Asthma — Causes, Triggers, Symptoms & Management Guide — Symptoms, Causes & Treatment | MyMedicPlus

Asthma is a chronic inflammatory disease of the lower airways defined by three pathophysiological characteristics: (1) variable and reversible airflow obstruction — airway narrowing that fluctuates over time and in response to treatment; (2) airway hyperresponsiveness — exaggerated bronchoconstriction to stimuli that do not affect non-asthmatic airways; and (3) airway inflammation — predominantly eosinophilic, IgE-mediated, Type 2 T-helper (Th2)-driven inflammation with elevated IL-4, IL-5, and IL-13 in allergic (atopic) asthma. It affects over 300 million people globally (approximately 1 in 13 individuals, ~8% of developed countries' populations) and causes 461,000 deaths annually — with the Global Burden of Disease Study estimating 24.8 million disability-adjusted life years (DALYs) lost — the vast majority of deaths preventable with appropriate preventive therapy. Asthma is characterised by recurring episodes of wheezing, breathlessness, chest tightness, and cough — typically worse at night and in the early morning, reflecting circadian variation in airway tone and bronchial inflammation. Phenotyping is increasingly important for management: allergic (atopic) asthma — most common form, onset in childhood or early adulthood, associated with atopic dermatitis and allergic rhinitis; non-allergic (intrinsic) asthma — adult-onset, often more severe, triggered by aspirin/NSAIDs (aspirin-exacerbated respiratory disease/AERD), exercise, cold air, or occupational agents; late-onset eosinophilic asthma — severe, corticosteroid-dependent, nasal polyp association; and obesity-associated asthma — non-eosinophilic, female predominance. Asthma is the third most common cause of hospitalisation in the United States and the most common chronic disease of childhood in most developed countries.

Asthma results from a complex interaction of genetic susceptibility, immune programming, and environmental exposures. Genetic predisposition: heritability of asthma is approximately 60-70%; key susceptibility genes include ORMDL3 (chromosome 17q21 — most replicated in childhood asthma GWAS), IL-4 receptor, ADAM33, PHF11, and genes of the IL-13 pathway. Atopy (IgE-mediated hypersensitivity) is the strongest risk factor — present in 80% of childhood asthma; the 'atopic march' describes the progression from atopic dermatitis in infancy to allergic rhinitis and asthma by school age. Allergen triggers: house dust mites (Dermatophagoides pteronyssinus and farinae — the leading perennial asthma trigger), pet dander (cat Fel d1 and dog Can f1 are highly potent allergens), grass/tree/weed pollens (seasonal triggers for allergic asthma exacerbations), mould spores (Alternaria and Cladosporium — highest risk for severe asthma attacks), and cockroach allergen (important in urban asthma in children). Non-allergic triggers: respiratory viral infections — rhinovirus is responsible for 50-80% of acute asthma exacerbations in children; influenza and RSV cause severe attacks requiring hospitalisation; tobacco smoke (active and passive — smoking in infancy/childhood increases asthma risk 2-fold, active smoking worsens control); air pollution (fine particulate matter PM2.5, nitrogen dioxide, ozone — each associated with increased emergency department visits); cold dry air — triggers exercise-induced bronchoconstriction via airway cooling and drying; aspirin and NSAIDs (aspirin-exacerbated respiratory disease — affects 10-20% of adult asthma patients, often with nasal polyps); beta-blockers (contraindicated in asthma); occupational sensitisers — isocyanates (spray painters, foam manufacturers), flour dust (bakers), latex, platinum salts, and wood dust — responsible for 10-15% of adult-onset asthma (occupational asthma). Risk factors for asthma development: family history of atopy, male sex in childhood (female predominance post-puberty), childhood obesity, low-birthweight, antibiotic use in infancy, caesarean delivery, and reduced microbial diversity in early life (hygiene hypothesis).

