Inflamatory diseases of the nose (1) 30.05.16 dr.davis

1. Dr. Davis Thomas

2. Atrophic Rhinitis

3. Definition
• Atrophic rhinitis is defined as a chronic nasal disease
characterised by progressive atrophy of the nasal mucosa
along with the underlying bones of turbinates.
• There is also associated presence of viscid secretion which
rapidly dries up forming foul smelling crusts.
• This fetid odour is also known as ozaena.
• The nasal cavity is also abnormally patent.
• The patient is fortunately unaware of the stench emitting
from the nose as this disorder is associated with merciful
anosmia.

4. Aetiology
The etiology of this problem still remains obscure.
Numerous pathogens have been associated with this condition,
the most important of them are
• 1. Coccobacillus,
• 2. Bacillus mucosus,
• 3. Coccobacillus foetidus ozaenae,
• 4. Diptheroid bacilli and
• 5. Klebsiella ozaenae.
These organisms despite being isolated from the nose of
diseased patients have not categorically been proved as the
cause for the same.

5. TYPES OF ATROPHIC RHINITIS
PRIMARY ATROPHIC RHINITIS
diagnosis of exclusion
CAUSES:
1. Hereditary
2. Endocrine dysfunction
3. Racial
4. Reflex sympathetic dystrophy syndrome
5. Nutritional deficiency
6. Autoimmune

6. SECONDARY ATROPHIC RHINITIS
CAUSES
1. Iatrogenic - surgery (commonest)
2. Trauma
3. Radiation
4. Granulomatous diseases
5. Infection

7. COMMONEST CAUSE OF UNILATERAL
ATROPHIC RHINITIS
GROSSLY DEVIATED SEPTUM
MECHANICAL THEORY OF ZAUFAL – It
states that skeletal defects due to gross septal
deviation to one side leads to unilateral atrophic
rhinitis on the roomy side.

8. Pathology:
1. Metaplasia of ciliated columnar nasal epithelium into
squamous epithelium.
2. There is a decrease in the number and size of compound
alveolar glands
3. Loss of cilia
4. Atrophy of nerves
5. Fibrosis of lamina propria

9. Type I
is characterised by the presence of endarteritis and
periarteritis of the terminal arterioles.
This could be caused by chronic infections.
 These patients benefit from the vasodilator effects of
oestrogen therapy.

10. Type II
 is characterised by vasodilatation of the capillaries,
these patients may worsen with estrogen therapy.
They also showed a positive reaction for alkaline
phosphatase suggesting the presence of active bone
resorption.

11. Triad of Atrophic Rhinitis
1. Fetor
2. Crusting
3. Atrophy.

12. Clinical features:
Nasal obstruction - crust formation
atrophic nerve endings
Thick crusts
Epistaxis
Anosmia
Offensive smell perceived by others
Headache
Impairment of hearing
Associated changes in pharynx & larynx

13. Clinical examination
Clinical examination of these patients show that their
nasal cavities filled with foul smelling greenish, yellow or
black crusts,
 the nasal cavity appear to be enormously roomy.
 When these crusts are removed bleeding starts to occur
Septal perforations &external deformity

14. Why nasal obstruction even in
the presence of roomy nasal
cavity?
• The nasal cavity is filled with sensory nerve endings close
to the nasal valve area.
• These receptors sense the flow of air through this area
thus giving a sense of freeness in the nasal cavity.
• These nerve endings are destroyed in patients with
atrophic rhinitis thus depriving the patient of this
sensation.
• In the absence of these sensation the nose feels blocked.

16. INVESTIGATIONS
ROUTINE BLOOD & URINE INVESTIGATIONS
To R/O underlying causes

17. Radiographic findings
Lateral bowing of nasal walls
Thin or absent turbinates
Hypoplastic maxillary sinuses

18. CT scan findings
1. Mucoperiosteal thickening of paranasal sinuses
2. Loss of definition of osteomeatal complex due to
resorption of ethmoidal bulla and uncinate process
3. Hypoplastic maxillary sinuses
4. Enlargement of nasal cavity with erosion of the lateral
nasal wall
5. Atrophy of inferior and middle turbinates

21. Conservative Treatment
1.Nasal douching - The patient must be asked to douche
the nose atleast twice a day with a solution prepared with:
Sodium bicarbonate - 28.4 g
Sodium biborate - 28.4 g
Sodium chloride - 56.7 g
mixed in 280 ml of luke warm water.
The crusts may be removed by forceps or suction.
2. 25% glucose in glycerin drops can be applied to the nose
thus inhibiting the growth of proteolytic organism.

