Rhinitis is an inflammation of the nasal mucosa
Allergic rhinitis -Seasonal -> hay fever Perennial Occupational Also known as ” allergic rhinoconjunctivitis” ( when conjunctivae are also involved ) or “hay fever ” ( seasonal AR )
Non allergic rhinitis -Infectious Vasomotor Hormonal Drug induced Structural Occupational Rhinitis medicamentosa Non-allergic rhinitis with eosinophilia syndrome.
Various other classification system exist based for e.g on etiology ( infective , mixed ) but our focus here is on allergic rhinitis- which is a type 1 allergic disease.
How common –Number of patients affected by allergies is increasing worldwide AR is a global problem estimated to affect 10 % to 20 % ( some papers quote up to 42 % ) of the entire population – hence AR is the most prevalent chronic non-communicable disorder BSACI reports that allergic rhinitis is common in UK and ○ affects 10-15 % of children ○ 26 % of adults No set diagnostic criteria exist for AR hence ○ diagnosis is based on subject reporting symptoms ○ tests are rarely used to confirm diagnosis ○ most studies focus on hay fever and may underestimate perennial AR Peak prevalence of rhinitis is reported to be in the 3rd and 4th decades with some evidence of remission in adult life ( AR symptoms develop before age 20 in 80 % of cases ) In childhood boys outnumber girls but in adulthood equal numbers suffer.
Most cases of rhinitis ( about 50 % ) are due to allergy Allergen -> inflammation induced by IgE mediated immune response to specific allergens – inflammatory mediators release driven by type 2 helper cells -Th2 cells ( histamine , other pro-inflammatory cytokines e.g leukotrienes and eicosanoids ) Once sensitization happens -exposure triggers a cascade of events and the response can be divided into an early phase and late phase response.
Cause – risk factors Dust mite fecal proteins Cockroach allergen Cat , dog and other dander’s Pollen grains Fungi and moulds Carpets which trap dust Occupational Education attainment. Genetic predisposition – most important factor in rhinitis development Patients with multiple food allergies Tonsillectomy Frequent URTIs Frequent antibiotic use in infancy Smoking Drinking.
major airway disease risk factor for development of asthma ○ 74 % to 81 % of asthmatic report symptoms of rhinitis ○ poor control of rhinitis is a risk factor for asthma exacerbation also associated with other conditions as sinusitis , anosmia , otitis media , nasal polyps , lower airway infection and even dental malocclusion affects QoL , school and work attendance often under-diagnosed and under-treated it is estimated that in UK only 18 % of subjects with rhinitis had seen a GP over the preceding 2 yrs concerning their hay fever it has been reported that children with AR are ↑ likely to have myringotomy tubes placed and have their tonsils and adenoids removed AR affects productivity , quality of sleep & cause emotional problems and even ability to drive ( some have shown that AR has the greatest negative impact on work productivity ↑ than that of heart disease & diabetes combined ) AR has a major financial impact on healthcare systems – both direct and indirect costs.
AR is an IgE mediated chronic inflammatory disorder which affects the nasal mucosa characterized by repeated episodes one or more of the following nasal congestion rhinorrhea ( anterior and posterior ) sneezing itching of the eyes , nosa and palate
Seasonal -widely recognised to occur in summer months lay term- hay fever
Perennial -occurs throughout the year- no universal definition gen accepted as > 9 months / year persistent tissue edema & infiltration with eosinophils, mast cells , TH2 lymphocytes and macrophages.
ARIA guidelines –Intermittent ( total duration of episodes of inflammation is < 6 weeks ) Persistent ( symptoms persist throughout the year ) Mild – patients are generally able to sleep normally & perform normal activities including school / work Moderate /Severe if they significantly affect sleep & ADL’s and or they are considered bothersome.
Rhinitis differentials -Infective rhinitis Non- allergic rhinitis ( differentiating is not always easy ) consider if ○ onset after age 20 ○ female ○ nasal hyperactivity ○ perennial symptoms Mixed allergic and non-allergic rhinitis Nasal polyps Sinusitis CSF rhinorrhoea Midline granuloma
Red flags -nasal crusting ○ unusual and if severe and high inside the nose consider chronic rhinosinusitis , nose picking , granulomatous polyangiitis , sarcoidosis or other vasculitides ( if associated with bleeding ) , cocaine , ozeana ( wasting of bony ridges & mucous membranes inside the nose ) ○ topical steroids do not usually cause crusting nasal bleeding / blood stained rhinorrhoea nasal deformity , perforations , ulceration or collapse symptoms which are unilateral for e.g obstruction , rhinorrhoea , persistent u/l epistaxis cervical lymphadenopathy nasal pain.
History-duration of symptoms magnitude of reactions patterns and chronicity seasonality ( pollen , moulds ) location of symptoms ( indoor or outdoor ) work / school environment if symptoms improve with holidays relationship to potential triggers – pollens , furred animals , textile / flooring upholstery , tobacco smoke , humidity levels family h/o atopic disease occupational history impact of symptoms on QoL co-morbidities ○ asthma ○ mouth breathing ○ snoring ○ sleep apnoea ○ sinus involvement ○ otitis media ○ nasal polyps previous treatment use of medications as beta blockers , NSAID’s , ACEi’s , hormone therapy , recreational cocaine.
