ALLERGIC RHINITIS

&
INTRINSIC RHINITIS
Dr. Neeraj Rauniyar
M.S. (ORL-HNS) , 2nd Year Resident
GMSM Academy of ENT and HN Studies
TUTH, IOM
 ROADMAP

• Definition
• Classification
• Pathophysiology
• Diagnosis
• Management
• Recent advances
• Controversies
 Definition

• Nasal hypersensitivity symptoms induced by an

immunologically mediated (most often IgE-dependent)
inflammation after the exposure of the nasal mucous
membranes to an offending allergen characterized by
rhinorrhoea, nasal obstruction or blockage, nasal
itching, sneezing, and postnasal drip that are reversible
spontaneously or under treatment.
(ARIA 2012 Revised)
 Prevalence
• Global health problem as prevalence is increasing
• Prevalence - 10% to 20% in the USA and Europe
(Ozdoganoglu et al., 2012)
• Prevalence – 0.8%-39.7%
(Scott-Brawn’s 7th edition)
• Higher in pediatric age group - 42%
(Wright et ;1994)
• Preschool children in China 20.1%
(Li et al., 2010)
• Peak age - 13 to 14.
• Approx. 80% -develop symptoms before age of 20
(Skoner et al, 2001)
 Risk Factors
• Atopy
– tendency to develop exaggerated IgE antibody
response to normally innocuous environmental
allergens
– Predispose to development of allergic disease
– Eg. allergic rhinoconjunctivitis, asthma, atopic
dermatitis
• Family H/O allergy especially allergic rhinitis
• Environment Factor
 higher socioeconomic status
 polluted environments
 Lifestyle changes
 early introduction of foods or formula
Co-morbidities
• 60% of asthmatics suffer from rhinitis

• 20-30% of patients with allergic rhinitis also have asthma

(Prim Care Respir J 2002)
• Children-ratio of asthmatics with AR to asthmatics without
AR is even higher
(Wright et al.,1996)
• 25% - 30% of acute sinusitis have AR

• 40% - 67% of unilateral chronic sinusitis

• 80% of chronic bilateral sinusitis

 Types of Allergic Rhinitis
• Seasonal
• Perennial

Frequency
ARIA
Classification
Severity
 Seasonal Rhinitis
 Pollen:
 Spring (March-June) = Trees
 Summer (May-August) = Grass
 Fall (August-October) = Weeds
 Mold:
 Spores in outdoors have seasonal
variation (reduced in winter,
increased in summer/fall due to
humidity).
 House dust mites:
 Generally “perennial” allergen, but
increased in damp autumn months.
• Symptoms of Seasonal Rhinitis

– Watery nasal discharge

– Nasal congestion
– Paroxyms of sneezing
– Itchy eyes, nose, ears, and throat
 Perennial Rhinitis
 Fungi/mold:
 Exposure peaks accompany
activities such as harvesting &
cutting grass .
 Pet Dander (cats, dogs):
 up to 4 months after pet removal.
 House dust mites:
 Live in bedding & carpets
 Dietary preference: human
epidermal scales.
 Cockroaches:
 Respiratory allergy
 Important allergen
• Symptoms of Perennial Rhinitis

– Little or no seasonal variation

– Symptoms - intermittent or continuous throughout year
– Nasal congestion
primary symptom
– Poor sense of smell -
– Watery nasal discharge & sneezing less prominent
• Patients with persistent rhinitis should be evaluated for
asthma (Bousquet et al., 2005)
Pathophysiology
 Diagnosis
• History
• Physical exam
• Laboratory tests
History
 Physical Examination
Face
allergic shiner
allergic salute
adenoid crease
• Anterior Rhinoscopy
Lungs
• Wheezing
• Persistent coughing

Other areas
• Stigmata of atopic diseases with nasal symptoms
– atopic eczema, asthma
 Differential Diagnosis
• Non-allergic rhinitis
– Infectious, NARES, intrinsic rhinitis , atrophic rhinitis, drug
induced, hormonally induced, rhinitis medicamentosa

• Structural/mechanical factors
– Septal deviation, turbinate hypertrophy, adenoid hypertrophy,
tumor, Polyp

• Inflammatory/immunologic
– Wegener’s, Sarcoidosis, SLE, Sjogren’s

• CSF rhinorrhoea
 Allergy Testing
• Nasal Cytology

• Skin Prick tests

• In vitro tests

• Nasal Allergen Challenge

 Nasal Cytology
• Anterior Inferior turbinate - most representative

• 5:1 Ratio of columnar to goblet cells in normal nasal

epithelium

• 1:4 Ratio in allergic response

• 20% or more Eosinophils inhalant allergy.

