Non Allergic Rhinitis by Dr Marjan

1. NON ALLERGIC RHINITIS
DR MARJAN

2. • The term ‘Non allergic rhinitis' is commonly applied to a variety of rhinitis
related problems that cause intermittent rhiorrhoea, nasal congestion, and
nasal obstruction unrelated to allergy.
• Nasal itching and sneezing lesser. Eye symptoms not prominant.
• 2 or more symptoms(including hypersecretion, post nasal drip) persists >9
months/year
• Occur more frequently in adults, increases with increase in age, more in females
• More likely to be perennial than seasonal.

3. PREVALENCE
• incidence: among in allergy clinic patients 28%-60% have NAR

4. AETIOLOGY
• Neurovascular disorder
• No specific antibodies
• Nonspecific reflex hypersensitivity
• Caused by various influences
• Change of temperature or humidity
• Alcohol , dust, smoke, mechanical irritation, stress, anxiety neurosis, endocrine disorders, rhinitis of
pregnancy.
• Certain precipitants such as perfume or strong odors are frequently identified
• Drugs: (e.g., antihypertensive agents as reserpine or betablockers, oral contraceptives)
• Drug abuse: (imidazoline & catechol derivatives,

5. PATHOPHYSIOLOGY
Nasal functiona and innervation
• Temp regulation, Olfaction, filteration, humidification of inspired air
• Nasal lining--> Ig A, protein, enzy for lubrication & protection
• Secretions trap the particulate matter and propels it towards natural ostia
• Frequency of 10-15 beats/min

6. INNERVATION
• Regulation of mucosal vasculature & glandular secretion- ANS
• Sympathetic --> NE & neuropeptide Y--> VC nasal musculature (decongestion)
• Parasympathetic-->ACh, NE & VIP--> increases nasal gland secretion
• Nasal sensation: 5th CN
• Afferent ethmoidal nerve--> sensory innervation to epithelium, vessels and glands
• C fibres(unspecialised afferent sensory fibres) react to pain & temp changes & osmalarity-
most imp in NAR

7. C fibres
• Stimulated by inflammatory mediators(histamine, bradykinin)--> involved in centrally
mediated reflexes.
• Stimulated by irritants: nicotine, smoke, formaldehyde & capsaicin
stimulated--> C fibres depolarise -->
--> release neuropeptides(substance P, calcitonin gene- related peptide)
--> increases vascular permeability & submucosal gland release
--> acute stimulation of glandular/endothelial & epitheial cells
--> Sensation of itching, rhinorrhea & burning

8. • Hyperresponsive afferant arc--> exaggerated efferent arc (parasympathetic--
>excessive nasal secretin and nasal congestion, if sympathetic is decresed --
>nasal congestion
• Problem can be intrinic epithelia or CNS regulation
• quite complex ,numerous factors
• intricate innervation by sensory, paraympathetic & sympathetic nerves
• other factors like inflammatoy cascades & multitudes of cellular and protein
reactions

10. NON ALLERGIC PERENNIAL RHINITIS
TYPES:
1.Vasomotor rhinitis / idiopathic rhinitis/ NANIPER
2. Non allergic occupational rhinitis
3. Hormonal rhinitis
4.Drug induced rhinitis
5.NARES
6.Rhinitis due to physical and chemical factors
7.Food induced
8. Emotion induced
9. NAR due to atomic obstruction/Atrophic rhinitis/ systemic disorder/ CSF fluid rhinorrhea

11. CLASSIFICATION OF RHNITIS

15. R A Settipane, et al., Update on nonallergic rhinitis, Ann Allergy Asthma Immunol 2001;86:494–508.

16. VASOMOTOR RHINITIS(IDIOPATHIC
RHINITIS)(VMR)
• Definition – “Heterogeneous group of patients with chronic nasal symptoms that
are not immunologic or infectious in origin and are usually not associated with
nasal eosinophilia”
• Dx by exclusion
• classified as either ‘runners’ (those with predominantly rhinorrhoea) or ‘blockers’
(those with predominantly nasal congestion and blockage),
• No specific cause found
• M/c form of NAR. at least 2/3 of all nonallergic rhinitis suffers
• Symptoms : rhinorrhoea, sneezing, nasal obstruction

17. PATHOPHYSIOLOGY
• Autonomic imbalance – Parasympathetic dominance
produce excessive rhinorrhea
• Some show more generalized autonomic dysfunction including both the
sympathetic and parasympathetic nervous systems
• Triggered mainly by irritants & change in atmospheric cnditions.

