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By SREEJITH T
OZAENA
Chronic inflammation of nose,
characterized by atrophy of nasal mucosa
and turbinate bones.
nasal cavities are roomy ,filled with foul
smelling crusts.
2 types
Primary
Secondary
PRIMARY ATROPHIC RHINITIS
AETIOLOGY HERNIA
HEREDITARY FACTORS
ENDOCRINE DISTURBANCES
RACIAL FACTORS
NUTRITIONAL DEFICIENCY
INFECTIVE
AUTOIMMUNE PROCESS
PATHOLOGY
Ciliated columnar epithelium replaced by
stratified squamous type.
Atrophy of seromucinous glands, venous
blood sinusoids and nerve elements.
Arteries in the mucosa, periosteum and
bone show obliterative endarteritis.
Bone of turbinates undergoes resorption
causing widening of nasal chambers.
Paranasal sinuses are small due to
arrested development.
CLINICAL FEATURES
MC females
foul smell from the nose
merciful anosmia
nasal obstruction - crust formation.
greenish or greyish black dry crusts
covering the turbinates and septum.
Epistaxis – on removal of crust.
nasal cavities appear roomy
atrophy of turbinates
nasal mucosa –pale
septal perforation
dermatitis of nasal vestibule
saddle deformity of nose
atrophic pharyngitis – Pharyngeal mucosa
appear dry and glazed with crusts
atrophic laryngitis – cough, hoarseness of
voice
hearing impairment
X-ray paranasal sinus - opaque
TREATMENT
Medical
Nasal irrigation and removal of crusts
25% glucose in glycerine
Local antibiotics
Oestradiol therapy
Placental extract
Systemic use of streptomycin
Potassium iodide
Surgical
YOUNG’S OPERATION
• Modified Young’s operation
NARROWING THE NASAL
CAVITIES
• Submucosal injection of teflon paste
• Insertion of fat, cartilage or teflon strips
under the mucoperiosteum of the floor,
lateral wall of nose, mucoperichondrium
of the septum.
• Section and medial displacement of
lateral wall of nose
SECONDARY ATROPHIC
RHINITIS
Syphilis
Lupus
Leprosy
Rhinoscleroma
Long standing purulent sinusitis
Radiotherapy to nose
Excessive surgical removal of turbinates
UNILATERAL ATROPHIC RHINITIS
Extreme deviation of nasal septum accompanied by
atrophic rhinitis on the wider side
IgE mediated immunologic response of nasal
mucosa to airborne allergens and is characterized
by
Watery nasal discharge
Nasal obstruction
Sneezing
Itching in the nose
2 Types
Seasonal
Perennial
ETIOLOGY
Inhalent allergens
Seasonal allergens – pollens
Perennial allergens – molds, dust mite,
dander from animals
Genetic predisposition
PATHOGENESIS
Inhaled allergens  IgE  blood basophil / mast
cell
Subsequent exposure  Ag +IgE 
degranulation of mast cells  release preformed
& newly formed chemical mediators 
vasodilatation, mucosal edema, infiltration of
eosinophils, excessive secretion from nasal
glands, smooth muscle contraction.
PRIMING EFFECT - mucosa earlier sensitized to
an allergen will react to smaller doses of
subsequent specific allergen and also get primed
to other nonspecific antigens to which patient was
not exposed  cause nonspecific nasal hyper -
reactivity
•ALLERGIC RESPONSE- 2 phases
Acute or early
phase
• Within 5–30 min
after exposure
• Sneezing,
rhinorrhoea, nasal
blockage,
bronchospasm
• Due to release of
vasoactive amines
Late or
delayed phase
• 2-8 hour after
exposure
• Swelling, congestion,
thick secretion
• Due to infiltration of
inflammatory cells at
the site of antigen
deposition
CLINICAL FEATURES
Seasonal nasal allergy
Paroxysmal sneezing(10-20
sneezes at a time)
Nasal obstruction
Watery nasal discharge
Itching of eyes, palate or pharynx
Perennial allergy
Frequent colds
Persistently stuffy nose
Anosmia due to mucosal edema
Postnasal drip
Chronic cough
Hearing impairment
SIGNS OF ALLERGY
Nasal signs
Transverse nasal crease
Pale and edematous nasal mucosa: bluish
Swollen turbinates
Thin, watery or mucoid discharge
Ocular signs
Edema of the lids
Congestion and cobblestone appearance of the
conjunctiva
Dark circles under the eyes(allergic shiners)
Otologic signs
Retracted tympanic membrane
Otitis media
Pharyngeal signs
Granular pharyngitis
Laryngeal signs
Hoarseness
Edema of the vocal cords
NEW ALLERGIC RHINITIS AND
ITS IMPACT ON ASTHMA (ARIA)
CLASSIFICATION
Duration of disease
INTERMITTENT
(symptoms are
present for)
• Less than 4 days
a week OR
• For less than 4
weeks
PERSISTENT
(symptoms are
