Allergic rhinitis is a hypersensitivity reaction of the nasal mucosa to allergens like pollen or dust mites. It causes sneezing, runny nose, nasal itching and congestion. Diagnosis involves assessing symptoms and examining the nose for swelling and discharge. Skin or blood tests can identify allergens. Treatment includes allergen avoidance, oral antihistamines like cetirizine or leukotriene inhibitors like montelukast, intranasal steroids, and immunotherapy for long term management.

1. Allergic rhinitis
Fahad zakwan
MD5

2. Definition
•hypersensitivity of the sinonasal mucosa to antigenic
materials.
•Characterized by recurrent attacks of:
Sneezing
Itching
Rhinorrhea (thin watery discharge from the nose)
Nasal obstruction

3. Types
•seasonal (hay fever)
•Perennial
•Perennial with seasonal
exacerbations

4. Predisposing factors:
•Genetic (50%) atopic
patient
•Temperature changes
•Emotional (anxiety)

5. The atopic syndrome
• The atopic syndrome is a hereditary disorder of
variable penetrance.
• Subjects are particularly susceptible to the
development of IgE-mediated allergic reactions
manifested by:
•infantile eczema;
•allergic asthma;
•nasal and conjunctival allergy

6. Exciting factors: (antigen)
•Inhalants: pollens (seasonal), house dust mites
(perennial)
•Ingestants: fish, milk, eggs.
•Injectants: penicillin.
•Infectants: fungal (allergic fungal sinusitis)
•Contactants: face powder.

8. Exposure to
allergens
PATHOPHYSIOLOGY

9. Mechanism (pathogenesis):
• When allergens are inhaled (1st time), the body produces
antibodies (IgE) which become fixed to the mast cells of
nasal mucosa.
• On re-exposure these antibodies cause the release of a
chemical mediators mainly histamine by the degranulation of
mast cells that leads to:
• swelling and edema of the nasal mucosa
• Vasodilatation and increased capillary dilatation
• Increased secretions
• Cellular infiltration (esinophils)

10. Antigen-presenting cells,
which include
macrophages and
Dendritic cells similar to
Langerhans cells in the
skin, take up allergen by
endocytosis

11. •APCs process
allergens, and co-
present it along with
HLA Class 2
molecules to CD4+ T
cells (Th2
lymphocytes)

12. •T cells undergo clonal
expansion
•They get activated
•They produce cytokines
•Signal B cells, causing
differentiation into
plasma cells
•Plasma cells produce IgE
class antibodies

13. •Allergen specific IgE
produced by Plasma
cells, bind to mast
cells, and Basophils,
resulting in Antigen
priming.

14. • Subsequent exposure to
allergen leads to cross linking
of IgE on cell surface
• Opening of Calcium channels
• Degranulation
• Release of preformed
mediators
• Histamine
• Prostaglandins
• Leukotrienes
• Kinins
• Cytokines

15. EARLY ALLERGIC RESPONSE
• Histamine results in Rhinorrhea, Sneezing, Itching, and some nasal
obstruction (Early allergic response)
• Edema, vasodilatation and plasma exudation; Increases glandular
secretion
• Upregulation of Adhesion molecules on vascular endothelial cells,
increased production of cytokines
• Other mediators of importance in Allergic Rhinitis:
• Prostaglandin D2 – Sustained nasal obstruction
• Leukotrienes (SRS-A) – Vascular permeability, Oedema,
• Eosinophil recruitment
• Kinins-Rhinorrhoea, Sneezing, Obstruction, Pain
• TH2 cytokines-IL-4, 5, 13, 6, 8, 10, TNF-alpha are important in
regulation of immune response

16. LATE ALLERGIC RESPONSE
• Severe exposure to allergens can result in a late phase response
• Eosinophils-Activated, increase local vascular permeability, mucus
secretion, further inflammatory cell influx, alteration of nasal epithelium
• Endothelial cells recruit leukocytes by releasing chemotactic factors and
modulation of adhesion factors.
• Trap circulating inflammatory cells at the site of allergic response,
especially eosinophils and basophils
• Basophils are a major source of histamine in the late phase response.
• Epithelial cells – Activated, and show increased expression of adhesion
molecules, expression and production of inflammatory mediators