 Skin Prick tests
• Simple, safe, rapid, efficient & cost effective

• Negative result usually requires no additional testing

• Positive result requires further testing of other antigens

in the group or family.

• Contain multiple antigens, (pollen, mold, weeds, dust

mite, animal dander)
• Rationale
– allergen introduced into skin causes degranulation of IgE-
sensitized mast cell with mediator release and formation of a
wheal and flare.

• Superficial skin reaction, does not penetrate dermis

• Highly specific, sensitive, convenient

• Requires positive (histamine) and negative (saline) control

Method
• Drop of standardized allergen extract-volar aspect of
forearm-pricked into skin-lancet

• Positive control (histamine) ,-ve control (saline or diluent) –

innoculated
• Separate lancet -each test

• Read -mean wheal diameter -15 mins

• Reactions ->2 mm - <5 yrs

>3 mm- >5 yrs
• +ve results - 2mm greater than –ve results
•Wheal size co-relate with amount of IgE
Whealing response
 Intradermal test
• 0.01-0.05 mL - antigen into – epidermis

• wheal and flare measured after 10-20 min

• can be used to detect most low-degree atopies

• does not permit accurate quantization of sensitivity

• Causes relatively minimal patient discomfort
• Disadvantages
– higher risk of anaphylaxis
– longer time
– Possible false positive
 Skin Endpoint Titration(SET)
 Modified method of IDT
 Serially diluted antigen extracts used
-determine minimal amount of antigen

 Endpoint response -lowest concentration of antigen -

produces -wheal
1. first wheal > 2 mm larger than negative control

2. followed by second wheal that is at least 2 mm

larger than preceding one.

 Endpoint signifies -safe starting point for

immunotherapy
 In vitro testing
 Includes
A) Total IgE
B) Phadiatop Test
B) Allergen-specific IgE antibody Test
• RAST (radioallergosorbent assay)
• CAP RAST
• ELISA test
 useful -if percutaneous testing not practical esp. when
- beta-blockers
- antihistamines (skin testing is unreliable)
- dermatographism, children cannot tolerate skin testing
 highly specific but not sensitive
(Agency for Healthcare Research & Quality,2005 )
• useful - identifying common allergens (e.g., pet dander, dust
mites, pollen, common molds)

• less useful - identifying food, venom, or drug allergies.

Indication of In Vitro Testing

• Impracticality of skin testing
– Skin disorder, unco-operatvie patients

• Clarification of skin test results

– Bizarre or borderline reactions

• Prevention of systemic reactions

– Prior history of anaphylactic reaction, severe asthma
 Total IgE
• AR patient  likely to have an elevated total IgE level
than the normal population

• Approx. 50% of patients with AR have normal levels of

total IgE, while 20% of non-affected individuals can
have elevated total IgE levels.
(Borish et al.,2005)
• Neither sensitive nor specific for allergic rhinitis

• Test is generally helpful in some cases when combined

with other factors.
 Phadiatop Test

• Multi-allergen screening test for aero-allergen

• Useful  difficult to pinpoint with reasonable certainty

the appropriate allergens to test for i.e. equivocal
history for allergy

• +Ve test  sensitive to one or more of the following

inhalants:
– house-dust mites
– grass
– Mould
– cat, dog
 RAST Test
Rationale
Stabilized allergen is incubated with patient seum, any
specific IgE bind to allergen & is identified by 2 nd incubation
with labelled anti-IgE
• Allergen bound to solid phase
• RAST Test  relation with IgE

• Very low (<20 kU/L) IgE  -ve test

• Very high IgE  false +ve test

• RAST graded as 0 – 6

0 = no significant specific IgE

1 = boderline value
2 – 6 = increasing level
CAP RAST
• Specific type of RAST
• Allergen is coupled to cellulose carrier and anti-IgE is
enzyme-labelled
• Different from generic RAST tests  allows to measure
exactly how much IgE is present to a specific allergen
• Higher sensitivity & specificity