18. SYMPTOMS
• Variable
Mainly
• – Nasal obstruction
• – Increased secretion
• Sneezing and pruritus and conjunctival symptoms are less common

19. INVESTIGATION FOR VMR
• Negative responses on skin or blood tests for specific IgE
• Nasal tissue cytologic analysis will not demonstrate eosinophils or other
inflammatory cells

20. TREATMENT
CONSERVATIVE TREATMENT
• Elimination of irritant factors
• Antihistamines
• Nasal decongestant drops
• Oral decongestant drugs
• Steroids sprays (e.g., beclomethasone)

21. SURGICAL TREATMENT
In recalcitrant cases
In 1961 GOLDIN- WOOD - transantral vidian neurectomy(Parasympathetic nasal fibers
divisions )
Complications: places internal max A, max N, Sup alveolar N in risk
Transpalatal-oronasal & orosinual fistula
Transethmoidal - bleeding from ethmoidal artery & vision problems
Endoscopic transnasal approach

22. OCUPATIONAL RHINITIS
Occupational rhinitis defined as rhinitis caused by exposure to airborne agents present in the work
place.
Prevalence 5-15%
Along with typical symptoms of NAR, will have impaired sense of smell,nosebleeds, crusting,
reduced mucociliary clearance, also have hyperreactivity
Baraniuk & kaliner- different chemical exposures as--immunologic, annoyant, irritational &
corrosive
• Immunologic (HMW agents with biologic source)
• annoyants- seen in pts with heightened olfactory awareness
• Irritational- when exposure is beyond threshold level.
• Corrosive(LMW compounds cause non- immunological inflammation),

23. CHART

24. PATHOPHYSIOLOGY
• Nose is the portal of entry & materials impact on the mucous surface as a
function of aerodynamic equivalent diameter(AED).
• Approx 80% of those that have an AED of more than 9 micrometre, 50% of
those with 2-9 micrometre AED & 40% of material wth less than 2 micrometre
stick to the nasal wall.

25. • Possible that damage and/or stimulation of the epithelial cells and neurons by the
irritants may lead to proinflammatory mediators and neuromediators, which
may predispose the nasal mucosa to inflammation and infection, subsequently
resulting in the symptoms of rhinitis
• Mainly by neurogenic mechanism: C fibres--> neuropeptide Y--> VD& edema &
inflammation
• Will have associated bronchial and ophthalmic manifestations

26. • episodic work related symptoms of rhinitis which usually manifest on weekdays &
abate during weekends & holidays.
• Risk factors for developing occupational rhinitis are:
o Exposure{intensity & duration}
o Atopy
o Smoking

27. • Occupational rhinitis frequently coexists with asthma & conjuctivitis.
• Prevention is the best approach .
• Antihistamines(2nd generation), sodium cromoglycate, topical steroids,
antihistamine nasal spray & saline douches are used. (trial & error)
• Treatment most effective in allergic occupational rhinitis
• IMMUNOTHERAPY- purified rhodent proteins, wheat flour extracts & natural
rubber latex.

28. EXERCISE-INDUCED RHINITIS
Due to autonomic dysfunction
Clinical findings
– Most common: Clear, watery rhinorrhea
– Acute nasal congestion
– Itching
– Sneezing
• Up to 20% of elite runners and swimmers experience symptoms during routine
workouts
Azelastie nasal apray is effective

29. HORMONAL RHINITIS
• Often associated with pregnancy (rhinitis of pregnancy)
• Also seen
in puberty
post menopausal

30. RHINITIS OF PREGNANCY
• Incidence: 20% to 30% of pregnant women
• Definition:
– New-onset nasal symptoms (usually congestion and/or rhinorrhea)
– Absence of other known cause
– Lasts >/= 6 weeks
– Better towards term
– Resolves within 2 weeks after delivery
• More in pregnant smokers (69%)
• Neither asthma nor rhinitis are risk factors for pregnancy rhinitis.