18. Symptoms
recurrent attacks of
• itching,
• sneezing,
• rhinorrhea (runners),
• obstruction (blockers),
• mild facial pain and headache.
• other allergic manifestations
(conjunctivitis, bronchial asthma,
eczema)

19. Signs
•Enlarged turbinates
(pale bluish)
•Polyps (bilateral,
multiple, glistening,
pale bluish, soft,
mobile, insensitive,
middle meatus)

20. PHYSICAL EXAMINATION
•The physical examination should focus on the
nose, but examination of facial features, eyes,
ears, oropharynx, neck, lungs, and skin is also
important.
•Look for physical findings that may be consistent
with a systemic disease that is associated with
rhinitis.

21. General facial features
• "Allergic shiners" are dark circles
around the eyes and are related to
vasodilation or nasal congestion.
• "Nasal crease" is a horizontal crease
across the lower half of the bridge of
the nose that is caused by repeated
upward rubbing of the tip of the nose
by the palm of the hand (ie,
the "allergic salute")

22. Nose
• The nasal examination is best accomplished with a nasal speculum or
an otoscope with nasal adapter. A rigid or flexible rhinolaryngoscope
may be used.
• The mucosa of the nasal turbinates may be swollen (boggy) and have
a pale, bluish-gray color. Some patients may have predominant
erythema of the mucosa, which can also be observed with rhinitis,
infection, or vasomotor rhinitis.
• While pale, boggy, blue-gray mucosa is typical for allergic rhinitis,
mucosal examination findings cannot definitively distinguish between
allergic and nonallergic causes of rhinitis.

23. •Assess the character and quantity of nasal
mucus.
•Thin and watery secretions are frequently
associated with allergic rhinitis.
•thick and purulent secretions are usually associated
with sinusitis;
•however, thicker, purulent, colored mucus can also
occur with allergic rhinitis.

24. • Examine the nasal septum to look for any deviation or septal
perforation, which may be present due to chronic rhinitis,
granulomatous disease, cocaine abuse, prior surgery, topical
decongestant abuse, or, rarely, topical steroid overuse.
• Examine the nasal cavity for other masses such as polyps or
tumors.
• Polyps are firm gray masses that are often attached by a stalk,
which may not be visible.
• After spraying a topical decongestant, polyps do not shrink, while
the surrounding nasal mucosa does shrink

25. Ears and eyes
•Perform otoscopy to look for tympanic membrane
retraction, air-fluid levels, or bubbles. Performing
pneumatic otoscopy can be considered to look for
abnormal tympanic membrane mobility. These findings
can be associated with allergic rhinitis.
•Ocular examination may reveal findings of injection and
swelling of the palpebral conjunctivae, with excess tear
production which are associated with allergic rhinitis.

26. Neck
•Look for evidence of lymphadenopathy or
thyroid disease.
Lungs
•Look for the characteristic findings of asthma.
Skin
•Evaluate for possible atopic dermatitis.

27. Investigations
•Skin prick test
•Serum IgE
•Nasal cytology: esinophils
•Nasal challenge test
•RAST
•C.T scan (polyps)

28. Allergy skin tests
• allergen introduced into skin
causes mast cell degranulation,
formation of wheal and flare
• mean wheal diameter at 15 mins
• >2 mm in children <5yrs,
• > 3 mm in older children and
adults

29. Total serum IgE
• This is a measurement of the total level of IgE in the blood.
• While patients with allergic rhinitis are more likely to have an
elevated total IgE level than the normal population, this test
is neither sensitive nor specific for allergic rhinitis.
• Therefore, this test is generally not used alone to establish
the diagnosis of allergic rhinitis, but the results can be
helpful in some cases when combined with other factors.

30. Total blood eosinophil count
•As with the total serum IgE, an elevated
eosinophil count supports the diagnosis of
allergic rhinitis, but it is neither sensitive nor
specific for the diagnosis.
•The results can sometimes be helpful when
combined with other factors.

