaena,
 Diptheroid bacilli and
 Klebsiella ozaenae.
 Recent studies have identified
 Bordetella bronchoseptica and
 Pasteurella multocida, and have suggested that
inoculation of these organisms into animals has produced
changes similar to atrophic rhinitis.

8.  Biochemical studies of the nasal aspirate in atrophic rhinitis
have noted a significant decrease in the total phospholipids
and also a change in the phospholipid profile.
 This suggests a possible role for surfactant deficiency in
the aetiopathogenesis.
 Surfactant deficiency in nasal secretion causing ciliary
dysfunction leading to stasis of nasal secretions and
crusting.

9.  Primary atrophic rhinitis usually commences at puberty and is
much more common in females, suggesting that endocrine
imbalance may have some role to play.
 The disease is more common in people of low socioeconomic
background and has been associated with poor nutrition and
iron-deficiency.
 Heredity is an important factor and there also appears to be a
racial influence.
 It is more common in yellow and Latin races and American
blacks are more susceptible as compared to natives of
equatorial Africa.

10.  Autoimmune:
 viral infection / malnutrition / immune deficiency
triggers destructive autoimmune process on nasal
mucosa
 Autonomic Imbalance:
 Excessive vasoconstriction from autonomic
imbalances as a reason for development of AR has
been described.
 Reflex Sympathetic Dystrophy Syndrome
(R.S.D.S.) causes vasodilatation & hyperaemic
decalcification of turbinates followed by
vasoconstriction

11.  Secondary Atrophic Rhinitis
 Long-standing purulent sinusitis
 Iatrogenic:
 Radical turbinectomy
 post-radiotherapy
 Tuberculosis, Syphilis,Leprosy, Rhinoscleroma
 Deviated nasal septum (atrophy in wider nasalcavity)

12. PATHOLOGY
 Patches of metaplasia -- ciliated columnar epithelium to
nonkeratinized or keratinized squamous epithelium.
 Lamina propria--- chronic cellular infiltration, granulation
tissue and fibrosis.
 Mucous glands are decreased in size and number.

13.  Vascular changes:
 Decreased vascularity,
 Periarteritis
 Endarteritis of the terminal arterioles.
 Taylor and young described vasodilatation of the
capillaries with increased alkaline phosphatase
activity leading to bone resorption

14.  Accumulation of lymphocytes & plasma cells.
 Squamous metaplasia from ciliated columnar
 Ciliary destruction & decrease in nasal glands
 Bone resorption
 Types:
 AR type I
 Common type (50–80 per cent of all cases),
 Endarteritis obliterans, periarteritis and periarterial
fibrosis of the terminal arterioles as a result of
chronic infections with round cell and plasma cell
infiltration.
 Benefit from the vasodilator effects of oestrogen
therapy.

15.  AR type II
 Less common (20–50 per cent of all cases)
 Capillary vasodilatation
 Endothelial cells of dilated capillaries have more
 Cytoplasm than normal and show a positive
alkaline phosphatase reaction suggesting active
bone resorption, which is a feature of the disease
 Not amenable to oestrogen therapy.

16. BIOPSY
Normal atrophic rhinitis

17. CLINICAL FEATURES
 Nasal crusting which is brown black or dark green
in colour
 Thick purulent discharge
 Foul smell due to the anerobic flora
 Anosmia
 Headache, epistaxis
 Nasal obstruction
 Pharyngitis sicca

18.  Causes of anosmia
 Loss of olfactory neural elements
 Thick secretion & crusts over olfactory area
 Degeneration of secretory glands
 Scanty mucous for dissolving odoriferous materials
 Causes of nasal obstruction
 Blunting of sensory nerve endings, thus resulting in
a diminished sensation of air flow.
 Crust formation

19. CLINICAL EXAMINATION
 Presence of fetor
 Changes in the nasal passages
 Atrophy of turbinates resulting in widening of the
cavity,
 Presence of green crusts and thick purulent
discharge.
 Occasionally, the condition may be complicated by
maggot infestation in the nose.