31. Pathophysiology:
• Oestrogens cause vascular engorgement,in the nose--> leading to nasal
obstruction and/or nasal hypersecretion.
• Beta-oestradiol and progesterone --> increase the expression of histamine H1
receptors on human nasal epithelial cells and mucosal microvascular endothelial
cells& induce eosinophil migration and/or degranulation.
• Preexisting chronic rhinitis can worsen, improve, or remain unchanged during
pregnancy

32. COMPLICATIONS
Uncontrolled rhinitis during pregnancy
– Severe snoring
– Increased risk of
• Gestational hypertension
• Preeclampsia
• Intrauterine growth retardation

33. TREATMENT
1. Reassurance
2. Saline douches
3. Diphenhydramine in first trimester- cleft lip & palate.
4. Chlopheriramine - cat B, can be used.
5. Decongestants not advised- gastroshisis
6. Topical & systemic streoids can be used but cautiously & with limitations
7. Intranasal cromolyn( cat B)

34. OTHER HORMONAL RHINITIS
• Growth hormone
• – Acromegaly can contribute to rhinitis symptoms
• Hypothyroidism
• – Evidence linking to rhinitis is limited and may merely represent the concomitant
occurrence of two common disorders

35. FOOD-INDUCED RHINITIS
• Watery rhinorrhea – Mostly bilateral & Begins soon after beginning to eat
• Virtually all foods
• Underlying mechanisms are largely unknown.
• Hot and spicy foods, in particular, which contain capsaicin, lead to a watery
rhinorrhoea termed ‘gustatory rhinitis’, probably as a result of the capsaicin
stimulating the sensory nerves to release neuropeptides and tachykinins.
• Alcoholic beverages induce symptoms as a result of vasodilation.

36. • Dyes and preservatives, as well as sulphites, appear to play a role in a very few
cases, whereas some foods may contain clinically relevant concentrations of
histamine or other biogenic amines.
• Some patient may acquire specific IgE to certain foods
• Consequently development of acute food-induced rhinitis
• Patients who experience recurrent nasal symptoms after eating virtually any food
are rarely found to have an atopic etiology

37. AGE - RELATED RHINITIS
• Important changes in nasal physiology in aging
– Decrease in total body water content
– Decrease in nasal blood flow
– Degeneration of mucous glands
– Collagen fibers in cartilage and elastic fibers in the dermis become progressively
atrophic
cause nasal block/ rhinorrhea

38. RHINITIS DUE TO PHYSICAL AND CHEMICAL
FACTORS
• In individuals with sensitized nasal mucous membranes.
Cold air-induced rhinitis
• Cold, dry air Skier's nose
• Watery discharge (most prominent feature)
• Congestion
• Burning of the nasal mucosa
• Develop within minutes of exposure to cold air
• Stop soon after the end of exposure
• Common in areas with low outdoor relative humidity

39. • Cod, dry air causes sensorineural stimulation--> increases tonicity & osmolarity of
nasal secretions--> release inflammatory mediators, afferent arc stimulation,
increased parasympthetic activity, increased epithelial shedding--> generation of
rhinitis symptoms

40. EMOTIONALLY INDUCED RHINITIS
• Emotional factors such as stress and sexual arousal have been documented to
affect the nose, as a result of autonomic stimulation.

41. DRUG-INDUCED RHINITIS
• Aspirin, other nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers,
angiotensin-converting enzyme (ACE) inhibitors, methyldopa, OCP, psychotropic
agents and nasal topical decongestants
• induce symptoms of rhinitis when they are administered either topically or systemically.
• predictable,(known side effects) or unpredictable, based on individual
hypersensitiVity ,in particular aspirin

42. • Intolerance to aspirin and/or NSAIDs --> predominantly rhinorrhoea (isolated
or part of a complex involving hyperplastic rhinosinusitis, nasal polyps and asthma)
• Intolerance to ACE I , methyldopa or OCP --> predominantly to nasal block.
• Persistent overuse of the topical nasal vasoconstrictors --> leads to nasal
decongestion by a mechanism involving a rebound effect following withdrawal of
these drugs, excessive use of these agents may also lead to nasal hyper-
reactivity and hypertrophy of the nasal mucosa, a condition known as ‘Rhinitis
medicamentosa’.