22. Conservative
• In patients with histological type I atrophic rhinitis oestradiol
in arachis oil 10,000 units/ml can be used as nasal drops.
• Kemecetine antiozaena solution - is prepared with
chloramphenicol 90mg, oestradiol dipropionate 0.64mg,
vitamin D2 900 IU and propylene glycol in 1 ml of saline.
• Potassium iodide can be prescribed orally to the patient in an
attempt to increase the nasal secretion.
• Systemic streptomycin injection
• Systemic use of placental extracts have been attempted with
varying degrees of success.

23. Surgical treatment
Aims
- to narrow the widened nasal cavity
- diminish drying and crust formation
- rest the mucosa and allow regeneration

24. Surgical management
1. Submucous injections of paraffin, .
2. Recently teflon strips, and autogenous cartilages
have been inserted along the floor and lateral nasal
wall after elevation of flaps.
3. Wilson's operation - Submucosal injection of 50%
Teflon in glycerin paste.
4. Witmack’s operation – rerooting of parotid duct
5. Lautenslager’s operation – medialisation of lateral
wall
6. Repeated stellate ganglion blocks have also been
employed with some success

25. 7. Young's operation
• This surgery aims at closure of one or both nasal cavities
by plastic surgery.
• After a period of 6 to 9 months when these flaps are
opened up the mucosa of the nasal cavities have found to
be healed.
• This can be verified by postnasal examination before
revision surgery is performed.
8.Modifications of this procedure has been suggested
(modified Young's operation) where a 3mm hole is left
while closing the flaps in the nasal vestibule. This enables
the patient to breath through the nasal cavities

26. COMPLICATIONS
Epistaxsis
Saddle nose deformity
Myiasis
Meningitis
Anosmia

27. Rhinosporidiosis

28. It is a chronic granulomatous fungal disease of the
nose caused by Rhinosporidium Seeberi/ Kinealyi.
Mode of Transmission:
1. Exact mode is not known.
2.Acquired by swimming in contaminated ponds.
3.Inhaling the dust of dried cowdung.
Malignant:- Deep seated and multiple, spreading
through systemic route. Generalised
Rhinosporidiosis.

29. Incidence:- 95% from India & Srilanka
Male: Female – 2:1
Tamil Nadu – Hyperendemic areas – madurai
& Ramnad, Thirumangalam, Rajapalayam,
Sivagangai (Large Ponds)
Affects –Nasal mucosa, Conjunctiva, Sclera,
Tonsils, Genitalia and Skin

30. Trauma – Predisposing factor – infective spores
enter through traumatised nasal mucosa and
multiply in the submucosa forming sporangia.
Spores are discharged into tissues and cause
reactive hyperplasia and lead to formation of
vascular mass.

31. CLASSIFICATION – Anatomical Sites
1. Nasal (78%)
a. Mucous membrane of septum
b. Spur in nasal floor
c. Lateral wall
2. Nasopharyngeal (16%)
a. Upper aspect of palate
3. Mixed
a. Naso – nasopharyngeal (6.3%)
b. Ethmoido – nasopharyngeal
c. Naso – lacrimal
4. Bizaree
a. Conjuntival
b. Tarsal
c. Cutaneous
d. Laryngeal

32. LIFE CYCLE – Ashworth (1923),
Karunaratne (1964)
• Earliest stage ( Trophic stage or Trophocyte)
• Round or oval cell – Chitinous wall – smaller – RBC –
vacuolated cytoplasm – vasicular nucleus – nucleolus
• First division – 50 µ - mitotic
• Cellulose layer – trophocyte - 100µ
• Free nuclei 2000 – sporangium – cytoplasm cleavage – spore -
150µ - 1000 spores
• 8–16 spherical bodies – Feulgen pasitive material (Spherules)
• 250µ–300µ - sporangia ruptures
• Spherule – lipoprotein coat – protein matrix

33. Staining Method
Spherule is made up of liproprotein coat with protein
matrix and feulgen positive centre
Bromophenol blue – spherules
Bismark brown – wall of spherules
Sudan black B – Lipoprotein coat.

36. Clinical Features
Symptoms
Nasal Obstruction
Nasal discharge
Epistaxis
Itching
Signs
AR – An irregular, friable, red, granular mass studded
with sporangia showing as white spots, usually
pedunculated.

39. Investigations
Routine Blood and Urine investigations.
Histamine level to be estimated – Histamine content
of Rhinosporidiosis is increased so proliferates quickly
and bleeds profusely.
X-Ray PNS.
Microscopic (KOH) examination of nasal discharge.
DNE.
HPE.