31. Nasal cytology
• A nasal smear can sometimes be helpful for establishing the diagnosis
of allergic rhinitis.
• A sample of secretions and cells is scraped from the surface of the
nasal mucosa using a special sampling probe.
• Secretions that are blown from the nose are not adequate.
• The presence of eosinophils is consistent with allergic rhinitis but also
can be observed with NARES.
• Results are neither sensitive nor specific for allergic rhinitis and
should not be used exclusively for establishing the diagnosis.

32. Imaging Studies
Radiography
•While radiographic studies are not needed to
establish the diagnosis of allergic rhinitis, they
can be helpful for evaluating possible structural
abnormalities or to help detect complications or
comorbid conditions, such as sinusitis or adenoid
hypertrophy.

33. CT scanning
• Coronal CT scan images of the sinuses can be very helpful for
evaluating acute or chronic sinusitis.
• In particular, obstruction of the ostiomeatal complex (a
confluence of drainage channels from the sinuses) can be
seen quite clearly.
• CT scanning may also help allocate polyps, turbinate
swelling, septal abnormalities (eg, deviation), and bony
abnormalities (eg, concha bullosa).

34. MRI
• For evaluating sinusitis, MRI images are generally less
helpful than CT scan images, largely because the bony
structures are not seen as clearly on MRI images.
• However, soft tissues are visualized quite well, making
MRI images helpful for diagnosing malignancies of the
upper airway.

35. PROCEDURES
Rhinoscopy:
• While not routinely indicated, upper airway endoscopy
(rhinolaryngoscopy) can be performed if a complication or
comorbid condition may be present.
• It can be helpful for evaluating structural abnormalities (eg,
polyps, adenoid hypertrophy, septal deviation, masses,
foreign bodies) and chronic sinusitis (by visualizing the areas
of sinus drainage).

36. Nasal provocation (allergen challenge)
testing:
• This procedure is essentially a research tool and is rarely indicated in the
routine evaluation of allergic rhinitis.
• The possible allergen is inhaled or otherwise inoculated into the nose.
• The patient can then be monitored for development of symptoms or
production of secretions, or objective measurements of nasal congestion
can be taken.
• Some consider this test the criterion standard test for the diagnosis of
allergic rhinitis.However, it is not a practical test to perform routinely, and
only an appropriately trained specialist should perform this test

37. Management
3-major treatment strategies:-
•Environmental control & allergen
avoidance
•Pharmacologic management
•Immunotherapy

38. 1. allergen avoidance and
environmental control
• Various recommendations for allergen avoidance had been suggested
in the past
• Total avoidance of exposure to passive smoking in pregnant women
• No ‘antigen avoidance diet’ is recommended
• reduce early life exposure to house dust mite
• no special avoidance of exposure to pets at home in infants and
preschool children
• Specific prevention measures eliminating or reducing occupational
allergen exposure

39. •clinicians should not administer and
patients do not use currently available
single chemical or physical preventive
methods aimed at reducing exposure to
house dust mites
•avoid exposure to indoor moulds at home
•avoid exposure to animal dander

40. 2. Pharmacologic management
• Most cases of allergic rhinitis respond to pharmacotherapy.
• Patients with intermittent symptoms are often treated adequately with oral
antihistamines, decongestants, or both as needed.
• Regular use of an intranasal steroid spray may be more appropriate for patients
with chronic symptoms.
• Daily use of an antihistamine, decongestant, or both can be considered either
instead of or in addition to nasal steroids.
• The newer, second-generation (ie, nonsedating) antihistamines are usually
preferable to avoid sedation and other adverse effects associated with the older,
first-generation antihistamines.
• Ocular antihistamine drops (for eye symptoms), intranasal antihistamine sprays,
intranasal cromolyn, intranasal anticholinergic sprays, and short courses of oral
corticosteroids (reserved for severe, acute episodes only) may also provide relief.