Classic symptoms of stable asthma are episodic and variable: recurrent wheeze (a high-pitched polyphonic expiratory sound from dynamic airway narrowing — from multiple airways), shortness of breath (dyspnoea), chest tightness, and cough — characteristically worse at night and in the early morning (reflecting circadian dip in cortisol and airway calibre), triggered by allergens, viral URTIs, exercise, cold air, or irritants, and varying spontaneously or with treatment. A diurnal variation in peak flow or FEV1 of above 10% is characteristic. Uncontrolled asthma features: use of reliever inhaler (salbutamol) more than twice weekly; night-time symptoms more than twice monthly; any limitation of activities. Exercise-induced bronchoconstriction (EIB): occurs in up to 90% of asthma patients — causing cough, wheeze, and dyspnoea during or within 15 minutes of exercise, resolving spontaneously in 30-45 minutes; pre-treatment with salbutamol or daily ICS typically prevents EIB. Acute severe asthma attack (status asthmaticus) features — classified by GINA as: moderate (able to speak in phrases; SpO2 above 92%; PEFR 51-69% best); severe (speaks in words only; SpO2 below 92%; RR above 25; PEFR below 50%); and life-threatening (silent chest — no wheeze from critically limited air entry; cyanosis; inability to speak; drowsiness, confusion, or exhaustion; SpO2 below 90%; PEFR below 33% best). Silent chest is an ominous sign indicating minimal air movement — paradoxically may be misinterpreted as improvement. Atypical presentations: isolated nocturnal cough (cough-variant asthma); chronic cough without wheeze; exercise-induced cough; and postnasal drip-triggered cough — all may represent asthma and should be investigated with spirometry.

NICE (2017) and GINA guidelines recommend a structured diagnostic pathway. Spirometry with bronchodilator reversibility test: the cornerstone of asthma diagnosis — demonstrates obstructive ventilatory pattern (FEV1/FVC ratio below 0.7 or below the lower limit of normal); significant bronchodilator reversibility defined as FEV1 improvement of above 12% and above 200 mL from baseline after 400 mcg inhaled salbutamol — confirms variable airflow obstruction and supports asthma diagnosis; normal spirometry does not exclude asthma (may be normal between episodes). Peak expiratory flow (PEF) variability: serial twice-daily PEF monitoring over 2-4 weeks showing diurnal variability of above 10-20% (amplitude percentage mean) is characteristic of asthma and helps confirm variable airflow obstruction in clinical practice. FeNO (fractional exhaled nitric oxide): FeNO is produced by airway epithelial cells under the influence of IL-4/IL-13 — elevated in eosinophilic airway inflammation; FeNO above 40 ppb (in adults) or above 35 ppb (in children) strongly supports eosinophilic asthma diagnosis and predicts good corticosteroid response; FeNO is measured using a handheld or tabletop device — NICE recommends FeNO as part of routine asthma diagnosis in the UK. Bronchial provocation/challenge testing: methacholine (PC20 below 8 mg/mL confirms hyperresponsiveness), mannitol, hypertonic saline, or exercise challenge — useful when spirometry is normal but clinical suspicion is high; particularly useful to confirm exercise-induced bronchoconstriction. Blood eosinophil count: elevated blood eosinophils (above 300 cells/microL in non-systemic eosinophilic conditions) suggests eosinophilic asthma phenotype and predicts response to anti-IL-5 biologic therapy. Skin prick testing and specific serum IgE (allergen panels) identify sensitisations to guide trigger avoidance and consider allergen immunotherapy. Chest X-ray: performed in all new asthma diagnoses to exclude other causes (COPD, pulmonary oedema, tumour); typically normal in asthma or shows hyperinflation during exacerbation. In children, the probability approach using FeNO, symptom pattern, and spirometry replaces a single diagnostic test.