present for)
• More than 4
days a week OR
• For more than 4
weeks
Severity of disease
MILD: None of the following
symptoms are present
• Sleep disturbances
• Impairment of daily activities, leisure and
sport
• Impairment of school or work
• Troublesome symptoms
MODERATE TO SEVERE
• One or more of the above symptoms are
present
INVESTIGATIONS
Total and differential count
Peripheral eosinophilia
Nasal smear
taken at the time of clinically active disease or after
challenge test
shows large number of eosinophils
present in non allergic rhinitis also eg:NARES
Skin test: helps to identify specific allergen
Skin prick test: drop of conc. allergen solution  volar
surface of forearm  introduce to the dermis  central
wheal and surrounding zone of erythema within 10-15 min
 +ve test
Specific IgE measurement: in vitro test to find specific
allergen
Radioallergosorbent test (RAST)
invitro test
measures specific IgE antibody concentration in serum
Nasal provocation test
COMPLICATIONS
Recurrent sinusitis
Nasal polypi
Serous otitis media
Orthodontic problems
Bronchial asthma
TREATMENT
Avoidance of allergen.
Treatment with drugs
Antihistaminics
Sympathomimetics (oral & topical)
Corticosteroids
Sodium cromoglycate
Anticholinergics
Leukotriene receptor antagonist
Anti IgE
Immunotherapy
allergen is given in gradually increasing doses till the
maintenance dose is reached
suppresses IgE formation
raise the titre of specific IgG antibody
subcutaneous, nasal, sublingual routes
STEP CARE APPROACH
RECOMMENDED BY ARIA
Mild intermittent disease  oral antihistamines,
intranasal cromolyn sodium
Moderate / persistent disease  intranasal
corticosteroids
Severe  combination therapy (oral nonsedating
antihistamines + intranasal steroids)
Severe and persistent  combination therapy + short
course of oral steroids & immunotherapy
Persistent nasal obstruction  intranasal
decongestants OR (oral decongestants +
antihistamines)
Avoid allergens and irritants in all forms of disease.
Nasal Cavity Inflammation and Atrophy Causes and Treatments

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Nasal Cavity Inflammation and Atrophy Causes and Treatments

  • 2. OZAENA Chronic inflammation of nose, characterized by atrophy of nasal mucosa and turbinate bones. nasal cavities are roomy ,filled with foul smelling crusts. 2 types Primary Secondary
  • 3.
  • 4. PRIMARY ATROPHIC RHINITIS AETIOLOGY HERNIA HEREDITARY FACTORS ENDOCRINE DISTURBANCES RACIAL FACTORS NUTRITIONAL DEFICIENCY INFECTIVE AUTOIMMUNE PROCESS
  • 5. PATHOLOGY Ciliated columnar epithelium replaced by stratified squamous type. Atrophy of seromucinous glands, venous blood sinusoids and nerve elements. Arteries in the mucosa, periosteum and bone show obliterative endarteritis. Bone of turbinates undergoes resorption causing widening of nasal chambers. Paranasal sinuses are small due to arrested development.
  • 6. CLINICAL FEATURES MC females foul smell from the nose merciful anosmia nasal obstruction - crust formation. greenish or greyish black dry crusts covering the turbinates and septum. Epistaxis – on removal of crust. nasal cavities appear roomy atrophy of turbinates
  • 7. nasal mucosa –pale septal perforation dermatitis of nasal vestibule saddle deformity of nose atrophic pharyngitis – Pharyngeal mucosa appear dry and glazed with crusts atrophic laryngitis – cough, hoarseness of voice hearing impairment X-ray paranasal sinus - opaque
  • 8. TREATMENT Medical Nasal irrigation and removal of crusts 25% glucose in glycerine Local antibiotics Oestradiol therapy Placental extract Systemic use of streptomycin Potassium iodide
  • 9. Surgical YOUNG’S OPERATION • Modified Young’s operation NARROWING THE NASAL CAVITIES • Submucosal injection of teflon paste • Insertion of fat, cartilage or teflon strips under the mucoperiosteum of the floor, lateral wall of nose, mucoperichondrium of the septum. • Section and medial displacement of lateral wall of nose
  • 10. SECONDARY ATROPHIC RHINITIS Syphilis Lupus Leprosy Rhinoscleroma Long standing purulent sinusitis Radiotherapy to nose Excessive surgical removal of turbinates UNILATERAL ATROPHIC RHINITIS Extreme deviation of nasal septum accompanied by atrophic rhinitis on the wider side
  • 11.
