Rhinitis and related topics of ENT. This presentation is a summary of Rhinitis up to the standards of the postgraduate level.

1. Rhinitis
• CONSULTANT : DR RAVI MEHER
• MODERATOR : DR SURVECHA
• PRESENTOR : DR AVINAV

2. Definition
• Inflammation of the nasal mucosa.
• Rhinitis is a group of disorders
characterized by inflammation and
irritation of the mucous membranes of
the nose.

3. Classification
A. Acute rhinitis
• a. Non-allergic:
1. Infective:
• Viral: Common cold (coryza or flu), rhinitis
associated
with influenza or other viral infections.
•Bacterial: Usually occurs as a secondary
infection following unresolved viral rhinitis.
2. Non-infective:
• Vasomotor rhinitis.
• Rhinitis due to chemical irritation.

4. b. Allergic e.g. Hay fever.

5. B. Chronic rhinitis:
a. Non-allergic:
1. Non-specific:
• Chronic catarrhal rhinitis.
• Chronic hypertrophic rhinitis.
• Chronic atrophic rhinitis.
• Rhinitis medicamentosa (drug-induced
rhinitis).
2. Specific:
• Scleroma.
• Rare types: Syphilis, tuberculosis, lupus and,
leprosy.
b. Allergic: Perennial allergic rhinitis.

6. • IgE mediated type I hypersensitivity
• Inflammatory changes in the nasal mucosa caused by exposure to
inhaled allergens
• Allergic rhinitis is subdivided into intermittent (IAR) or persistent
(PER) disease and the severity into mild or moderate/severe
ALLERGIC RHINITIS

7. >/= 2 symptoms of:
• Anterior or posterior rhinorrhea
• Sneezing
• Nasal blockage and/or
• Itching of the nose during >/= 2 consecutive days for
>1hour on most days

8. • AGE: More in adolescents
ETIOLOGY
• PREDISPOSING FACTORS
• PRECIPITATING FACTORS
• INDUSTRIALIZATION
• GENETIC
• FOCAL SENSITIVITY
• IgA DEFICIENCY
• PSYCHOLOGICAL FACTORS
• LIVING CONDITIONS
• ENVIRONMENTAL FACTORS
• EXOGENOUS
• ENDOGENOUS

9. COMMON ALLERGENS
• INHALANT- pollen and dust, fungus, animal dander
• FOOD ALLERGY

10. PATHOLOGY
• INFILTRATION
• EDEMA
• RHINORRHEA
• CONGESTION
• INFECTION
• POLYPS
• PARANASAL SINUSES

11. HYGIENE HYPOTHESIS
• Larger family size, more frequent infections and unhygienic contact
may all be protective
• Reduced exposure to infective agents reduces the Th1 response and
leads to an overdrive of the Th2 immune response leading to
excessive production of IgE and consequent atopy

13. ARIA CLASSIFICATION

14. ALLERGIC RHINITIS
SEASONAL PERENNIAL
• SNEEZING
• WATERY RHINORRHEA
• NASAL OBSTRUCTION
• ITCHING OF EYES & NOSE
• ITCHING THROAT & EARS
• LOSS OF SMELL & TASTE
• SINUSITIS
• EUSTACHIAN TUBE DYSFUNCTION
• SNEEZING & ITCHING LESS
COMMON
• OCAL PHENOMENON
• In response to chemical mediators
leading to mucosal edema a/w
sneezing & rhinorrhea

15. CLINICAL FEATURES
SYMPTOMS SIGNS
• Irritation of the nose
• Recurrent sneezing
• Rhinorrhea
• Nasal obstruction
• Anosmia
• Headache
• ACUTE: Pale mucosa with watery
secretions
• CHRONIC: bluish or purplish
mucosa due to venous stasis
• Polyps may be present
Atopic march  Sequential development of allergic diseases, often starting
in infants with atopic eczema then the development of
allergic rhinitis and finally allergic asthma

16. ANTERIOR RHINOCOPY
ASYMPTOMATIC SYMPTOMATIC
• Normal nasal mucosa • Pale, boggy, bluish, edematous nasal
mucosa
• Bulky turbinates with coating of clear
or mucoid secretions

17. DARRIER’S LINE
 Transverse dark horizontal crease on the
dorsum of nose superior to the tip of nose
ALLERGIC SHINERS
• The dark circles under the eyes
are caused by rerouting the
blood away from the congested
nasal mucous membrane