Symptoms –Rhinorrhoea ( clear , U/L , coloured ) Nasal obstruction ( partial , complete , U/L or B/L , alternating ) Nasal crusting , nasal itching Eye symptoms ( intense itching , redness , swelling of the white of the eye , watering , lid swelling ) Lower respiratory tract symptoms -as cough , wheeze , SOB Other symptoms as snoring , sleep problems , repeated sniffing , throat clearing , pollen food syndrome , allergic shiners ( dark circles under eye due to nasal congestion )
Examination -Outward signs for e.g ○ persistent mouth breathing ○ rubbing at the nose or an obvious transverse nasal crease ○ frequent sniffling or throat clearing ○ allergic shiners Nose ○ swelling of the nasal mucosa ○ assess nasal airflow ○ depressed / widened nasal bridge ○ pale thin secretions Sinuses – palpation Posterior oropharynx – for signs of post nasal drip Chest- auscultate for wheeze Skin – check for dermatitis
AR is mainly diagnosed by a thorough clinical history , examination and in some cases by allergy testing ( availability may vary widely in primary care )
Allergic specific IgE can be tested by skin prick tests ( SPTs ) or serum immunoassay A normal level of IgE does not r/o allergy and a significant allergic disease is possible with low levels of IgE Skin prick tests ( SPT ) can help in identifying specific allergic triggers of rhinitis but the results should be interpreted in the clinical context BSACI guideline recommends that SPT should be carried out routinely to determine if the rhinitis is allergic or non-allergic RAST tests are expensive and provide in vitro measure of a patients specific IgE levels against a particular antigen It should be noted that the presence of sensitising IgE antibodies to a particular antigen does not imply that the allergen has any clinical relevance and the numerical values do not correlate with severity of clinical reactions.
Exercise caution in requesting / ordering RAST tests as false positives & false negative results can happen . A negative specific IgE test does not r/o an immediate allergy while positive test may not be clinically relevant. Establishing a diagnosis solely based on IgE tests can be inaccurate.
Symptoms can be managed but AR resists cure Treatment is usually in a stepwise fashion based upon severity of symptoms , patient choice , historic response to Rx ( always consider the possibility of co-existing asthma in all patients )
Mild intermittent symptoms with no impact on QoL/ sleep/ school work -give information about hay fever ( if suspected ) from Allergy UK / NHS allergen avoidance if a specific allergen has been identified self- management strategies as nasal irrigation use oral non-sedating antihistamine OTC as cetirizine / loratadine on PRN basis ○ antihistamines work on neurally mediated symptoms of itch ( also reduce itch at other sites as conjunctiva , palate and skin ) , sneeze and rhinorrhoe and have only a modest effect on nasal congestion ○ 2nd generation antihistamines ( e.g cetirizine , desloratadine , diphenhydramine , fexofenadine ) work for longer and are largely non sedating and have no clinically significant anti-cholinergic activity activity intranasal antihistamine as azelastine work faster & are more effective than oral preparations in relieving rhinitis and in decreasing nasal obstruction ○ They work within 15 minutes & can be used on demand as rescue therapy for symptom breakthrough ○ SEs include local nasal irritation and taste disturbance consider intranasal sodium cromoglycate ( mast cell stabiliser with anti-inflammatory activity ) use PRN if antihistamines cannot be used.
Moderate /severe and or persistent symptoms with impact on QoL regular intranasal corticosteroid ( INS ) – mainstay of treatment in AR ○ educate how to use ( BSACI information leaflet ) ○ advice that onset of action is 6-8 hrs after the 1st dose and clinical improvement may take a few days to be apparent & max effect may take up to 2 weeks ○ INS reduce nasal congestion , improve ocular symptoms and ↓ lower airway symptoms in patients with concurrent asthma ○ consider nasal drops if patient has severe nasal obstruction in head upside down position ○ mometasone furoate , fluticasone furoate and fluticasone propionate have negligible systemic absorption and are suitable for use in children ○ about 10 % of users may suffer with local irritation , sore throat & epistaxis ○ for patients who suffer with sore throat a preparation free of benzalkonium such as rhinocort , flixonase nasules can be tried ○ it is recommended to avoid using INS with moderate ( beclomethasone ) or high systemic bioavailability ( betamethasone , dexamethasone ) Consider regular antihistamine ( AH ) use
Check -compliance, technique , dose – revisit diagnosis ? is it something else
consider adding ipratropium bromide ( to INS + antihistamines ) regular tds use can decrease neurogenic rhinorrhoea but has no effect on other nasal symptoms
Combination therapy-spray containing azelastine + fluticasone propionate ( Dymista® ) leads to better symptom control than using either agent alone including ocular symptoms
Anti- leukotrienes can be as effective as loratadine in seasonal AR but less effective than INS consider if oral antihistamines & or INS are not effective or well tolerated Montelukast is licensed in UK for people who suffer with seasonal AR and asthma.
Chromones- Sodium cromoglycate & nedocromil Na inhibit the degranulation of sensitized mast cells inhibiting the release of mediators Sodium cromoglycate spray needs to be used several times a day not as effective as INS but some patients may benefit with reduced sneezing , rhinorrhoea and nasal itching.
an alternative diagnosis is suspected / red flags nasal blockage which fails to respond to pharmacotherapy structural abnormalities as septal deviation symptoms persist despite optimum treatment in primary care further testing as SPT is being considered to ascertain diagnosis.
Video how to use nasal spray from Asthma UK https://www.asthma.org.uk/advice/inhaler-videos/nasal-spray/
American Academy of Allergy Asthma and Immunology on Hay fever https://www.asthma.org.uk/advice/inhaler-videos/nasal-spray/
BSACI on rhinitis https://www.bsaci.org/patients/most-common-allergies/rhinitis/
Uptodate com patient information https://www.uptodate.com/contents/allergic-rhinitis-beyond-the-basics
NHS Inform Scot on allergic rhinitis https://www.nhsinform.scot/illnesses-and-conditions/ears-nose-and-throat/allergic-rhinitis
Hayfever and asthma – patient information from the National Asthma Council Australia https://www.nationalasthma.org.au/living-with-asthma/resources/patients-carers/brochures/hay-fever-allergic-rhinitis-and-your-asthma
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