ELISA test
– Allergen bound to fluid phase
Modified RAST (MRT)
• Involves an additional washing procedure in order to
reduce non-immunologically bound radioactivity
• Increased sensitivity to RAST
Comparison of SPT & RAST
Test SPT RAST
Time for result Immediate Days-weeks
Cost Cheap Expensive
Safety Safe Very safe
Sensitivity Sensitive Slightly less
Affected by therapy Yes No
Other requirements Training for Trained operator &
performance & interpreter
interpretation
 Nasal allergen challenge
Rationale
 Allergen introduced- nose & any reaction is measured
& compared to placebo

 Gold standard test

 Rarely necessary

 Indications:-
- +ve history & –ive SPT
- prior to immunotherapy –occupational allergy
 Allergen –suitable form ( not containing phenol or other
irritants)
• Diluents of allergen – employed initially

• Allergen-gradually increasing concentration –

monitoring URT & LRT symptoms
• Subjective –symptom scores, VASs

• Objective –sneeze count, nasal inspiratory peak flow ,

rhinomanometry , acousrtic rhinometry , spirometry,
pulmonary peak flow
• Disadvantages
– Time consuming
– Excessive lab facilities
– Trained staff
– Resuscitation equipment
 Treatment modalities
• Allergy avoidance & Environmental control measures
• Pharmacotherapy
• Immunotherapy
• Surgery rarely
Allergy avoidance & Environmental control

• A) Primary measure
– Early use of antibiotics
– Increased vaccination Are implicated
– Restriction of allergen exposure in causation
– Smoking during pregnancy
– Formula feeding
– Obsessional house dust mite avoidance
B) Secondary measure
1)Allergen avoidance

 impractical & difficult to implement, not effective when

used alone.

 sensitive to pollen
- minimize time spent outdoors at times of high pollen
count.
- keep windows of homes & cars closed
- employ AC
2) Allergic to dust mite:

- encasing mattresses, pillows & quilts in impermeable

covers (controversial)

- washing bedding weekly ( 55 C–60 C; 131 F–140)

- High-efficiency particulate air (HEPA) filters -reduce

allergen load

- Insecticides

- sensitive to humidity - dehumidification (controversial)

3) allergic to cats & dogs

- get rid of animals.

- weekly washing can reduce allergens
( controversial)

4)Cockroach infestation
- sealing and controlling food supply
- using chemical control and traps .
- cockroach extermination reduce allergen levels
by 80% to 90%
Pharmacotherapy
Strength of evidence for treatment of rhinitis
intervention SAR PAR
Children Adult Children Adult
oral anti-H1 A A A A
intranasal A A A A
anti-H1
INS A A A A

intranasal A A A A
Cromolyn Na
subcutaneous A A A A
IT
Sublingual IT A A A A

allergen D D D D
avoidance
A: recommendation based on RCT or meta-analysis
(Prim Care Respir J 2002)
D: recommendation based on the clinical experience
SAR: seasonal allergic rhinitis PAR: perennial allergic rhinitis
 H1-antihistamines
• acts - stabilizing H1-receptor - smooth muscle cells,
nerve endings, and glandular cells - reduction in
almost all symptoms rapidly

• only modest effect - nasal congestion

• Levocetrizine more effective than loratadine in improving
AR as show by meta-analysis
A/E (Mosges et al,. 2011)
• 1st gen  sedation, psychomotor retardation, learning
impairment as crosses BBB
• QTc prolongation & arrhythmias 
astemizole, hydroxzine, diphenhydramine
 Intranasal corticosteroids

• Single most effective agents

• Improve all nasal symptoms-nasal

congestion, rhinorrhea, itching &
sneezing

• Currently available INS -

beclomethasone dipropionate,
budesonide, fluticasone, flunisonide
mometasone & triamcinolone
acetonide
MOA:- diffuse across cell membrane- bind specific
intracellular receptors, form complex -
transported into nucleus, binds to glucocorticoid
response elements (GREs)

• transcription of GRE-associated genes either

downregulated or upregulated

• leads -reduction in inflammatory cells & their associated

cytokines in nasal mucosa
( Luisi et al.,1991)
• Goal: control symptom with lowest possible dose.
 A/E of INS
 Local : nasal burning , stinging, dryness, and epistaxis.
( 5% to 10%)

 Systemic side effects :

 minimal or no suppression
hypothalamic-pituitary-adrenal axis
(Wilson et al.,1998)
 Osteocalcin - marker of bone turnover &
eosinophilia unaffected
 No increased likelihood of bone fracture regardless of
dose (Suissa et al., 2004)
 Decongestants
• Topical and oral form.