40. Treatment
Wide excision of the mass along with basal cautery.
Dapsone 100 mg daily to prevent recurrence (arrest
the maturation of spores).
Side effects – Methaemoglobinemia
Hepatotoxicity
Recurrence – 1) Incomplete removal
2) Submucosal presence of spores
3) Multiple sites.

41. Rhinoscleroma

42. It is a chronic granulomatous disease of the nose,
caused by Gram negative, non motile, encapsulated,
diplobacillus, Klebsiella Rhinoscleromatis (Frisch
Bacillus).
Site – Nose, nasopharynx, oropharynx, larynx, trachea
and bronchi.
Common in females.
Predisposing factors – Poor hygiene and low socio
economic status.

43. Pathogenesis:
Droplet infection
Clinical features:
1) Atrophic stage.
2) Granulomatous stage – Tapir Nose (Subdermal
infiltration of the nodules in lower part of nose &
upper lip giving a woody feel).
3) Cicatricial stage – Hebra Nose (Scarring, enlargement
& disfigurement of the nose).

44. Histology
Mikulicz cells – Presence of scattered large foam cells
with a central nucleus and vacuolated cytoplasm
containing the bacilli.
Russel bodies – Plasma cells with eosinophilic,
homogenous inclusion bodies .

45. Investigations
Biopsy & HPE
Culture of the organism in Mc-conkey agar medium
and staining by PAS and Giemsa stains.
X Ray skull lateral view – ‘V’ shaped soft palate
attachment – Palatal sign – Gothic arch deformity

46. Treatment
Tetracycline – 6 weeks
Steroids – prevent recurence
Excision of cicatrized tissue.

47. Rhinitis Medicamentosa
The prolonged usage of Sympathomimetic nasal
decongesant drops and sprays leads to Tachyphylaxis
resulting in rebound vasodilatation & engorgement of
nasal mucosa leads to nasal obstruction.

48. Rhinitis Sicca :
It is a form of rhinitis characterised by dryness of
nose, limited to the anterior part of nasal cavity. It
occurs in people who work in hot and dry
surroundings.
Rhinitis Caseosa:
It is a chronic nasal disease characterized by the
presence of caseous cholesteatoma like material with
granulations in the nose. It is also called nasal
cholesteatoma.

49. Stewart’s Granuloma
It is also called peripheral sinonasal T-cell lymphoma.
It presents as an indurated swelling of the nose, nasal
vestibule and septum.
HPE – dense collection of cells especially
lymphocytes.
Treatment : Radiotherapy.

50. Wegener’s Granuloma
It is an autoimmune disease of unknown aetilogy
characterised by necrotising granuloma and vasculitis
of the upper and lower airways, systemic vasculitis
and focal necrotising glomerulonephritis.
Diagnosis by nasal biopsy.
Treatment : Saline nasal douching
Cyclophosphamide 1-2 mg/kg/day
High dose of steroids.

51. Tuberculosis
Syphilis
Leprosy

52. RHINOLITH
Synonym – nasal calculus
Defined as concretion or calcareous mass in the nose

53. Pathogenesis
Neglected foreign body/ blood clot /
inspissated mucus -nidus
↓
Granulations formation
↓
Calcium, mg CO 3 or PO4 gets deposited
↓
Hard rhinolith
↓
Enlarges & nerosis of septum

54. CLINICAL FEATURES
 Unilateral nasal discharge
Nasal obstruction
Occasional epistaxis
Sometimes asymptomatic
AR – irregular , grey or greyish black mass along the
floor
On probing – gritty sensation

55. Diagnosis
- History , examination
- X- ray PNS
Treatment
surgical excision – endoscopic
lateral rhinotomy

56. NASAL MYIASIS
SYNONYM – maggots in the nose
Suppurative conditions of nose / unhygenic living
condition
↓
attracts flies – chrysomiya , lay eggs
↓
hatch & grow into larvae
↓
Crawl into nasal cavity & surrounding regions

57. Predisposing factors
 atrophic rhinitis
 chronic suppurative rhinosinusitis
 syphilis & leprosy
 fungating malignant masses

58. Clinical features
Irritation of nose
Watering of eyes
Swelling & puffiness of eyelids, lips
Thin blood stained nasal discharge to epistaxsis
Foul smell
Formication – Crawling sensation in the nose.
AR- multiple maggots with purulent, foul smelling
nasal discharge

59. complications
Destruction of surronding structures – nose , palate ,
orbit
Inhalation into tracheobronchial tree
Intracranial spread
Psychological

60. Treatment
Handpicked with nasal dressing forceps
Instillation of 25% chloroform or turpentine oil
Douching with warm saline
Treat complications
Treat underlying cause

61. THANK YOU