  • 12. IgE mediated immunologic response of nasal mucosa to airborne allergens and is characterized by Watery nasal discharge Nasal obstruction Sneezing Itching in the nose 2 Types Seasonal Perennial
  • 13.
  • 14. ETIOLOGY Inhalent allergens Seasonal allergens – pollens Perennial allergens – molds, dust mite, dander from animals Genetic predisposition
  • 15. PATHOGENESIS Inhaled allergens  IgE  blood basophil / mast cell Subsequent exposure  Ag +IgE  degranulation of mast cells  release preformed & newly formed chemical mediators  vasodilatation, mucosal edema, infiltration of eosinophils, excessive secretion from nasal glands, smooth muscle contraction.
  • 16. PRIMING EFFECT - mucosa earlier sensitized to an allergen will react to smaller doses of subsequent specific allergen and also get primed to other nonspecific antigens to which patient was not exposed  cause nonspecific nasal hyper - reactivity
  • 17. •ALLERGIC RESPONSE- 2 phases Acute or early phase • Within 5–30 min after exposure • Sneezing, rhinorrhoea, nasal blockage, bronchospasm • Due to release of vasoactive amines Late or delayed phase • 2-8 hour after exposure • Swelling, congestion, thick secretion • Due to infiltration of inflammatory cells at the site of antigen deposition
  • 18. CLINICAL FEATURES Seasonal nasal allergy Paroxysmal sneezing(10-20 sneezes at a time) Nasal obstruction Watery nasal discharge Itching of eyes, palate or pharynx
  • 19. Perennial allergy Frequent colds Persistently stuffy nose Anosmia due to mucosal edema Postnasal drip Chronic cough Hearing impairment
  • 20. SIGNS OF ALLERGY Nasal signs Transverse nasal crease Pale and edematous nasal mucosa: bluish Swollen turbinates Thin, watery or mucoid discharge Ocular signs Edema of the lids Congestion and cobblestone appearance of the conjunctiva Dark circles under the eyes(allergic shiners)
  • 21.
  • 22. Otologic signs Retracted tympanic membrane Otitis media Pharyngeal signs Granular pharyngitis Laryngeal signs Hoarseness Edema of the vocal cords
  • 23. NEW ALLERGIC RHINITIS AND ITS IMPACT ON ASTHMA (ARIA) CLASSIFICATION Duration of disease INTERMITTENT (symptoms are present for) • Less than 4 days a week OR • For less than 4 weeks PERSISTENT (symptoms are present for) • More than 4 days a week OR • For more than 4 weeks
  • 24. Severity of disease MILD: None of the following symptoms are present • Sleep disturbances • Impairment of daily activities, leisure and sport • Impairment of school or work • Troublesome symptoms MODERATE TO SEVERE • One or more of the above symptoms are present
  • 25. INVESTIGATIONS Total and differential count Peripheral eosinophilia Nasal smear taken at the time of clinically active disease or after challenge test shows large number of eosinophils present in non allergic rhinitis also eg:NARES Skin test: helps to identify specific allergen Skin prick test: drop of conc. allergen solution  volar surface of forearm  introduce to the dermis  central wheal and surrounding zone of erythema within 10-15 min  +ve test Specific IgE measurement: in vitro test to find specific allergen
  • 26. Radioallergosorbent test (RAST) invitro test measures specific IgE antibody concentration in serum Nasal provocation test
  • 27. COMPLICATIONS Recurrent sinusitis Nasal polypi Serous otitis media Orthodontic problems Bronchial asthma
  • 28. TREATMENT Avoidance of allergen. Treatment with drugs Antihistaminics Sympathomimetics (oral & topical) Corticosteroids Sodium cromoglycate Anticholinergics Leukotriene receptor antagonist Anti IgE
  • 29. Immunotherapy allergen is given in gradually increasing doses till the maintenance dose is reached suppresses IgE formation raise the titre of specific IgG antibody subcutaneous, nasal, sublingual routes
  • 30. STEP CARE APPROACH RECOMMENDED BY ARIA Mild intermittent disease  oral antihistamines, intranasal cromolyn sodium Moderate / persistent disease  intranasal corticosteroids Severe  combination therapy (oral nonsedating antihistamines + intranasal steroids) Severe and persistent  combination therapy + short course of oral steroids & immunotherapy Persistent nasal obstruction  intranasal decongestants OR (oral decongestants + antihistamines) Avoid allergens and irritants in all forms of disease.