BPTBuddy

Description

IgE-mediated inflammation of the nasal mucosa
Cardinal four: sneezing, rhinorrhoea, nasal obstruction, itch (nose, palate, eyes)
- Itch and sneezing separate it from non-allergic rhinitis

ARIA classification - drives treatment intensity

Axis	Categories
Duration	Intermittent <4 days/wk or <4 consecutive weeks; Persistent >=4 days/wk AND >=4 weeks
Severity	Mild = no impairment; Moderate-severe = sleep disturbance, impaired daily/school/work activity, or troublesome symptoms

The old seasonal/perennial split is superseded - Australian house dust mite and grass seasons overlap

Differential

Non-allergic rhinitis - vasomotor, occupational, hormonal (pregnancy), gustatory, NARES (eosinophilic)
Rhinitis medicamentosa - rebound from >5 days topical decongestant
Drug-induced - ACE inhibitors, alpha-blockers, NSAIDs, cocaine
Chronic rhinosinusitis +/- nasal polyps
Unilateral: foreign body, tumour, CSF rhinorrhoea, granulomatosis with polyangiitis

~1 in 5 Australians (~19%) - one of the highest rates worldwide
Onset usually childhood/adolescence; peak prevalence 20-40
M=F in adults; M>F in children
Grass pollen dominant in temperate Australia (Oct-Dec); house dust mite year-round, worse in humid coastal regions
Alternaria and Aspergillus in inland/agricultural areas

Sensitisation -> allergen-specific IgE on mucosal mast cells
Re-exposure -> early phase (minutes): histamine, tryptase, leukotrienes
- -> sneeze, itch, watery rhinorrhoea, vascular engorgement
Late phase (4-12h): eosinophil, basophil and Th2 lymphocyte infiltration
- -> nasal blockage, hyperreactivity, priming (lower allergen doses trigger symptoms as the season progresses)
United airways - same epithelium, same Th2 process as asthma
- Chronic mucosal inflammation -> bronchial hyperresponsiveness

Clinical diagnosis. Test to identify the allergen, not to make the diagnosis.

Clinical

Symptom-exposure relationship, seasonality, pets, workplace, bedding
Allergic salute, transverse nasal crease, allergic shiners, Dennie-Morgan folds, mouth breathing
Rhinoscopy: pale, boggy, blue-grey oedematous turbinates + clear secretions
- Erythematous mucosa suggests infection or non-allergic rhinitis
Examine for polyps, septal deviation, post-nasal drip; check the chest

Allergen identification

Skin prick testing - first-line
- Panel: house dust mite, moulds (Alternaria, Aspergillus), grasses, animal dander, plus pollens and cockroach
- Wheal >=3 mm above negative control; antihistamines withheld 3-5 days
Specific IgE where SPT is unavailable, skin disease present, or antihistamines cannot be ceased
A positive test without matching history is sensitisation, not allergy - do not treat it

When to image or scope

Unilateral symptoms, bleeding, facial pain, anosmia, treatment failure -> nasendoscopy +/- CT sinuses
Plain sinus X-rays have no role

A. Allergen avoidance

House dust mite: mattress and pillow encasing, hot wash bedding, remove bedroom carpet
Pollen: stay indoors on high-count and windy days, close car windows, shower after outdoor exposure
Avoidance improves symptoms but does not alter the natural history of the disease
Single-measure mite avoidance has repeatedly failed in trials - only bundled measures help

B. Pharmacotherapy - matched to the dominant symptom

Symptom	Best agent
Blockage	Intranasal corticosteroid
Sneeze/itch/rhinorrhoea	Antihistamine (intranasal or oral H1)
Watery rhinorrhoea alone	Intranasal ipratropium (anticholinergic)
Eye symptoms	Topical ocular antihistamine or sodium cromoglycate

Intranasal corticosteroid is the single most effective agent for moderate-severe or persistent disease
- Mometasone, fluticasone, budesonide
- Takes days to weeks for full effect - start before the season and use continuously, not PRN
- Technique matters: spray away from the septum, do not sniff hard - the main causes of failure and of epistaxis
Second-generation oral antihistamines - cetirizine, loratadine, fexofenadine
- Avoid sedating first-generation agents - impair driving, sleep architecture and school performance
Combination intranasal corticosteroid + antihistamine (azelastine/fluticasone) - superior to either alone in moderate-severe disease
Topical decongestants: maximum 3-5 days - rhinitis medicamentosa
Saline irrigation - cheap, useful adjunct
Montelukast - modest benefit; neuropsychiatric warning, reserve for coexisting asthma

C. Allergen immunotherapy - the only disease-modifying option

Subcutaneous or sublingual desensitisation is the only treatment that alters the disease course
- 3-5 years of therapy; benefit persists for years after cessation
- May prevent progression to asthma and new sensitisations
Indications: moderate-severe disease inadequately controlled on optimal pharmacotherapy, or unacceptable medication burden, with a demonstrated IgE-specific trigger matching the history
SCIT: risk of systemic reaction - must be given where adrenaline and observation for 30 min are available; not in uncontrolled asthma
SLIT: first dose supervised, then home dosing; local oropharyngeal itch common

D. Treat what travels with it

Assess and treat asthma in every patient - control of rhinitis improves asthma control and reduces exacerbations
Chronic rhinosinusitis, otitis media with effusion, obstructive sleep apnoea

Asthma - up to 80% of asthmatics have rhinitis; ~20-40% of rhinitis patients have asthma
Atopic dermatitis, food allergy, eosinophilic oesophagitis
Chronic rhinosinusitis with nasal polyps
Pollen-food (oral allergy) syndrome - birch/grass cross-reactivity
Otitis media with effusion, adenoid hypertrophy, dental malocclusion in children
Obstructive sleep apnoea, sleep fragmentation
Thunderstorm asthma - grass pollen + rye grass; rhinitis with grass sensitisation is the key risk group, Melbourne 2016

Chronic, relapsing; often improves in later adult life
Allergic march: eczema and food allergy in infancy -> rhinitis -> asthma
Untreated: impaired sleep, daytime somnolence, measurable impairment of school and work performance
Immunotherapy is the only intervention shown to change the trajectory

Complications

Poorly controlled asthma
Recurrent sinusitis, nasal polyps, anosmia
Rhinitis medicamentosa from decongestant overuse
Epistaxis and (rarely) septal perforation from poor intranasal steroid technique
Growth velocity concern with intranasal steroids is small and dose-dependent - use the lowest effective dose in children

7 of 7 sections written · drafted 2026-09-08