1. OBJECTIVES 1-DESCRIBE ALLERGIC RHINITIS 2-DESCRIBE NASAL POLYPOSIS

2. Allergic Rhinitis
Definition: it is IgE mediated hypersensitivity disease due to abnormal reaction of the mucous membrane of the nasal airway to certain allergens characterized by recurrent attacks of sneezing, itching, watery nasal discharge and nasal obstruction.

3. Predisposing factors:
Hereditary (atopy) → if the two parents has allergic rhinitis 75% of offspring get allergic rhinitis, if one parent has allergic rhinitis 50% of offspring may get allergic rhinitis.
Physical → changes in the humidity and content of the inspired air may render the nasal mucosa more susceptible.
Infection → bacterial and viral infection may alter the permeability of the tissue to allergens.

4. Precipitating factors:
Allergens are divided into:
B- Exogenous (coming from outside the-body) includes:
Inhalants: e.g. pollens, house-dust mite, animal emanation.
Ingestions e.g. egg, fish, milk.
Contacts to nasal mucosa e.g. make up, powders, nasal drops and sprays.
Drugs e.g. aspirin (aspirin induced rhinitis may be associated with nasal polyp and late onset asthma), β-blockers and ACE inhibitors.
Infection (not proved) e.g. bacteria, viral, fungal.
B- Endogenous → coming from within the body e.g. tissues coming from tissue injury.

5. Mechanism of allergy:
Allergen is captured by allergen specific cells via their surface immunoglobulin receptors → internalized → processed into peptides → expressed on the B cell surface in association with MHC class II molecules→ activation of CD4 T-lymphocytes → production of interleukin 4 by activated CD4 T-lymphocytes → production of IgE by plasma cells → binding of IgE to high affinity receptors on mast and basophil cells with binding of allergens to IgE which has bounded to mast and basopil cells → release of pharmacologically active mediators e.g. histamine, prostaglandin D2 leukotrienes → vasodilatation, increase vascular permeability & glandular secretion resulting in oedema, itching, sneezing, watery rhinorrhoea, nasal obstruction ...etc.

6. Pathology:
A- Local mucosa changes:
Oedema.
Infiltration of eosinophils and plasma cells.
Vasodilatation → stasis of blood → blue colour of inferior turbinate.
Watery discharge: Due to seromucinous glands activity. It contain eosinophils
Polyps: Due to edematous mucosa
Superadded infection may occur which may cause some degree of fibrosis.

7. B- Involvement of the sinuses:
Mucosal thickening.
Polyps.
Fluid effusion into the sinuses, it is clear and sterile but sometimes it becomes thick due to infection.

8. Clinical types:
A- Seasonal allergic rhinitis (the symptoms occur in certain season. The patient is symptoms free all over the year and become symptomatic only during that season as in allergic rhinitis due to tree pollen in which the symptom occurs only in spring)
B- Perenial allergic rhinitis (the symptoms present all over the year and usually it is due to house dust mite or domestic pets as dogs, cats...etc).

9. Symptoms: include:
Paroxysms of sneezing.
Watery rhinorrhoea.
Nasal Obstruction.
Itchiness of the nose, eyes and palate.
Redness of the eyes in hay fever.

10. Signs:
In patient with current symptoms the allergic mucosa appears pale or bluish, bogy with swelling and watery discharge.
If the patient is seen when asymptomatic the nasal mucosa appears entirely normal

11. Investigations:
1- Skin prick test: injection of the antigen intradermal in the anterior aspect of the arm. Injection of normal saline at another site as a control. After ½ hour we compare the site of antigen injection and the site of normal saline injection. If we find redness and swelling at antigen injection site in comparison to normal saline injection site → the patient is allergic to that antigen. Skin test is rapid accurate and inexpensive but it is invalid in patients on anti-histamine and patients with severe eczema.

12. 2- Serum IgE measurement: IgE increases in allergic rhinitis patients.
(PRIST) plasma reactive immuno-sorbent test → measure total plasma IgE.
(RAST) radio-allergo-sorbent test → measures plasma level of specific IgE.
3- Nasal smear → presence of eosinophils in the nasal discharge.
4- Nasal provocation test → the potential allergen is sprayed into the nose and note the number of sneeze, amount of discharge. If the patient is allergic to that allergen → ↑ number of sneezing, ↑ amount of discharge and ↑ in nasal resistance using rhinomanometry.

13. Treatment:
1- Allergen avoidance: such as avoidance of house dust mite by using mattress covers, avoidance of animal allergen by washing the animal once weekly and avoidance of pollens by wearing sun glasses & keeping windows shut in cars and buildings.

14. 2- Drugs:
Corticosteroids: it is effective in controlling nasal symptoms of allergic rhinitis in the majority of patients. It can be used as topical corticosteroids (drops or sprays) like dexamethasone or as a short course of oral corticosteroids e.g. prednisolone 20 mg/ 1 day for 5 days.
Sodium cromoglycate, Is an alternative prophylactic treatment for allergic rhinitis. It is safe drug, it is the first choice in children but it is less effective than corticosteroids.