41. SECOND-GENERATION ANTIHISTAMINES
• They compete with histamine for histamine receptor type 1 (H1) receptor
sites in the blood vessels, GI tract, and respiratory tract, which, in turn,
inhibits physiologic effects that histamine normally induces at the H1
receptor sites
• All are efficacious in controlling symptoms of allergic rhinitis (ie, sneezing,
rhinorrhea, itching) but do not significantly improve nasal congestion. For
this reason, some second-generation antihistamines are available as
combination preparations containing a decongestant.
• They are often preferred for first-line therapy of allergic rhinitis, because of
their excellent efficacy and safety profile.
• They can be used prn or daily

42. Cetirizine
• Competes with histamine for H1 receptors in GI tract, blood vessels,
and respiratory tract, reducing hypersensitivity reactions.
• Once-daily dosing is convenient.
• Bedtime dosing may be useful if sedation is a problem.
DOSE:
• <2 years: Safety and efficacy not established
• 2-6 years: 2.5 mg (0.5 teaspoon) oral solution PO qDay; can increase to 5 mg
PO qDay or 2.5 mg PO twice daily; not to exceed 5 mg qDay
• >6 years: 5-10 mg PO qDay, depending on severity of symptoms; not to
exceed 10 mg qDay

43. Levocetirizine
DOSE:
•<6 months: Safety and efficacy not established
•6 months to 5 years: 1.25 mg PO qDay (evening)
•6-12 years: 2.5 mg PO qDay (evening)
•>12 years: 5 mg PO qDay (evening)

44. Fexofenadine
DOSE:
•<2 years: Use not recommended
•2-12 years: 30 mg PO BID
•>12 years: 60 mg PO BID OR 180 mg PO
qDay

45. Loratadine
DOSE:
•<2 years: Safety and efficacy not
established
•2-6 years: 5 mg PO qDay
•>6 years: 10 mg PO qDay; not to exceed
10 mg qDay

46. LEUKOTRIENE RECEPTOR ANTAGONISTS
• Alternative to oral antihistamine to treat allergic
rhinitis.
• One of the leukotriene receptor antagonists,
montelukast (Singulair), has been approved in the
United States for treatment of seasonal and perennial
allergic rhinitis.
• When used as single agent, produces modest
improvement in allergic rhinitis symptoms

47. Montelukast
• Selective leukotriene receptor antagonist that inhibits the cysteinyl
leukotriene (CysLT 1) receptor.
• Selectively prevents action of leukotrienes released by mast cells and
eosinophils.
• When used as a single agent, has been shown to result in a
reduction of seasonal allergic rhinitis symptoms, similar in degree to
that of loratadine.
• <2 years: Safety and efficacy not established
DOSE:
• 2-6 years: 5 mg (chewable tablet) or 4 mg (granules) PO once daily
• 6-15 years: 5 mg (chewable tablet) PO once daily
• >15 years: 10 mg (conventional tablet) PO once daily

48. FIRST-GENERATION ANTIHISTAMINES
• The older, first-generation H1 antagonists (eg,
diphenhydramine, hydroxyzine) are effective in
reducing most symptoms of allergic rhinitis, but they
produce a number of adverse effects (eg, drowsiness,
anticholinergic effects).
• They can be used prn, but adverse effects may limit
their usefulness when taken on a daily basis

49. Chlorpheniramine
• One of the safest antihistamines to use during pregnancy.
• Competes with histamine on H1-receptor sites on effector cells in blood vessels
and respiratory tract.
DOSE:
• <2 years: Safety & efficacy not established
• 2-6 years: 1 mg PO q4-6hr; not to exceed 6 mg/day
• 6-12 years: 2 mg PO q4-6hr; not to exceed 12 mg/day or sustained release HS
• >12 years
• Tablets or syrup: 4 mg PO q4-6hr; not to exceed 24 mg/day
• Extended-release tablets: 8 mg PO q8-12hr or 12 mg q12hr; not to exceed 24 mg/day
• Extended-release capsules: 12 mg PO qDay; not to exceed 24 mg/day
• Sustained-release capsules: 8-12 mg PO q8-12hr, up to 16-24 mg/day

50. Diphenhydramine
DOSE:
•2-6 years old: 6.25 mg q4-6hr; not to
exceed 37.5 mg/day
•6-12 years old: 12.5-25 mg PO q4-6hr;
not to exceed 150 mg/day
•>12 years old: 25-50 mg PO q4-6hr; not
to exceed 300 mg/day