• Topical vasoconstrictor
-catecholamine (eg, phenylephrine)
-imidazoline (eg, oxymetazoline)

• oral vasocontrictor
-phenylephrine
- pseudoephedrine
 action via 1 and 2 adrenoreceptors
 reduction in blood flow - nasal vasculature - increased
nasal patency
 5 to 10 mins topically
 30 mins - orally.
 Nasal decongestion - last
 8 hours - topical use
 24 hours - extended-release oral decongestants
 Nasal congestion only affected
(Cohan et al.,1979)
 monotherapy with vasoconstrictors - limited role
 oral decongestants + antihistamine- all cardinal
symptoms of AR
 A/E -topical decongestants
• nasal burning, stinging, dryness, and, less commonly,
mucosal ulceration.
• Tolerance and rebound congestion -used for longer than 1
week (rhinitis medicamentosa)

A/E -oral decongestants

• CNS stimulation - insomnia ,nervousness, anxiety &
tremors,
• CVS- tachycardia, palpitations & increases in blood
pressure.
 Mast cell stabilizers
 Cromolyn sodium- inhibits degranulation of sensitized
mast cells thus blocking release of inflammatory
mediators.

 Allergen challenge studies – effective in reducing –early &

late-phase allergic reaction
(Orie et al.,1996)

 Indicated in both seasonal and perennial AR

(Cohan et al.,1969)
 Onset of relief - first week treatment
• 4% intranasal solution - recommended for adults and
children aged 2 and older.

• solution four times daily.

• symptoms - under control, less frequent dosing

• Poorly absorbed systemically -excellent safety record.

• A/E -Topical
– sneezing, nasal irritation, and unpleasant taste
 Antileukotrienes

 High concentrations LTC4 - in nasal secretions atopic

individuals after allergen challenge ( Wang et al.,1995)

 LTD4 increase nasal mucosal blood flow & nasal

airway resistance (Bisgaard et al.,1986)

 Blockage of the LT
- 5-lipoxygenase (5-LO) inhibitors:-Zileuton
-Receptor blockade -cys-LT1 receptor :-Montelukast &
zafirlukast.
 Receptor antagonists
 Zafirlukast performed no better than placebo - seasonal AR
( Pullerits et al.,1999)

 Other study - reduction in upper respiratory responses to cat

exposure
(Phipatanakul et al.,2000)

 Montelukast - clinical efficacy in seasonal AR

(Chervinsky et al.,2004)
 Antihistamine + antileukotriene treatment started 6 weeks before
the pollen season  preventing AR symptoms during natural
allergen exposure
( Kurowski et al., 2004)
• Montelukast + loratadine -superior reducing day time
nasal symptoms in seasonal AR (Meltzer et al.,2000)

• Not better controlled with combination than once daily

fexofenadine (Wilson et al.,2004)

• leukotriene antagonists do not appear more effective

than nonsedating antihistamines

• less effective than INS

(Ratner et al.,2003)
• Useful- concomitant mild persistent asthma and
intermittent AR.
 Immunotherapy (IT)
• Repeated administration of allergen extract –induce state of
immunological tolerance

• Reduction in clinical symptoms & requirements for

medication - subsequent natural allergen exposure
(Bousquet et al; 1998)
Indications
• IgE -mediated disease (+SPT/RAST)
• AR –severe symptoms ,fail to usual treatment
• Inability to avoid allergens
• Patients who understand risks & limitations of treatment
• Limited spectrum of allergen sensitivities (1 or 2)
Contraindications:
• age < 5 yrs
• use of beta-blockers
• Other medical/autoimmune disease
• pregnancy
• uncontrolled asthma FEV1 < 70%
Efficacy
 Highly effective -selected patients (Grade A)
 Grass pollen induced rhinitis-50% reduction in sx & 80%
reduction in rescue medication (Wallker et al.,2001)
 Reduction in seasonal bronchial hyperresponsiveness
 Treatment for 3 to 4 yrs –improvement for 3 yrs following
discontinuation (Durham et al.,1999)
• Children with seasonal rhinitis IT for 3 yrs-2 to 3 fold
reduction in developing asthma
(Moller et al.,2002)
• Offers long term disease modification & prophylaxis