15. Antihistamines: (to control sneezing, itching and rhinorrhoea)
Old antihistamine e.g. chlorpheniramine with sedative side effects.
H1 specific histamine receptor antagonists e.g. loratadine,cetrizin with no sedative side effects
Topical vasoconstrictors e.g. phenylephrine; which are effective against nasal blockage.
Topical anticholinergics e.g. ipratropium bromide; which are effective against watery rhinorrhoea.

16. 3- Immunotherapy (hyposenstization): after identification of allergen which causes allergic rhinitis; we inject that allergic in very low concentration; then gradually we increase the concentration of the allergen. The idea of hypo-sensitization is to produce blocking IgG to neutralize IgE and prevent the symptoms and sign of allergic rhinitis when the patient is exposed to the allergen.
Immunotherapy is more useful in:
Children.
When there is only single allergen causing allergic rhinitis and mostly useful when the allergen is pollen or house dust mite.

17. Complications of allergic rhinitis:
Sinusitis: due to mucosal oedema → blockage of sinus drainage.
Eustachian tube dysfunction → otitis media with effusion.

18. Nasal polyps:
1- Simple nasal polyps
2- Antrochoanal polyp (Killian's polyp)

19. Simple nasal polyps:
Definition: pedunculated portion of oedematous mucosa of the nose and\or paranasal sinuses.
Aetiology:
Allergy.
Infection.
Vasomotor rhinitis (non-infective non allergic rhinitis, also it is called idiopathic rhinitis characterized by watery rhinorrhoea, nasal obstruction and sneezing).
Bernouilli phenomenon: the increased speed of the air flowing through the nose decreases the pressure in the nasal cavity → pulling of the mucosa → polyp.
Polysaccharide changes: alteration in polysaccharide ground substance.

20. Conditions associated with polyps:
Asthma (late onset asthma present in 20−40% of patients with polyp).
Aspirin hypersensitivity present in 8% of patients with polyp.
Cystic fibrosis: 8% of patients with cystic fibrosis have polyps.
Kartagener's syndrome (immotile cilia syndrome) characterized by bronchiectasis, sinusitis, situs inversus & infertility in male.
Young's syndrome: characterized by bronchiectasis sinusitis & azoospermia.

21. Pathology:
It is oedematous mucosa show infiltration of many cells mainly eosinophils and plasma cells, most commonly arise from the ethmoidal sinuses due to complex anatomy & poor blood supply.

22. Clinical features: Nasal polyps mainly occur in an adult male, usually bilateral and multiple, characterized by:
Nasal obstruction
Watery rhinorrhoea.
Sneezing.
Anosmia.
Epistaxis.
Pain.
Postnasal drip
O\E there is pale translucent (poor blood supply) swellings, probing show Insensitive (poor nerve supply) mobile swellings

23. Note:
Simple nasal polyp is rare before 10 years, so if polyp found in children up to 2 years we have to exclude meningocoele and encephalocoele, and polyp found in children between 2−10 years we have to exclude cystic fibrosis by sweat test.

24. Investigations:
Radiology (plain X-ray and CT scan) may show mucosal thickening, opaque sinus, and fluid level due to obstruction sinus drainage loss of nasal translucency
Investigation to exclude allergy like:
1- Radio allegro-sorbent test (RAST),
2- Plasma reactive immuno-sorbent test (PRIST)
3- Skin prick test.
Biopsy is essential when the polyp is unilateral, so post operatively the polyp sends for histopathological examination.

25. Treatment:
A-Medical treatment:
1-Corticosteroids:
Topical steroid like betamethason drops used for 1 month, 2 drops each nostril twice daily → successful in 50% of patients or beclomethosone (beconase) nasal spray for 1 month.
Short course systemic steroid prednisolone 20 mg/day for 5 days.
2-Antihistamines.
3-Topical decongestant to relieve obstruction (used no more than 2 week to avoid rhinitis medicamentosa).

26. B-Surgical treatment: FESS is the surgical treatment of choice
B-Surgical treatment: FESS is the surgical treatment of choice. Other procedures include:
Minor procedures: polypectomy by cold-wire snare, or by using Tilley Henckelled forceps.
Major procedures: Ethmoidectomy (intranasal or external ethmoidectomy, transantral ethmoidectomy).

27. Antrochoanal polyp (Killian's polyp)
It arises from the maxillary sinus mucosa and prolapse through the ostium in the middle meatus into the nasal cavity. It is more common in adolescent male, it is unilateral translucent in color, seen in the posterior part of nasal cavity and it may be difficult to see it by anterior rhinoscopy but it is easy to see it by mirror examination of postnasal space, clinically it causes anterior nasal discharge and nasal obstruction which is greater on expiration than in inspiration due to ball-valve effect.

28. Pathologically there must be no eosinophils infiltration.
Plain X-ray shows total unilateral opacity of maxillary sinus.
It has been postulated that antrochoanal polyp is due to faulty development of maxillary sinus ostium; it is always large.
There is no medical treatment and it should be treated surgically .Endoscopic surgery(ESS) is the treatment of choice. Other procedures may include simple polypectomy . Cald well luc operation (contraindication for patient age < 16 ) may be used for multiple recurrence.