45. • Other drugs -- Mechanism?
– Induce changes in nasal function by causing inflammation, through neurogenic effects
– Unknown mechanisms
• Evidence is anecdotal and not supported by investigation
• Apart from rhinitis medicamentosa, drug-induced rhinitis may be further classified into:
• – Local inflammatory type
• – Neurogenic type
• – Idiopathic (unknown) type
• In these mechanism, nasal mucous membrane is often normal (different from rhinitis
medicamentosa)

46. LOCAL INFLAMMATORY TYPE
• Main drugs: Aspirin and NSAIDs
– Including
• ASA exacerbated asthma (AEA)
• “Triad” of nasal polyposis, asthma and aspirin or other NSAIDs sensitivity
• Principle mechanism : Inhibition of cyclooxygenase-1 (COX-1)

49. NEUROGENIC TYPE
• Sympathetic
• Parasympathetic
• Sensory fibres

50. SYMPATHETIC
• - Adrenergic sympathetic neuron fibres contain
Norepinephrine & Neuropeptide-Y (NPY)

51. PATHOPHYSIOLOGY

53. IDIOPATHIC TYPE

54. NARES-
• Mullarkey and colleagues: characterized the condition on the basis of a presence of > 20%
eosinophils in nasal smears of symptomatic patients with perennial symptoms of episodes
profuse watery rhinorrhoea, nasal pruritis, incomplete nasal obstruction,,epiphora,sneezing
and occasional loss of smell.
• There is lack of evidence of allergy, as indicated by negative SPT &/or absence of serum IgE
antibodies to specific allergens.

55. • Triad of nasal polyposis , intrinsic asthma, intolerance to aspirin-sampter’s triad.
• NARES may be an early expression of the triad
• In 1/3rdcases it is isolated.
• 50% of NARES patients without a history of respiratory symptoms, bronchial
responsiveness is associated with an increase in the number of sputum
eosinophils
• NARES is a variant of vasomotor rhinitis, and referred to the condition as
‘perennial intrinsic rhinitis’.

56. • Mostly found in middle-aged patients
• Extremely infrequently in childhood
• <2% of children with nasal eosinophilia
• Prevalence general population: Unknown
Prevalence -- 13 and 33% in patients with non-allergic rhinitis(About 1/3 of cases of
nonallergic rhinitis)
PREVALENCE

57. PATHOPHYSIOLOGY
• Not clearly understood
• Eosinophilia may contribute to nasal mucosal dysfunction
• May be due to release of toxic substances contained in eosinophil granules
– Major basic protein
– Eosinophil cationic protein
Result: May damage nasal ciliated epithelium and prolong mucociliary clearance

59. SYMPTOMS
• Usually more intense nasal symptoms than vasomotor or allergic rhinitis
• Perennial nasal symptoms and signs
• Congestion
• Clear discharge being most prominent
• Sneezing
• Pruritus
• Anosmia

60. INVESTIGATION
• Nasal smears:
– If 10% of cells are Eo = Elevated Eo
– In NARES, usually large numbers of Eo (5–20%) found
– No systemic allergy as assessed by allergy skin or blood testing

61. NASAL SMEARS
• Both nostrils should be sampled
• Samples collection
– Blowing mucus into transparent wrap
– Cytology brush
– Probe
– Ultrasonic nebulization of hypertonic saline
--Nasal lavge
• Transfer samples to slides, fixed, and then treated with Hansel stain
• Nasal biopsy is more accurate

62. DIAGNOSIS & TREATMENT
• Nasal eosinophilia in patients with nonallergic rhinitis
• Generally regarded as a good prognostic indicator for response to treatment with
topical steroid therapy
• If eosinophilic infiltration is massive (e.g., in aspirin sensitivity syndrome) - Use
of oral glucocorticoid may be required to control symptoms