A/E of IT
• Local rxns – trivial
• Systemic reactions-10%-updosing phase
• Mild rhinitis, asthma responding –antihistamines or
inhaled bronchodilators
• Occasionally – severe systemic rxns-general urticaria ,
severe asthma or anaphylaxis
Protocol
– Updosing phase-
weekly inj -8 to 16 wks
– Maintainance phase-
4- 8 wkly intervals-3-5yrs
– Hospital basis
– Observed  1 hour
Mechanism of ITX
• Blunting seasonal increase-allergen specific IgE
• Blocking of IgE Abs
• Inhibition recruitment & activation –inflammatory cells
• Modulation of T –lymphocyte functions
Routes of Immunotherapy
• Sublingual route (SLIT)/Subcutaneous route (SCIT)

• SLIT  efficacy  less than SCIT

• Allergen –drops or tablets under tongue-retained for

several minutes -swallow

• Dose of allergen is greater than subcutaneous

immunotherapy
 Recent meta-analysis –confirmed efficacy

[Grade A]
 UK grass pollen sublingual immunotherapy trial-
-3o% reduction-symptoms
- 38% reduction –rescue medication use
(Till et al; 2004)
 Immunotherapy effective not only as a therapeutic agent
but also as a preventive
(Finegold 2002)
Novel ITX approaches
• Using adjuvants
– Bacterial DNA sequences (CpG)
– Allergen peptides
– Short length allergen peptides
 Human monoclonal antibody

 Omalizumab - recent developments in the treatment of atopic

diseases
 Modulation of allergic inflammation.

 expensive for routine treatment of AR primarily indicated -

severe asthma.
 Effective-both allergen challenge studies & clinical trials.

 Multiple randomized, double-blind, placebo-controlled studies -

efficacy in seasonal and perennial AR
(Vignola AM et al.,2004)
 Surgery

• Marked septal deviation

• Turbinate hypertrophy

• Endoscopic sinus surgery- rhinosinusitis

[Grade B]
 Recent advances in treatment
Gene therapy
An easy, effective, and convenient treatment
delivering the allergen or the therapeutic protein in the
form of plasmid DNA in vivo to modulate allergic immune
responses
(Chuang et al,. 2009)
Endonasal Phototherapy
• Combination of UV-A (25%), UV-B (5%) and visible light
(70%)
• Reduces the number of inflammatory cells and the level of
mediators
(Demirbas et al., 2011)
• Effective modality in the treatment of
allergic rhinitis patients refractory to antiallergic drugs
• positive effects on the quality of life
(Cingi et al., 2009)

• Pioglitazone
– activation  inhibits the inflammatory process 
attenuates allergic inflammation & induces production of
regulatory T lymphocytes ( Wang et al., 2010)
 Conclusion
• Prevalence  increasing
• ARIA classification is evidence based & treatment plan
acc. to it is easy
• Pathophysiologically release of mediators from different
cells leads to C/F
• Diagnosis by history, exam and allergic test esp. SPT &
RAST
• The strategy to treat allergic diseases is based on:
(i) patient education, (ii) environmental control &
Allergen avoidance, (iii) pharmacotherapy, and (iv)
immunotherapy
• INS ,antihistaminics & allergen avoidance  main
modality
• Allergen avoidance, INS & ITX  resistant cases
INTRINSIC RHINITIS
 Various terms used

 Non-allergic Non infectious Perennial rhinitis

(NANIPER)
 Intrinsic rhinitis
 Intrinsic Rhinopathy
 Vasomotor rhinitis

 Vasomotor rhinitis – commonest term

 Intrinsic Rhinitis

Definition
• Condition persisting for >9 months each year and
produces ≥ 2 symptoms including
 Hypersecretion
 Blockade
 Sneezing
 PND
(Scott-Brown’s 7th edi.)
 Classification
 Idiopathic rhinitis (Vasomotor rhinitis, or non-allergic
non-infectious perennial rhinitis (NANIPER)

 Non-allergic occupational rhinitis

 Hormonal rhinitis

 Drug induced rhinitis

 Others – Non allergic rhinitis with eosinophilia syndrome

(NARES), food induced rhinitis, emotional rhinitis,
rhinitis due to chemical & physical factors, atrophic
rhinitis (Bosque et al; 2001))
 Prevalence
 7-21 % --general population

 20-50% -rhinitic population

(Jassen et al;1998)

 1000 patients -18 clinics USA

-23% - intrinsic rhinitis
-34% - mixed rhinitis
(Settipane et al ;2001)