51. Hydroxyzine
DOSE:
•<6 years old: 50 mg/day PO
divided q6hr
•>6 years old: 50-100 mg/day PO
divided q6hr

52. DECONGESTANTS
• Stimulate vasoconstriction by directly activating alpha-adrenergic receptors of the
respiratory mucosa.
• Pseudoephedrine produces weak bronchial relaxation (unlike epinephrine or
ephedrine) and is not effective for treating asthma.
• Increases heart rate and contractility by stimulating beta-adrenergic receptors.
• Used alone or in combination with antihistamines to treat nasal congestion.
• Numerous preparations are available containing combinations of various
decongestants, expectorants, or antihistamines.
• Alternatively, a separate decongestant and antihistamine can be administered to
allow for individual dose titration of each drug.

53. Pseudoephedrine
• Stimulates vasoconstriction by directly activating alpha-
adrenergic receptors of the respiratory mucosa.
DOSE:
Nasal Congestion
• <2 years: Safety and efficacy not established
• 2-6 years: 5-30 mg PO q4-6hr PRN
• 6-12 years: 30 mg PO q4-6hr, OR 4 mg/kg/day divided q6hr;
not to exceed 120 mg/day
• >12 years: 60 mg PO q6hr PRN (immediate release);
alternatively, 120 mg PO q12hr (extended release) or 240 mg
PO q24hr (extended release)

54. NASAL CORTICOSTEROIDS
• Nasal steroid sprays are highly efficacious in treating allergic rhinitis.
• They control the 4 major symptoms of rhinitis (ie, sneezing, itching,
rhinorrhea, congestion).
• They are effective as monotherapy, although they do not significantly
affect ocular symptoms.
• Greater benefit may occur when nasal steroids are used with other
classes of medication.
• They are safe to use and not associated with significant systemic
adverse effects in adults

55. EXAMPLES:
• Mometasone (Nasonex)
• Beclomethasone (Beconase AQ, QNASL)
• Budesonide inhaled (Rhinocort Aqua)
• Fluticasone (Flonase)
• Ciclesonide (Omnaris)
• Fluticasone furoate (Veramyst)
• Triamcinolone (Nasacort AQ)

56. INTRANASAL ANTIHISTAMINES
Azelastine
DOSE:
•<6 years: Safety and efficacy not established
•6-12 years: 1 spray per nostril q12hr
•>12 years: 1-2 sprays per nostril q12hr

57. administration
• Patients should tilt the head slightly
forward, insert the nasal adapter into
one nostril, and point the tip of the
adapter toward the
inflamed nasal turbinates
and away from the nasal septum.
• Patients should pump the drug into
one nostril while holding the other
nostril closed and should concurrently
inspire through the nose.
• Repeat for the other nostril.
• If sneezing occurs, patients should
wait until sneezing has stopped, then
clear the nasal passages and repeat
administration of the dose.

58. 3. IMMUNOTHERAPY
• Involves repeated administration of an allergen
extract subcutaneously to induce immunological
tolderance with reduction in clinical symptoms
and medication requirement suring subsequent
natural allergen exposure.
• Indicated in patients with patients with severe
allergic rhinitis whose symptoms fail to respond to
conventional treatment.
• More useful in patients with a limited spectrum of
allergies, esp in seasonal hayfever, inability to
avoid allergens.

59. • Mechanism appears to be modulation of T lymphocyte functions
• IgE sensitivity should be confirmed before starting.
• Reduction in risk of bronchial asthma, may prevent development of new
allergies
• Special protocols are available, which includes an updosing phase of
weekly injections for 8-16 weeks, followed by maintainence injections at
4-8 weekly intervals for 3-5 years.
• Local reactions may occur
• Systemic reactions are rare, may lead to rhinitis and asthma, which
responds to treatment.
• Rarely anaphylaxis may occur.

60. Reference
• Diseases of the Ear, Nose and Throat (P.D. BULL MBBCh,
FRCS),University of Sheffield(Ninth Edition)
• Mediscape references, Allergic rhinitis (full article)