Intrinsic Rhinitis and Rhinitis Medicamentosa

Spectrum of Disease
Vasomotor rhinitis
Non-Allergic Rhinitis with Eosinophilia Syndrome (NAREs)
Occupational rhinitis: flour, animal, wood, latex, paint
Rhinitis medicamentosa: Prolonged use of decongestant nasal drops
Drug-induced: propranolol, O.C.P., antidepressants
Endocrine: hypothyroid, pregnancy, menstruation
Miscellaneous: honeymoon / emotional/ non airflow / addiction

Pathogenesis:
Overactivity of Parasympathetic nervous system of nose
Nasal congestion (due to nasal vasodilatation)
Nasal block (due to nasal vasodilatation)
Watery rhinorrhoea (due to ed nasal glandular secretions)
Trigger Factors:
Emotional stress, sudden change in temperature, humidity , blasts of cold air, dust, smoking & traffic fumes
Clinical Features
Symptoms - perennial
Nasal block (blockers)
Profuse watery rhinorrhoea (runners)
Paroxysmal early morning sneezing
Postnasal drip
Signs
Turbinates congested & hypertrophied
Sequelae
Nasal polyp, hypertrophic rhinitis, sinusitis

1. Intrinsic Rhinitis
(Non-allergic Non-infective rhinitis,
Vasomotor rhinitis)
Prof. (Dr.) Krishna Koirala
18-07-2023

2. Spectrum of Disease
•Vasomotorrhinitis
•Non-AllergicRhinitiswithEosinophiliaSyndrome(NAREs)
•Occupationalrhinitis:flour,animal,wood,latex,paint
•Rhinitismedicamentosa:Prolongeduseofdecongestant
nasaldrops
•Drug-induced:propranolol,O.C.P.,antidepressants
•Endocrine:hypothyroid,pregnancy,menstruation
•Miscellaneous:honeymoon/emotional/nonairflow/
addiction

3. Autonomic nerve supply of nose

4. •Deep petrosal nerve (sympathetic) + Greater Superficial
petrosal nerve (Parasympathetic)Vidian nerve (Nerve of
Pterygoid canal)Pterygopalatine ganglion Nasal
glands
Parasympathetic
stimulation 
Vasodilatation,
Increased nasal
secretions
Sympathetic
stimulation
Vasoconstriction ,
Decreased nasal
secretions

5. Vasomotor Rhinitis

6. •Pathogenesis:
–Overactivity of Parasympathetic nervous system of nose
•Nasal congestion(due to nasal vasodilatation)
•Nasal block(due to nasal vasodilatation)
•Watery rhinorrhoea(due to ed nasal glandular
secretions)
•Trigger Factors:
–Emotional stress, sudden change in temperature, humidity ,
blasts of cold air, dust, smoking & traffic fumes

7. Clinical Features
•Symptoms -perennial
–Nasal block (blockers)
–Profuse watery rhinorrhoea (runners)
–Paroxysmal early morning sneezing
–Postnasal drip
•Signs
–Turbinates congested & hypertrophied
•Sequelae
•Nasal polyp, hypertrophic rhinitis, sinusitis

8. ALLERGIC INTRINSIC
Allergen exposure Yes No
Nasal itching +++ Minimal
Sneezing +++ +
Rhinorrhoea ++ +++
Nasal obstruction ++ +
Hyposmia ++ +

9. ALLERGIC INTRINSIC
Nasal mucosa Pale Congested
Nasal polyps ++ Rare
Absolute Eosinophil
Count
ed Normal
Nasal smear
eosinophil
ed Normal
Skin prick test Positive Negative
Treatment
Steroid spray, Anti H1,
Nasal decongestant
Ipratropium,
Botulinum

10. Treatment of
Vasomotor Rhinitis

11. General Measures
•Sleepwithheadendelevatedby30
0
•Sleep+workinacoolenvironment(notcold)
•Keepbodywarm
•Regularexerciseprogramtoimprovevasomotor
tone
•Avoidanceoftriggerfactors

12. Medical Treatment
•Antihistamines:
–Systemic: Cetirizine, fexofenadine, loratadine, levocetrizine,
ebastine
–Topical: Azelastine spray
•Nasal Decongestants
–Systemic: Phenylephrine, pseudoephedrine
–Topical : Xylometazoline, oxymetazoline, saline
•Topical and systemic steroids

