Seasonal Allergic Rhinitis


Hayfever, also known as seasonal allergic rhinitis, can ruin the joys of spring and summer for many sufferers. It is essentially a symptomatic allergic reaction; caused by exposure to certain allergens that are found in abundance during spring and summer, such as tree pollens, grass pollens etc. Other allergens such as weeds, mould spores etc, may be amongst inducers of the reaction.


The pathophysiology of seasonal allergic rhinitis is a two phase process.

· This phase is associated with the rapid onset (over a period of minutes) of acute nasal symptoms (i.e. sneezing and rhinorrhoea) and the emergence of ocular symptoms (i.e. itching, redness, and watering). These symptoms are caused by histamine release, particularly from mast cells in the nasal mucosa. This early-phase histamine release, together with the effects of other potent pro-inflammatory cytokines (e.g. leukotrienes) and eicosanoids (e.g. prostaglandins and kinins) also increases vascular permeability, leading to oedema formation. This peaks within 15-20 minutes of exposure to the allergen.


· This happens several hours (6-12 H) after the exposure to allergen (pollens). It is characterised by cellular recruitment of basophils, neutrophils, T-lymphocytes, monocytes, and eosinophils, and by the release of multiple mediators, including cytokines, prostaglandins, and leukotrienes, which perpetuate the inflammatory response. This late-phase inflammatory reaction is associated with tissue remodelling, further tissue oedema, and the development and perpetuation of nasal congestion, considered by patients to be one of the most troublesome symptoms of AR. As a result of mucosal inflammation, tissues become primed and react more vigorously to allergen exposure. These late-phase reactions and modifications in tissue responsiveness contribute to bronchial hyper-responsiveness.


Seasonal allergic rhinitis is a common problem in the UK, affecting around 20% of the population although, even that may be an under-representation as the true prevalence is unknown. Many people are undiagnosed for their seasonal disorder and self-treated with over the counter products. It appears that both genetic and environmental factors can contribute to the development of allergic rhinitis. Examples include personal/family history of atopy/allergies, exposure to allergens, cigarette smoke, air pollution etc.


Obtaining a complete history of the presenting complaint is central to diagnosing that of seasonal allergic rhinitis. Clinicians should also gather family history, occupational exposure to allergens, triggers/alleviating factors, previous self-treatment fails/successes, and effect of the condition on the patient’s quality of life.


Clinicians would however seek to rule out differentials such as Non-allergic rhinitis (Patient will not have symptoms linked to spring/summer), infective rhinitis (purulent discharge, systemically unwell, secondary bacterial infection), Nasal polyps (symptoms will not fit in with the exposure to pollens/allergen, nasal examination may also reveal that this will be more of a chronic issue, nasal obstruction/snoring may be reported), sinusitis (patient has had a cold/viral upper respiratory tract infection and continued with symptoms, so regardless of the season of summer, this could be the reason for presentation. And there are some other differentials such as adenoids hypertrophy (usually in children), Unilateral rhinorrhoea caused by leakage of CSF, tension headache (watery eyes, stuffy nose with headache) etc.


Let’s fix it:

Non Pharmacological Options:

· Saline nasal irrigation

· Identification and avoidance of trigger allergen (if possible)

· In many cases, complete avoidance is not practical but should be considered to reduce the amount of medication that is required to treat the disorder


House Dust Mites

· Major allergen found in houses

· Wash sheets and blankets in hot water (60°C) every week

· Use anti-mite covers in mattresses, beds and pillows

· Vacuum-clean beds each week

· For indoors, use of exhaust circulation-type cleaner is recommended

· Clean furniture in the bedroom with damp rags


Pollen

· Avoid going outdoors on days when pollen counts are high

· Use of air conditioning

· Keep doors and windows closed at home and when inside cars

· Wear a mask and use glasses during heavy pollen dispersal period

· Avoid wearing of wool coats

· Shake the dust off (eg suit and hair) before entering the house


Pets

· Do not allow animals in the house

· If this is not possible, exclude pets from the bedroom or keep them outdoors

· Clean the rooms and improve the ventilation


Others

· Discourage smoking by patient (active smoking), household members and visitors (passive smoking)

· Minimize contact with irritants (eg perfumes, hair spray and other odours, air pollution from traffic)

· Reduce the growth of moulds at home by decreasing humidity or dampness and eliminating sites for mould growth


Pharmacological options:

The management options are guided by the severity and frequency of symptoms.

For mild to moderate (however intermittent symptoms) OR mild persistent symptoms, either intranasal antihistamine spray {Azelastine (Rhinolast), Ipratropium (Rinatec)} OR oral non-sedating antihistamine (such as Loratadine, Cetirizine, Acrivastine, Desloratadine, Levocetirizine, Mizolastine, Fexofenadine) can be used. The nasal sprays described above are only available on prescription. However, there is a good choice of non-sedating oral antihistamine available via self-selection counter from both chemists and other retailers.

For moderate to severe (intermittent symptoms) or who fail to respond to the above regime, intranasal corticosteroids for regular use during the period of allergen exposure should be used. These include Beclometasone, Fluticasone, Triamcinolone (All of these available on self-selection or OTC from chemists), Mometasone (only available on prescription). It’s best to advise patient that it works well when used daily during high allergen exposure period, regardless of daily symptom peaks or troughs.

For severe/uncontrolled acute presentation a clinician may consider a short course of oral steroid. This will help gain control of the crisis situation whilst other options can be explored in a few days’ time.


Resistant cases/treatment failures: It’s best to check compliance and technique of nasal spray use. Change in strategy is guided by symptoms of patients. For example, for severe nasal stuffiness a short term add-on nasal decongestant (no longer than 7 days) may be used. For ongoing nasal itching the nasal corticosteroid may be replaced with steroid-antihistamine combo (Dymista) and vice versa. A regular oral antihistamine may be considered as an add-on. Other co-existing symptoms such as allergic conjunctivitis and secondary bacterial conjunctivitis, may also need treating too. For a hayfever sufferer who is also asthmatic, addition of Leukotriene receptor antagonist (Montelukast, Zafirlukast) can be useful too.

Indication for referral: An assessment by immunologist or ENT specialist may be indicated if despite escalation of treatment, the patient continues to struggle or has a structural abnormality/obstruction or diagnostic uncertainty.


Alternative/Complimentary therapies: Pollen Barrier Balm (Hay-max balm), Acupuncture (Qi-chi Acu-pressure band), Homeopathic remedies (Arsen alb), Flower remedies (Luffa, Pollinosan), Herbal (HayfeGUARD, Lizorm, Allergforte). The aforementioned examples are only few from the range of available products.


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