18. ALLERGIC SALUTE
DENNIS MORGAN’S CREASE

19. CONCOMITANT ALLERGY
• EYES: Itching & watering of eyes
• EARS: Eustachian tube block
• ALLERGIC PHARYNGITIS: Hyperplasia of submucosal lymphoid tissue
• ASTHMA: Attacks of bronchospasm may follow attacks of nasal allergy
• SKIN: allergic eczema
• Larynx: vocal cord edema, dry cough

20. IN VIVO IN VITRO
• SKIN TESTS- SUBCUTICULAR,
INTRADERMAL SKIN TESTS
• NASAL PROVOCATION TEST
• NASAL CYTOLOGY
• RAST
• FLOUROALLERGOSORBANT TEST
• PAPER
IMMUNOALLERGOSORBANT
TEST
INVESTIGATIONS
• NON SPECIFIC- NASAL SMEAR FOR EOSINOPHILS, TOTAL WBC COUNT and
Differential count, AEC, Histamine test
• SPECIFIC

22. SUBCUTICULAR -PRICK/SCRATCH TEST
• Used for SCREENING
• Prick the epidermis of forearm with a drop of test extract solution
(allergen with histamine & saline as control)
• Examine the area :
After 10 minutes for Histamine control
After 20 minutes for Allergen
• Measure the wheal response around the prick

24. OTHER TESTS
• Diagnostic nasal Endoscopy
• X RAY PNS
• CT PARANASAL SINUSES

25. Treatment
•The prevention of allergic rhinitis
• Methods of reducing allergen exposure
• Pharmacological treatment of allergic rhinitis
• Immunotherapy for allergic rhinitis
• Surgical treatment
• Complementary therapie

26. The prevention of allergic rhinitis and reducing
allergen exposure
• Children should Breast-feed atleast first 3 months after birth
• Reducing Allergen Exposure- by regular washing of beddings/ pillows
& Sufficient ventilation to reduce humidity
• At peak pollen times: Windows closed, use Sunglasses/masks
• Exclude pets from bedrooms / keep them outdoors

27. • Wash bedding regularly
• Wash pillows and duvets in hot water
• Sufficient ventilation of dwellings to decrease humidity (use
dehumidifiers)
• Good quality vacuum cleaner
•Eradicate cockroaches with appropriate insecticidal bait
• Food allergy

28. Pharmacological treatment of allergic rhinitis
ANTIHISTAMINES
First-line treatment for these symptoms in patients who have no problem with nasal obstruction.
Little effect on nasal blockage. 1st gen antihistamines (chlorphenamine, diphenhydramine) rarely
used (sedative effects) ketotifen additional effect - mast cell stabilizer.
2nd genoral antihistamines (loratadine and cetirizine) - non- sedating, safe long-term use, can be
used for children. (rapid onset of action and will give symptom reduction on a once daily dosing.)
Topical antihistamines (azelastine) used intranasally to achieve rapid symptom control and
can be combined with a topical nasal steroid. (disadvantages - bitter taste)

29. • Intra nasal glucocorticoids:
Most effective
First-line treatment of choice in patients who complain of nasal block.
Steroids have an effect on the production of pro-inflammatory
mediators within the cell nucleus their effect is slow to occur and long
lasting
It can take two weeks for full benefit to be noticed

30. SYSTEMIC GLUCOCORTICOSTEROIDS
Oral steroids may occasionally be useful in patients with severe
symptoms to allow reduction of mucosal swelling and subsequent use of
topical medication or to cover a short period when symptom control is
particularly bad. Prednisolone 20–40 mg/day is normally sufficient but
oral steroids may cause serious side effects so their use should be
considered carefully and length of treatment be kept as short as
possible. For this reason depot injectable steroids, while effective at
symptom control, are not recommended as once injected their effects
cannot be stopped.

31. LEUKOTRIENE RECEPTOR ANTAGONISTS (LTRAS)
Cysteinyl leukotrienes are a family of eicosanoid inflam- matory mediators (LTC4,
LTD4 and LTE4) produced in leukocytes, mast cells, eosinophils, basophils and
macro- phages by the oxidation of arachidonic acid by the enzyme arachidonate 5–
lipoxygenase. Their effects are to cause bronchoconstriction, increase vascular
permeability and attract inflammatory cells and as such are involved in the
processes underlying asthma and allergic rhinitis. 63 In the UK montelukast (a
leukotriene receptor antagonist) is licensed for the treatment of allergic rhinitis
associated with asthma. In studies it was found to be as effective as loratadine in
reducing nasal symptoms but less effective than a topical nasal steroid. 64
Combined use of cetirizine and montelukast was shown not to improve symptom
control above each drug individually in one study 65 but to be more effective when
combined in another. 66 There is a significant variation in responsiveness to LTRAs
and a closely monitored trial of treatment may be useful in some patients. It now
has a place in the updated ARIA treatment guidelines (Figure 91.3).

