Asthma

Asthma affects approximately 1 in 12 adults in the UK. The diagnosis should be suspected in patients presenting with fluctuating respiratory symptoms (wheeze, breathlessness, chest tightness, and cough) that are worse at night or in the early morning. According to NICE NG80, diagnosis in adults involves a combination of clinical assessment and objective tests. Initial tests include spirometry (FEV1/FVC < 0.7 indicating obstruction) and a Bronchodilator Reversibility (BDR) test (improvement in FEV1 by 12% and 200ml). Fractional Exhaled Nitric Oxide (FeNO) testing is recommended for adults to identify eosinophilic inflammation (positive if >40 ppb). If diagnosis remains uncertain, Peak Expiratory Flow (PEF) monitoring over 2 to 4 weeks (diurnal variability >20%) is used. Management aims for 'no daytime symptoms, no night-time awakening, and no rescue medication use'. The stepwise ladder begins with low-dose Inhaled Corticosteroids (ICS) as first-line maintenance, followed by the addition of a Long-Acting Beta Agonist (LABA). Acute exacerbations are categorized by severity: Moderate (PEF 50-75% best), Severe (PEF 33-50%, RR >25, HR >110, inability to complete sentences), and Life-threatening (PEF <33%, SpO2 <92%, silent chest, cyanosis, exhaustion, or normal pCO2 on ABG). Critical care referral is mandatory for life-threatening features or worsening acidosis.

The pathophysiology of asthma involves a complex Type 2 (T2) helper T-cell mediated immune response. In response to environmental triggers, Th2 cells produce cytokines (IL-4, IL-5, IL-13) that drive IgE production by B cells and the recruitment of eosinophils to the airway mucosa. This leads to chronic inflammation, goblet cell hyperplasia, and mucus hypersecretion. Mast cell degranulation releases histamine, leukotrienes, and prostaglandins, causing immediate smooth muscle contraction (bronchoconstriction). Over time, chronic inflammation leads to 'airway remodelling,' characterized by subepithelial fibrosis, smooth muscle hypertrophy, and increased vascularity. This can result in fixed airflow obstruction that mimics COPD. The 'hygiene hypothesis' suggests that reduced exposure to microbes in early childhood shifts the immune system toward a Th2-mediated allergic phenotype rather than a Th1-mediated protective response. Genetic factors play a role, with associations found in genes coding for ADAM33 and orosomucoid-like 3 (ORMDL3). Environmentalปัจจัย such as atopy (family history of eczema/hay fever) and allergens (pollen, dust mites, pet dander) are primary drivers of symptoms.

Clinical presentation typically includes episodic symptoms with clear triggers. A history of atopy (eczema, allergic rhinitis) increases the likelihood. Physical examination may be normal between attacks, but during an exacerbation, an expiratory polyphonic wheeze is classic. In severe cases, accessory muscle use (sternocleidomastoid) and Harrison’s sulci (in children) may be seen. Complications include status asthmaticus (a life-threatening prolonged attack), pneumothorax, and respiratory failure (Type 1 initially, Type 2 if exhausting). Long-term complications include fixed airflow limitation and side effects of systemic corticosteroids (osteoporosis, weight gain, adrenal suppression). High-risk features for asthma death include a history of intubation, recent hospital admission, and psychological distress. Clinicians must screen for vocal cord dysfunction or GORD, which can mimic or exacerbate asthma. Occupational causes must be excluded in all new-onset adult cases; failure to do so is a common medicolegal pitfall.

Bedside: PEF diary (2-4 weeks looking for >20% variability). Bloods: Eosinophil count (elevated in T2-high asthma), Total IgE and Specific IgE (RAST) to identify triggers. Imaging: Chest X-ray (usually normal, used to exclude complications like pneumothorax or infection). Special Tests: FeNO testing (Positive if >40 ppb in adults, >35 ppb in children); Spirometry (FEV1/FVC < 0.70); Bronchodilator Reversibility (BDR) test (400mcg Salbutamol, positive if FEV1 increases >12% and >200ml); Bronchial provocation test (Methacholine or Histamine) if other tests are inconclusive.

**Chronic Management — NICE NG80 Stepwise Approach (Adults):**
Step 1: SABA prn (e.g. Salbutamol 100mcg) — use as reliever at all steps.
Step 2: Add low-dose ICS (e.g. Beclometasone 200mcg/day). This is the most important step.
Step 3: Add LABA to ICS (combination inhaler, e.g. Salmeterol/Fluticasone or Formoterol/Budesonide). MART (Maintenance And Reliever Therapy) can be used where ICS/Formoterol is prescribed — the same inhaler serves as both maintenance and reliever, simplifying therapy and reducing exacerbations. LTRA (e.g. Montelukast) may be added at this step as an adjunct, particularly in those with allergic rhinitis or exercise-induced symptoms.
Step 4: Increase ICS dose (medium-dose ICS/LABA) or add LAMA (e.g. Tiotropium — licensed add-on for uncontrolled asthma in adults).
Step 5: High-dose ICS/LABA; refer to specialist. Consider anti-IgE (Omalizumab) or anti-IL5 (Mepolizumab) biologics for severe eosinophilic or allergic asthma.

**Acute Management (O-SHIT-ME mnemonic):** Oxygen (target 94-98%), Salbutamol 5mg nebulised (driven by air if mild, oxygen if severe), Hydrocortisone IV 100mg or Prednisolone PO 40-50mg, Ipratropium bromide 0.5mg nebulised (add in acute severe/life-threatening), Theophylline/Aminophylline infusion (senior advice only), Magnesium Sulphate 2g IV over 20 mins (senior review, for acute severe not responding), Escalation (ICU/intubation).

**Discharge criteria:** Stable on 4-hourly SABA, PEF >75% of best/predicted, inhaler technique checked, GP follow-up within 2 working days, written asthma action plan provided.