13. Drug SneezeRhinorrhoeaNasal
block
ed smell
Antihistamine+++ ++ + 0
Steroid spray+++ +++ +++ +
Cromoglycate + + + 0
Topical nasal
decongestant
0 0 ++++ 0
Ipratropium 0 ++ 0 0

14. Steroid spraysStrength /
puff
Acute attack
dose
Maintenance
dose
Beclomethasone 50 g 2 puffs BD 1 puff OD
Budesonide 64 g 2 puffs OD-BD 1 puff OD
Fluticasone 50 g 2 puffs OD-BD 1 puff OD
Mometasone 50 g 2 puffs OD-BD 1 puff OD

15. Surgical Treatment
1.Toreducesizeofnasalturbinatesthusto
relievenasalobstruction
2.Sectioningparasympatheticsecretomotor
fibersofnose(Vidianneurectomy)torelieve
excessiverhinorrhea

16. Surgeries to reduce the size of turbinate
•Formucosalhypertrophy
–Onsurface:Electrocautery,Laser
–Submucosal:Electrocautery(Submucosaldiathermy),
cryotherapy,radiofrequencyablation
•Forbonyhypertrophy
–Submucousresectionofinferiorconcha
•Formucosal+bonyhypertrophy
–Partial/totalturbinectomy

18. •Trans -septal approach
•Trans -antral approach (Golding Wood)

19. Rhinitis Medicamentosa
(Rebound Nasal Congestion)
•Inflammationofthenasalmucosaleadingtorebound
nasalcongestioncausedbytheoveruseoftopicalnasal
decongestants(>10-14days)
•Subsetofdrug-inducedrhinitis
•Prolongedusetachyphylaxismorefrequentdose
•Nasalmedicationscontainingbenzalkoniumchloride
(antimicrobialpreservative)causemorerebound
congestionbyinducingmucosalswelling

20. Physiology of Nasal Congestion
•Thenasalmucosalvascularsystem
–Resistancevessels(arterioles)whicharepredominantly
regulatedbyalpha-2adrenoreceptors
–Capacitancevessels(venousplexus)regulatedbyboth
alpha-1andalpha-2adrenoreceptors
•Stimulationofthesereceptorsleadstothedecongestanteffect
(vasoconstrictionofthelargevenoussinusoidsandcollectingveins)
decreasedbloodflowdecreasednasaledemaandrhinorrhea
•Parasympatheticnervoussystemstimulationcontributestonasal
congestion

21. Types of intranasal decongestants
(adrenoreceptor activity)
•Beta-phenylethylamine derivatives (primarily
alpha-1 agonists)
–Ephedrine, Phenylephrine
•Imidazoline derivatives (primarily alpha-2 agonists)
–Oxymetazoline ,Xylometazoline
•Imidazolines produce the effect mainly via alpha-2
adrenoreceptors (more effective due to their
vasoconstrictive effect to both capacitance and
resistance vessels in the nasal mucosa)

22. Offending drugs : Oxymetazoline , Xylometazoline
•Oxymetazolineisanadrenergicα1-andα2-agonistand
adirect-actingsympathomimeticdrug
•Itcausesvasoconstrictionofdilatedarteriolesand
reducesbloodflowbystimulatingadrenergicreceptors
•Contractssmoothmuscleofvenouserectiletissue
presentinnasalturbinatesmucosalshrinkageand
decreaseairwayresistance

23. Pathophysiology
•Chronicvasoconstrictionleadstoischemiaofthenasal
mucosaleadingtointerstitialedema
•Fatigueoftheconstrictormechanismsoccursresultingin
reactivehyperemiaandcongestionleadingtoreduced
sensitivitytoendogenouscatecholaminesthe
adrenoreceptorsbecome refractorytonasal
decongestants,necessitatinghigherdosageofmedication
(tachyphylaxis)
•Alterationinvasomotortoneresultsinincreasedvascular
permeabilityandedema
•Thebeta-adrenoreceptoractivitymayoutlastthealpha
effectsleadingtoreboundvasodilatation

24. Pathogenesis

25. Clinical Features
•Chronicnasalblockrequiringincreaseddose&
frequencyoftopicaldecongestantsafterits
prolongeduse
•Nasalmucosaappearshyperemic,granular&
boggyinearlystagesandpale&anemicinlater
stages

26. Treatment
•Immediatewithdrawaloftopicaldecongestant-
Substitutewithsystemicnasaldecongestants
•Nasalcorticosteroidsprays&oralcorticosteroids
•Rhinostatsystem:Decreasingconcentrationof
decongestants
•PatientEducation:
–Avoidtopicaldecongestantusefor>10days