21. INVESTIGATIONS
 General : hemogram
 Specific Investigations
Saccharine test: decreased nasal muco-
ciliaryclearance time
 Serum iron & protein levels: malnutrition
 Culture & sensitivity of nasal discharge
 Diagnostic Nasal Endoscopy
 X-ray P.N.S.: maxillary sinusitis

23.  C.T. scan P.N.S.
 Mucoperiosteal thickening
resorption of ethmoid bulla & uncinate process
 Hypoplasia of maxillary sinuses
 Roomy nasal cavities
 Erosion & bowing of lateral nasal wall
 Atrophy of turbinates

26.  Other Specific Investigations
Chest X-ray: T.B., bronchiectasis
 Serology for syphilis: V.D.R.L.
 Sputum for AFB, Mantoux test: T.B
 Nasal smear study: Leprosy
 Complement fixation test & biopsy:Rhinoscleroma

27. COMPLICATIONS AND SEQUELAE
 Nasal septal perforation and saddle nose
deformity:
 Severe cases left untreated may be complicated by
destruction of nasal bone and cartilages lead to
septal perforations and saddle nose deformities.
 Secondary rhinosinusitis
 Local and systemic spread of infection: Spread
of infection to the pharynx, larynx, lungs and ears,
and intracranial spread in immunocompromised
patients is possible

28.  Atrophic pharyngitis and laryngitis. Pharyngitis
sicca is a frequent co-morbidity in AR with a dry
pharyngeal mucosa. Dislodged crusts may cause
choking episodes
 Chronic dacryocystitis.
 A rare complication of ar in the form of dacryocystitis
has been noted
 Nasal myiasis.
 Seen in neglected cases of primary ar, especially in
patients of lower socioeconomic status living in poor
hygienic conditions.
 The putrefied nasal debris and foul smell attract flies of
the genus chrysomia (c. Bezianna vilteneauve).

29. TREATMENT
 Aims to restore nasal hydration and minimalisation
of crustings
 Medical and conservative treatment
 Surgical treatment

30.  Regular nasal cleansing is the basis of conservative
treatment.
 Alkaline Nasal Douche
 Sodium bicarbonate (28.4g) --loosens nasal crusts
 Sodium biborate (28.4g) –Antiseptic
 Sodium chloride (56.7g) --makes solution isotonic
 Mixed in 280 ml of warm water to make the solution

31.  Glucose–glycerine nose drops.
 Mixing 75g of gycerine and adding 25g of glucose
 25% glucose is used to inhibit saprophytic infection and
proteolytic bacteria (glucose on fermentation produces
lactic acid and an acidic pH that inhibits bacterial growth),
and promote the growth of commensal flora.
 Glycerine helps as a lubricant and hygroscopic agent
(adsorbs water from the atmosphere and moistens mucosa,
and hence impedes crust formation).
 Glycerine may also cause some degree of irritation and
hence improve vascularity.
 These nose drops should be applied three or four times a
day after douching the nose.

32.  Liquid paraffin nose drops
 Effective in lubricating the nasal mucosa and in
removal of crusts
 Long-term use is not recommended in view of
reports of paraffin granulomas and inhalational
lipoid pneumonias.

33.  Oestradiol in arachis oil.
 available for instillation into the nose as drops and
sprays (10 000 units/ml)
 oestrogens are only useful for Young and Taylor
Type I AR
 oestradiol may worsen the situation in the Type II
variety.

34.  Kemicetene antiozaena solution.
 90 mg of chloramphenicol
 0.64 mg of oestradiol diproprionate
 900 IU of vitamin D2 and propylene glycol in each
millilitre.
 This is used in the form of nose drops after
douching.

35.  Chloramphenicol/streptomycin drops.
 use after douching.
 Local treatment with injection of a mixture of
streptomycin and novocaine has been tried with
satisfactory results.

36.  Injections of human placental extract have been
administered both systemically and locally
(submucosal/intranasal) and have been noted to
result in an improvement.
 The extract (0.5 ml) is injected into each nasal
cavity per week for 24 weeks

37.  Action of Placental extract
 Progesterone leads to hyperplasia of nasal mucosa
& glandular secretion
 Oestrogen leads to vasodilatation
 Biogenic stimulator of metabolic & regenerative
process
 Intra-placental serum boosts up immunity
 Mechanical narrowing of nasal passage

38.  Antibiotics and antimicrobials
 Systemic (intravenous) aminoglycoside (Tobramycin)
therapy for two weeks in addition to topical gentamicin.
 Good results have been reported in one study where
Rifampicin 600 mg once daily for 12 weeks was
administered.
 More recently, ciprofloxacin in a daily dose of 500–750
mg bid for one to three months has been tried
successfully, i.e. measured by the disappearance of
crusts, odour and K. ozaenae.

39.  Iron, zinc, protein and vitamin (A and D)
supplements.
 Recommended especially in cases of malnutrition
and established deficiencies.
 The use of potassium iodide by mouth with the
object of increasing nasal secretion has been
recommended.

40.  Prostheses:
 Non-surgical closure of the nasal vestibule using
prostheses
 including occlusion of the nostril with an obturator made
from dimethylpolysiloxane.
 This is useful in cases of secondary AR where formal
closure of the nostril is contraindicated in view of the
treatment necessary for the primary disease.
 Another similar device made of clear acrylic resin called a
‘pin-hole nasal prosthesis’ has been described more
recently.