63. OTHER RHINITIS WITH HIGH NASAL EO
• BENARS = blood eosinophilia nonallergic rhinitis syndrome
– A subtype of NARES
– Associated with elevated blood eosinophils
• Phaeohyphomycosis of maxillo-ethmoid sinus( mycotic infxn)
• Churg-Strauss syndrome(EGPA)- marked blood vessel inflammation

64. RHINITIS WITH OTHER CELL INFILTRATION

65. NASAL MASTOCYTOSIS
• = Basophilic/metachromatic nasal disease
• A histologic diagnosis
• Unknown etiology
• Hallmark: Mast cell infiltration (frequently >2,000/mm3) without nasal eosinophilia
• Nasal symptoms:
– More likely to be secretion/rhinorrhea and congestion/blockage
– Without significant sneezing/pruritus

66. O/E: Pale nasal mucosa
• This condition are not predisposed to develop aspirin sensitivity, nasal polyps, asthma, or
sinusitis.
• Treatment: Inflammatory condition
– Topical anti-inflammatories
– Intranasal cromolyn
– Intranasal/oral corticosteroids

67. DIFFERENTIAL DIAGNOSIS
• Allergic rhinitis ( excluded by appropriate allergy tests)
• Polyps & sinusitis
• Congenital and acquired anatomical abnormalities (e.g. nasal septal deviation, adenoid
hypertrophy, hypertrophy of nasal turbinates, choanal atresia): Rhinorrhoea, post-nasal
drip and nasal blockage Benign and malignant tumours, , granulomas
• Ciliary defects and cerebrospinal rhinorrhoea.
• Tumours can lead to unilateral nasal obstruction, bleeding and pain.
• Rhinorrhoea and nasal congestion, in the absence of pruritis, are also characteristic
features of nasal mastocytosis, an extremely rare condition, in which eosinophils are
absent and tests for IgE-mediated disease are negative.

68. LOCAL CAUSES

69. SYSTEMIC CAUSES

70. DIAGNOSIS AS A STEP-WISE APPROACH
• Thorough case history, step-wise exclusion of possible differential diagnoses, as follows.
• If the case history is suggestive of clinically relevant non-infectious rhinitis:
1. check possible stimuli, severity and duration of disease;
2. check drug use (systemic and topical), exposure at work place, hormonal status (pregnancy,
hypothyroidism, acromegaly) and involvement of other organs (asthma, hormonal status);

71. BRANDT & BERNSTEIN

72. PHYSICAL EXAMINATION
• O/E- mucosa is boggy & edematous with clear mucoid secretions.
• Mucosal injection, lymphoid hyperplasia,- tonsils, adenoids,BOT
• Chemical exposure- areas of blanched mucosa sorrounding prominant vessels
• Atrophy of mucosa- seen in aging,prior surgery & drug abuse.
• Look for anatomic abnormalities & features of infection.

73. 1. exclude other nasal disease (rigid nasal endoscopy);
2. exclude allergy: skin prick test, serum IgE-antibodies or nasal provocation testing in
selected cases;
3. exclude chronic rhinosinusitis (nasoendoscopy +/− computed tomography (CT) scan);
4. perform nasal cytology (eosinophilia), and if shown to be positive then perform oral
Aspirin challenge.
5. Acoustic rhinomanometry - to r/o Nasal valve collapse
6. Validated sell testing
7. Intranasal cold , dry air- as a reproducible diagnostic tool in VMR ( VAS, PIF)

74. THERAPY FOR NONALLERGIC PERENNIAL
RHINITIS
First, evaluate the severity , confirm the need for therapy.
1.Avoidance--> patient education(specific stimuli (drug-induced, food-induced or
occupational rhinitis, chemicals? irritants induced rhinitis) first-line therapy
2.Limited exposure--> eg: occupational rhinitis::use masks/rotective coverings)
3. Vigorous exercise--> decrease nasal congestion by stimulating adrenergic
receptors