32. SODIUM CROMOGLICATE
Sodium cromoglicate nasal spray has modest effects on rhinitis symptoms
but must be used four times daily, which limits compliance. It has no side
effects and can be used on young children. Cromoglicate eye drops can be
effective against ocular itching.
DECONGESTANTS
Topical (e.g. xylometazoline) and systemic decongestants (e.g.
pseudoepedrine) are available and have a place in allergic rhinitis
management The disadvantage is of rebound vasodilation when their use is
stopped leading to a worsening of symptoms and of rhinitis medicamentosa
with longer term use. A maximum length of treatment of 7–10 days
therefore is advised. Systemic decongestants may also have side effects such
as insomnia, tachycardia and tremor.

33. IPRATROPIUM
Topical ipratropium bromide spray is effective at controlling watery
rhinorrhoea and can be a useful addition to a topical steroid if
rhinorrhoea is not being well controlled. Side effects are infrequent but
include prostatic symptoms and worsening of glaucoma.
NASAL DOUCHING
Saline nasal douches may help with symptom control and can physically
remove an allergen from the nasal mucosa. If pollen levels are high
regular douching may be of benefit.

34. MANAGEMENT
I. PATIENTS WITH INTERMITTENT SYMPTOMS:
A) MILD:
Oral H1 BLOCKER
Or
INTRANASAL H1 BLOCKER
+/-
DECONGESTANT
Or Montelukast

35. II. MODERATE-
SEVERE
INTERMITTENT
OR MILD
PERSISTENT
Oral H1 BLOCKER
Or
INTRANASAL H1 BLOCKER
+/-
DECONGESTANT
Or Montelukast
Or Intranasal
Corticosteroid
IN PERSISTENT CASES:
Review after 2-4 weeks
• If failure- STEP UP
• IMPROVED- Continue
for 1 month

36. iii.
MODERATE-
SEVERE
PERSITENT
INTRANASAL CORTICOSTEROID
H1 BLOCKER OR MONTELUCAST
Review after 2-4 weeks:
IMPROVED: Step down & continue
treatment for > 1 month

37. IF FAILURE:
Review
Add or increase
intranasal
corticosteroid
dose
01
RHINORRHEA:
Add Ipratropium
02
BLOCKAGE: Add
Decongestant or
Short term Oral
Corticosteroid
03

40. IMMUNOTHERAPY
INDICATIONS:
• Evidence of IgE mediated disease
• Inability to avoid allergens
• Inadequacy of drug therapy
• Limited spectrum of allergen sensitivities
• Symptoms that span for > 1 season
• Anti IgE antibody – (Omalizumab)

41. PROCEDURE
• Serial SC Injections of immunogenic extracts of relevant allergens
• Given in progressively increasing doses until a maximal tolerated dose
is achieved
• This is the potent immunogenic dose  significantly greater than that
required for a specific IgG response

42. MECHANISM
• Increase in IgG blocking Antibodies, which inactivates allergen specific
T cells
• Increase in allergen specific IgE Antibodies & reduced allergen specific
IgE production
• Prevention of rise in chemotactic factors

43. FOLLOW UP
• Injections are administered once weekly or twice weekly until effects
are noted
• Then once a week for a total of one year
• Maintenance Therapy- Every 3 weeks for 3 years

44. Surgical:
VIDIAN NEURECTOMY
INDICATIONS:
• Intractable secretomotor rhinopathy
• Senile rhinorrhea
• Chronic Epiphora
• Crocodile tears
• Recurrent polyposis

45. ROUTES
TRANSANTRAL TRANSNASAL
• CLASSIC- GOLDING WOOD
PROCEDURE
• SUBPERIOSTEAL
• TRANS-SEPTAL
• DIRECT
TRANSPALATAL

46. NON-ALLERGIC RHINITIS
Any nasal condition in which the symptoms are
identical to those seen in allergic rhinitis but an allergic
etiology has been excluded
• Rhinitis symptoms in the absence of identifiable
allergy (by allergy testing), structural abnormality,
immune deficiency, sinus disease or other causes

47. NON-ALLERGIC RHINITIS
• Idiopathic rhinitis or vasomotor rhinitis or NANIPER
• Non-allergic occupational rhinitis
• Hormonal rhinitis
• Drug-induced rhinitis
• Other forms -NARES, rhinitis due to physical & chemical factors, food-
induced rhinitis, emotion-induced rhinitis, atrophic rhinitis

48. • In patients with perennial non-allergic rhinitis this condition persists
for > 9 months/ year
• >/=2 symptoms of hypersecretion, blockage, sneezing & post-nasal
drip