41. NASAL OBTURATORS

42.  Decongestants or antihistamines.
 Strongly contraindicated in AR as they worsen the
pathology and hence the clinical course of the
disease.

43. SURGICAL MANAGEMENT
 Aim of Surgery:
o Decrease trauma of air turbulence
 Nasal closure
 Volume reduction
o Increase nasal secretions
 Parotid duct implantation into maxillary sinus
o Increase vascularity of nasal mucosa
 Denervation procedures
 Nasal implantation of maxillary sinus mucosa

44.  The principles of surgery may be divided largely into four
groups.
1. Decreasing the size of the nasal cavities: redudes
turbulence of air currents in roomy air cavities and thus
preventing drying and crustings.
2. Promoting regeneration of normal nasal mucosa.
This may be achieved by allowing the nasal cavities to
rest by temporary closure (complete or partial) of the
nostrils

45. 3.Increasing lubrication of the dry nasal mucosa. This is
achieved by increasing the secretory abilities of the nasal
cavities or by introducing secretions from elsewhere
4.Improving vascularity of the nasal cavities.
 This is achieved either by blocking the sympathetic
nervous system (stellate ganglion block or cervical
sympathectomy)
 subserving the nose or by introducing grafts (e.G.
Placenta, maxillary mucosal flaps, buccal flaps) that
improve vascularity

46. Types of surgery
Nasal closure: Young
Modified Young
Volume reduction: Lautenslager
Wilson
Sublabial implants
Vestibuloplasty
Denervation: Cervical sympathectomy
Stellate ganglion block
Sphenopalatine ganglion block
Salivary irrigation: Parotid duct implantation

47.  Young’s operation:
 Only 1 nostril closed
completely by raising 2 circumferential flaps (inner mucosal
& outer cutaneous) in nasalvestibule & suturing them in
midline.
 Modified Young’s operation
 Similar to youngs but keeping a 3 mm opening on both
sides.
 Recannalisation done after few months with a tri-radiate
(Mercedes Benz) incision

50.  Advantages of Modified Young
 Progress of disease can be monitored with 2.7 mm nasal
endoscope
 Glucose in glycerine drops can be instilled
 Both nostrils can be operated at one sitting
 Nasal breathing preserved
 No complaints of de-nasal voice
 Better cosmetic result

51. Vestibuloplasty :
 Ghosh described an alternative surgical technique
of vestibuloplasty, wherein a posteriorly based skin
flap is raised in the lateral wall of the nasal
vestibule and sutured on itself, thus decreasing the
lateral flow of air into the nasal cavity

52.  Lautenslager’s operation:
 Fracture & medial
displacement of lateral nasal wall
 Wilson’s operation: submucosal injection of Teflon
paste

53.  Raghav Sharan’s operation.
 The mucosa of the maxillary antrum is elevated and
brought into the nasal cavity on each side through the
antrostomy.
 The benefits are perhaps three-fold: decreasing the size
of the cavity, and improving lubrication and vascularity

54.  Cervical Sympathectomy
 Stellate ganglion block/ cervical chain block:
 through an anterior paratracheal approach, 10-15 cc of 1
per cent xylocaine is injected slowly.
 The success of the procedure is judged by the
appearance of Horner’s syndrome, congestion of the
ipsilateral tympanic membrane and congestion of the
ipsilateral nasal mucosa.
 It is reported that foetor and crusting are relieved within
eight to 10 blocks and that this is maintained for up to four
to eight days after cessation of blocks.
 risk of transient recurrent laryngeal nerve palsy

55.  Sublabial implantation: bone, cartilage,
fat,placental bits, hydroxyapatite + fibrin
paste,Plastipore, acrylic resin, silastic
 Parotid duct implantation into maxillary sinus
{Wittmack’s operation}

56.  Rhinitis Sicca
 Mild form of atrophic rhinitis
Seen in hot, dry, dusty places (bakers, goldsmiths);
alcoholics & anaemics
 Crusting present anteriorly only
 Bone atrophy & foetor are absent
 Tx: Nasal douching + change of surrounding

57.  Rhinitis Caseosa
 Synonym: Nasal cholesteatoma
 Chronic inflammation with deposition of foul
smelling cheesy material in nasal cavity.
 Nasal obstruction---stasis of secretions & exfoliated
cells---putrefaction---caseation
 Treatment: 1. Removal of cheesy debris
 2. Correction of nasal obstruction

58. REFERENCES
 Scott brown 7th edition
 Dutt, S., & Kameswaran, M. (2005). The aetiology
and management of atrophic rhinitis. The Journal of
Laryngology & Otology, 119(11), 843-852.
doi:10.1258/002221505774783377
 Hazarika 3rd edition
 Dhingra 6th edition