Treatment follows the GINA (Global Initiative for Asthma) 2024 step-up/step-down approach based on symptom control and exacerbation frequency. Step 1 (mild intermittent — symptoms less than 2 days/week): as-needed low-dose ICS-formoterol (preferred over SABA alone — reduces exacerbation risk; GINA 2024 preferred track). Step 2 (mild persistent): daily low-dose ICS controller plus as-needed SABA reliever; or as-needed low-dose ICS-formoterol. Step 3 (moderate persistent): low-to-medium ICS + LABA (salmeterol/fluticasone propionate — Seretide; formoterol/budesonide — Symbicort; formoterol/fluticasone furoate — Relvar); add LTRA (montelukast 10 mg/day) if LABA is insufficient or not tolerated. Step 4: medium-high dose ICS/LABA; add tiotropium 5 mcg (soft mist inhaler — Spiriva Respimat) for add-on bronchodilation in adults with history of exacerbations; azithromycin 250-500 mg three times weekly for persistent uncontrolled asthma. Step 5 (severe uncontrolled — refer to specialist severe asthma service): biologic agents targeting specific inflammatory pathways — anti-IgE: omalizumab (Xolair — SC monthly; IgE-dependent allergic asthma, elevated serum IgE, sensitised to perennial allergen; reduces exacerbations by 25-50%); anti-IL-5: mepolizumab (Nucala 100 mg SC monthly), reslizumab (IV), benralizumab (Fasenra 30 mg SC monthly then 8-weekly — depletes eosinophils completely); anti-IL-4/IL-13: dupilumab (Dupixent 200-300 mg SC fortnightly — superior for nasal polyp comorbidity and steroid-dependent asthma); anti-TSLP: tezepelumab (Tezspire 210 mg SC monthly — broadest phenotype coverage, reduces exacerbations 70-82% in PATHWAY trial). Biologics reduce severe exacerbations by 50-75%. Acute asthma management: mild-moderate — repeated salbutamol 2.5-5 mg nebulised (or 4-10 puffs via spacer every 20 minutes for 1 hour); ipratropium bromide 0.5 mg added for moderate-severe attacks; systemic corticosteroids (prednisolone 40-50 mg/day orally for 5 days or IV hydrocortisone 100 mg 6-hourly); supplemental oxygen targeting SpO2 94-98%; magnesium sulphate 1.2-2 g IV over 20 minutes for severe attack not responding to initial bronchodilators (significantly reduces hospitalisation rate). Allergen immunotherapy (SCIT or SLIT) is disease-modifying for allergic asthma.

Poorly controlled asthma causes progressive fixed airflow obstruction through irreversible airway remodelling — smooth muscle hypertrophy, subepithelial fibrosis, and goblet cell hyperplasia — reducing lung function permanently over years. Frequent acute exacerbations cause hospitalisation, ICU admission, and mechanical ventilation requirements. Near-fatal and fatal asthma attacks (status asthmaticus) occur when severe bronchospasm and mucus plugging cause refractory hypoxia — typically from delayed or inadequate treatment or non-adherence to preventer therapy. Systemic corticosteroid dependence from frequent oral prednisolone courses causes osteoporosis (vertebral fractures), type 2 diabetes, Cushing's syndrome, cataracts, and adrenal suppression. Children with uncontrolled asthma have significantly more school absence, exercise avoidance, disrupted sleep, and impaired physical and social development. The 461,000 annual asthma deaths globally — the vast majority preventable with consistent ICS use and trigger avoidance — are predominantly in low-income countries with limited access to inhaled corticosteroids.

Allergen avoidance is the first step: use allergen-impermeable mattress and pillow covers for house dust mite allergy; HEPA air purifiers and keeping pets out of bedrooms for pet allergy; monitor daily pollen counts and keep windows closed during high pollen periods for seasonal allergic asthma. Quit smoking and eliminate secondhand smoke exposure — passive smoke is a major trigger and worsens long-term lung function. Maintain a healthy weight — obesity impairs diaphragmatic function, reduces lung volumes, and significantly worsens asthma control; each 5% weight loss reduces respiratory symptoms. Aerobic exercise (swimming is particularly beneficial as a moist-air environment reduces EIB) improves cardiorespiratory fitness and asthma control when properly managed with pre-exercise bronchodilator use if needed. Keep up-to-date influenza vaccination (reduces asthma exacerbation risk 20-40%) and pneumococcal vaccination. Identify personal triggers via a symptom and peak flow diary. Correct inhaler technique (spacers improve lower respiratory deposition from 20% to 60%), reviewed at every consultation. Every asthma patient should have a written Personalised Asthma Action Plan (PAAP) specifying when to increase treatment, when to start prednisolone, and when to call 999.

Seek emergency care immediately (call 999/112 or go to A&E) for: severe asthma attack with marked breathlessness at rest making talking in short sentences or single words difficult; use of accessory muscles (neck muscles, between ribs); respiratory rate above 25 breaths per minute; oxygen saturation below 92%; peak flow below 50% of personal best (severe attack) or below 33% (life-threatening attack); not responding to back-to-back salbutamol puffs; or a silent chest (no wheeze audible — a grave sign). Call 999 for any life-threatening attack features. Contact a GP urgently for: asthma symptoms that are significantly worse than usual and not responding to reliever inhaler; needing reliever inhaler more than 3 times per week (suggests poorly controlled asthma requiring step-up of preventive treatment); waking at night with cough or wheeze more than once per week; or limiting exercise significantly. All asthma patients should have a written Asthma Action Plan from their GP or asthma nurse, specifying when to increase treatment and when to call 999.