 30% associated – nasal polyposis

(Settipane et al,
1977)
 Aetiopathogenesis of Intrinsic Rhinitis
• Autonomic imbalance
– Parasympathetic hyperactivity
– Sympathetic hypoactivity
• Non-IgE-mediated inflammatory responses
• Neurotransmitters
– adrenaline
– Acetylcholine
- VIP

 Sympathetic system – nasal resistance to airflow

 Parasympathetic system  nasal glands  increase

parasympathetic outflow  glandular hypersecretion
 Eosinophilic intrinsic rhinitis- (Nasal obstruction
syndrome)
-autonomic imbalance, local inflammation &
recruitment of inflammatory cells

-nasal obstruction

-relieved – inhaled corticosteroid

-8 % with nasal polyposis –intolerance to aspirin

(Dark Lee ,et
al.,1972)
 14% associated –asthma
(Mularkey et al.,1980)
• Non eosinophilic intrinsic rhinitis (Rhinorrhoea
syndrome)
-autonomic imbalance

-increase parasympathetic outflow

-rhinorrhoea

-anticholinergic for teatment

Turbinate enlargement
• Inferior turbinate enlargement- nasal obstruction
• Swelling of submucosa
• Dilatation of submucosal venous
sinusoids
(Cauna et al.,1975)
• Under adrenargic control
• Collapse on sympathetic stimulation
• Facilitated by vasoconstrictor
drugs
• Turbinate mucosa -oedematous with eosinophils &
mast cells (Cauna et al.,1972)
 Clinical picture
• Nasal obstruction
• Sneezing
• Nasal itching
• Rhinorrhoea
• Hyposmia
• PND
• Sneezing
• Itching Allergic rhinitis

• Nasal congestion
• Significant hyposmia Intrinsic rhinitis
• Childhood rhinitis – Allergic

• Adulthood rhinitis – Intrinsic

 C/F of Eosinophilic & Non-Eosinophilic IR

Symptom Eosinophilic Non- Eosinophilic

Obstruction Moderate/Severe Mild

Rhinorrhorea Mild/Moderate Severe
Sneezing/Pruritis Minimal Minimal
Hyposmia Usual Rare
Aspirin Sensitivity + -
Sign
Mucosal Swelling Marked Mild
ITH Marked Mild
Polyp Frequent Never
Sinus Mucosal Thicking Frequent Rare

Treatment INS Anticholinergic

 Diagnosis
• History
• Examination
• Investigations
 Treatment
1)Medical
2) Surgical
 Medical treatment

 Controversial

Eosinophilic IR
-INS
• Topical  Fluticasone, Mometasone
• Systemic  short duration
-Alfa receptor agonists-
• Topical  xylomethazoline
• Systemic pseudoephindrine
-Mast cell stabilizers
• Topical  cromoglycate
• Systemic  Ketotifen
Non eosinophilic rhinitis-

- Anticholinergic
• Topical  ipratropium
• Systemic  hyosine

-Anticholinergic / sympathomimetic
• imipramine ( orally)
• Cholorphenaramine ( orally)
 Surgical treatment
For eosinophilic rhinitis
Inferior turbinate reduction
• Linear thermal cautery
• Silvernitrate cautery past
• Laser cautery -recent
• Submucosal diathermy equally effective
• Cryotherapy
• Radical trimming- recurrance

For Non- eosinophilic rhinitis

Vadian Neurectomy
• Excision
• Diathermy
• Division of vidian nerve
 Recent Advances in treatment

Radiofrequency volumetric tissue reduction (RFVTR)

 Radiofrequency (RF) heating

induced submucosal tissue
destruction & tissue volume
reduction

 According to size of turbinate

 probe -inserted - 2-3 points

along length of turbinate
• Temp. maintained - 60°C to 90°C

• Protein denaturation -tissue coagulation occurs

at 49.5°C
Vidian neurectomy
• Severe rhinorrhoea not responding –ipratropium &
other medications
(Golding-Wood ,1973)
 Transantral approach
 Transnasal approach
 Transphenoid approach (Lee et al., 2011)
• High relapse rate
• Reinnervation  with in 1 year
 Conclusion
 Intrinsic rhinitis is common disease

 Thorough history and examination to reach at positive

diagnosis of IR after excluding allergy

 For eosinophilic IR INS

 For Non-eosinophilic IR  ipratropium

 Various other drugs to be prescribed before going for

surgery
Thank you