75. • Topical steroids and antihistamines are the two main classes of drugs ( Fluticasone
Propionate, Budesonide, Beclomethasone and Azelastine, respectively, have been
approved by the Food and Drug Administration (FDA)
• Azelastine nasal spray --> control of rhinorrhoea, post-nasal drip, sneezing and nasal
congestion.
• Topical nasal steroids -->y used for treatment of more severe symptoms, (more useful in
patients with inflammatory pathogenesis is a prominent, eg NARES.
• Recent evidence suggests that in patients who do not respond to treatment with nasal
steroids, treatment with non-conventional therapies such as silver nitrate, botulin toxin
and particularly intra-nasal capsaicin may be beneficial

76. TOPICAL NASAL CORTICOSTEROIDS
• Different preparations are available
• How to use::point the nozzle upwrds and away from the septum
• Fluticasone propionate &beclomethasone--> FDA
• Budesonide--> pregnancy, cat B

77. • Acts on nasal mucosa--> decreased neutrophl and eosinophil cemotaxis &
basophil mediators release. Also decrease mucosal edema and
inflammation
• DECONGESTANTS -topical or systemic --> to decrease mucosal edema, so
used initially for increased penetration of nasal spray.
• NORMAL SALINE-- incresed mucociliary clearance , rinsing increases efficacy of
steroids
• ADE- infrequent. m/c :septal irritation,nasal dryness & crusts, epistaxis,throat
dryness and headache.
• Only 20 % is absorbed 80% swallowed( eliminated by first pass metabolism)

78. ANTIHISTAMINES
• Oral- limited use, except in sneezing or itching .
• Can be used orally/ parenterally/ topically.
1st generation- most potent,most effective
central/motor/cognitive impairment(anxiety, dizziness, tremor,insomnia,nausea, euphoria)S/E (
as it is lipophilic/ crosses BBB)
& anticholinergic S/E- so effective in rhinorrhea
Chlorpheniramine , Diphenhydramine, Clemstine

79. 2nd generation- desloratidine, loraidine,cetrizine, levocetrizine, fexofenadine
• AZELASTINE( topical antihistamine)H1 receptor antagonist- AR
• Prevent synthesis of leukotrienes, kinins, cytokines & prevent expression of
intercelluar dhesion molecules & prevents generation of SO free radicals-NAR
• NARES & VMR
• Funtl MRI- decreased bood flow to olfactory and sensory processing areas of brain, thus
rduces its response to odorants
• Very useful in presence of mixed rhinitis
• OLAPATIDINE n/s(0.6%) - FDA approved for pts >12 years of age

80. ANTICHOLINERGIC
• ORAL - Decreases rhinorrhea- S/E - blurred vision,drying of eyes & mouth, thickened secretion
• Intra-nasal anticholinergics (Ipratropium Bromide)- selectively inhiits nasal secretion- useful in patients with
nasal secretion as the predominant symptom.
• S/E- epitaxis and dryness- rare, incidence decrease with prolonged use.
• 0.03%-AR & NAR
• 0.06%- a/c viral rhinitis
• In children as yoing as 6 years & in pregnancy (cat B)
• Initially 2sprays 2-3 times/day, symptom improvement within 1 week, tapered to one spray/twice daily(lowest
dose)

81. • Nasal decongestants should be avoided or limited to 10 days
• Intra-nasal capsaicin --> significant and long-term effect in NANIPER
• Once daily for 5 weeks with intranasal capsaicin --> significantly improve all
symptoms throughout a 6-month follow-up in patients suffering from severe
chronic non-allergic rhinitis with nasal vasoconstrictor abuse
• In cases where nasal obstruction is resistant to medical treatment and if the
inferior turbinate is hyperplastic, surgical intervention to reduce the size of the
turbinate
• Endoscopic transnasal vidian neurectomies have also been performed by
excision, diathermy and cryotherapy.

82. SURGERY
• In recalcitran cases
Correction of anatomical deformity (nasal poly, spur,DNS, HIT)
Tissue conservation & mucosal sparing are used whenever possible to maintain normal
physiology & prevent atrophic rhinitis

83. COMPLICATION
• Chronic rhinitis--> sinusitis
• nasl polyps
• ETD
• laryngel dysfunction
• COM
• hearing loss
• Sleep disorderd breathing
• disorders of smell, malaise, and fatigue

84. • THANK YOU