49. NANIPER
Imbalance between sympathetic & parasympathetic nervous systems
Imbalance in neuronal control of the end organs in the nose

50. Types of Non Allergic Rhinitsi
• Idiopathic rhinitis:
• Nasal blockage
• Rhinorrhoea
• Sneezing
The prevalence of sneezing, conjunctival symptoms and pruritis is lower than that in allergic rhinitis
• Runners: predominantly rhinorrhoea
• Blockers: predominantly nasal congestion and blockage, many patients suffer from more than one
type of these symptoms

51. NON ALLERGIC OCCUPATIONAL RHINITIS
Rhinitis caused by exposure to airborne agents
present in the work place
Sneezing, nasal discharge &/or blockage
Act via both immunologic (IgE-mediated) & non-
immunologic mechanisms
Non-immunologic triggers : Irritant or toxic small
molecular weight compounds such as aldehydes,
isocyanates, aircraft fuel and jet stream exhaust,
solvents
Physical (long-term exposure to cold air)

52. • Damage &/or stimulation of the epithelial cells and neurons by the
irritants
 Proinflammatory mediators and neuromediators
 Predisposes nasal mucosa to inflammation & infection rhinitis
• Occupational exposure to Vanadium pentoxide, a constituent of
fuel oil ash and a known respiratory irritant increase the number of
polymorphonuclear cells in nasal lavage

53. HORMONAL RHINITIS
• Often associated with pregnancy
• Puberty also induce symptoms of rhinitis
• Neither asthma nor rhinitis were, apparently, risk factors for pregnancy
rhinitis
• Estrogens cause vascular engorgement in the nose, leading to nasal
obstruction &/or nasal hypersecretion

54. NARES
• Presence of > 20% Eosinophils in
nasal smears
• lack of evidence of allergy
NARES patients frequently develop nasal polyps and asthma later on in life
 NARES may be an early expression of Sampter’s triad
Bronchial responsiveness is associated with an increase in the number of
sputum eosinophils, but not with an increase in nasal eosinophils
SYMPTOMS:
Perennial sneezing attacks
Profuse watery rhinorrhea
Nasal pruritis
Incomplete nasal obstruction
Anosmia

55. • Individuals with sensitized nasal
mucous membranes  Cold &
dry air  rhinorrhea  SKIER’S
NOSE
• Chemicals & air pollutants
derived from cigarette smoke &
liquid petroleum fuels 
exacerbate symptoms of rhinitis
in non-allergic
Rhinitis due to physical or chemical factors:

56. DRUG-INDUCED RHINITIS
• NSAIDs
• Beta-blockers
• ACE inhibitors
• Methyldopa
• Oral contraceptives
• Psychotropic agents
• Nasal topical decongestants
Aspirin &/or NSAIDs  Rhinorrhea
ACE inhibitors, methyldopa or OCP  nasal blockage

58. RHINITIS
MEDICAMENTOSA
• Decongestants induce
vasoconstriction through alpha1
adrenergic receptors  shrinks
congested mucosa & improve
airway
• Hypoxia & toxic metabolite
accumulation  Reflex
vasodilation
• Increased vascular permeability
• Rebound congestion
• Sub-Epithelial interstitial
fibrosis

59. FOOD-INDUCED RHINITIS
• Certain foods & alcoholic beverages can induce non-allergic rhinitis
• Hot and spicy foods contain capsaicin
stimulates sensory nerves to release neuropeptides & tachykinins
 watery rhinorrhea termed ‘gustatory rhinitis
• Alcoholic beverages  Vasodilation  Symptoms
EMOTIONALLY INDUCED RHINITIS
• Stress and sexual arousal affect the nose, likely as a result of
autonomic stimulation

60. MIXED RHINITIS
A combination of allergic and non-allergic rhinitis, a group not
considered in the other studies.
Both non-allergic & mixed rhinitis occur more frequently in adults
than in children
More common in females
More likely to be perennial than seasonal

61. Occupational rhinitis
Symptoms arising out of causes and conditions attributable to a
particular work environment and not to stimuli encountered outside
the workplace.
The prevalence of occupational rhinitis in the general population is still
unknown.
• Occupational rhinitis is either allergic or irritant.
• Occupational rhinitis frequently coexists with asthma and
conjunctivitis.
• Exposure, atopy and smoking are risk factors.

62. • History of work-related symptoms with improvement in weekends
and holidays is typical.
• Nasal provocation is the main diagnostic test.
• Prevention is the best approach.
• Medical therapy is similar to that for other types of rhinitis.

63. THANKYOU