Asthma (โรคหอบหืด)

• ICD10:
  • J45.0 Predominantly allergic asthma
  • J45.1 Nonallergic asthma
  • J45.9 Asthma, unspecified
  • J46 Status asthmaticus
• ICD11:
  • CA23 Asthma
  • CA23.0 Allergic asthma
  • CA23.1 Nonallergic asthma
  • CA23.2 Exercise-induced bronchoconstriction

Overview

Asthma is a chronic inflammatory respiratory disorder characterised by episodic symptoms of wheezing, shortness of breath, chest tightness, and cough. These symptoms are due to reversible narrowing of the airways, typically in response to various stimuli or triggers. The disease manifests through airway inflammation, bronchial hyperreactivity, and intermittent airflow obstruction that is often reversible spontaneously or with treatment. Although it affects individuals of all ages, it frequently begins in childhood and may persist into adulthood.

The underlying pathology involves a complex interplay of immune cells such as eosinophils, mast cells, and T-helper 2 (Th2) lymphocytes, resulting in airway remodelling over time if not adequately controlled. Chronic airway inflammation leads to structural changes including smooth muscle hypertrophy, subepithelial fibrosis, and goblet cell hyperplasia. Because of its chronic nature and recurrent symptoms, asthma significantly impacts patients’ quality of life and can lead to hospitalisation or death if untreated.

Management focuses on controlling airway inflammation, preventing exacerbations, and maintaining normal pulmonary function. Treatment strategies are guided by symptom severity, frequency, and the Global Initiative for Asthma (GINA) guidelines, which promote stepwise management to optimise disease control.

Epidemiology

Asthma is one of the most common chronic diseases worldwide, affecting approximately 300 million people. Its prevalence varies across countries, with higher rates reported in developed nations due to environmental and lifestyle factors. In the United States, around 8% of adults and 10% of children are affected, while in developing countries, underdiagnosis and limited access to care contribute to morbidity and mortality.

The disease shows a strong genetic predisposition. Children with one asthmatic parent have about a 25% chance of developing asthma, which increases to 50% if both parents are affected. Environmental factors, including exposure to tobacco smoke, air pollution, and indoor allergens such as dust mites, mould, and animal dander, are major contributors to asthma development and exacerbation.

Asthma is more common in boys during childhood but occurs more frequently in women during adulthood. The global burden of asthma includes substantial healthcare costs and productivity loss. Mortality rates have declined over recent decades due to improved management, though preventable deaths still occur, particularly in low-income countries where access to inhaled corticosteroids and emergency care remains limited.

Microbiology

Although asthma is not an infectious disease, microbial factors can contribute to its onset and exacerbations. Respiratory viral infections, particularly rhinovirus, respiratory syncytial virus (RSV), influenza virus, and parainfluenza virus, are major triggers of asthma attacks, especially in children. These infections induce airway inflammation through epithelial damage, cytokine release, and immune system activation, resulting in transient airway hyperreactivity.

In addition to viruses, bacterial pathogens such as Mycoplasma pneumoniae and Chlamydia pneumoniae have been associated with chronic airway inflammation and may play a role in the persistence or severity of asthma symptoms. Colonisation of the airways by these atypical bacteria has been shown to exacerbate bronchial inflammation by stimulating macrophages and T-cells to release proinflammatory cytokines, including IL-1β, IL-6, and TNF-α.

Emerging evidence also suggests a role for the airway microbiome in modulating immune responses in asthma. A reduction in microbial diversity in early childhood has been linked to increased susceptibility to allergic airway diseases. Commensal bacteria in the respiratory and intestinal tract, particularly Bifidobacterium and Lactobacillus species, are believed to promote immune tolerance, while dysbiosis may predispose to Th2-dominant inflammatory responses. Hence, the interaction between host immunity and the microbiome plays a pivotal role in asthma pathogenesis and its clinical course.

Pathophysiology

Clinical Presentation

Asthma presents with episodic symptoms that vary in frequency and intensity, often triggered by allergens, exercise, cold air, or respiratory infections. The cardinal symptoms include wheezing, breathlessness, chest tightness, and cough, particularly at night or early in the morning. Symptoms typically improve either spontaneously or after use of bronchodilators.

Sign & Symptom	Pathogenesis	Frequency	Specificity
Wheezing	Airflow limitation due to bronchial constriction	++++	++++
Dyspnoea	Increased airway resistance and hyperinflation	++++	+++
Cough (especially nocturnal)	Airway hyperresponsiveness and mucus hypersecretion	+++	++
Chest tightness	Smooth muscle spasm and dynamic airway collapse	+++	++
Prolonged expiratory phase	Air trapping and reduced expiratory flow	++	+++

Physical examination during an asthma attack may reveal expiratory wheezing, use of accessory muscles, and tachypnoea. In severe cases, patients may exhibit a silent chest (ominous sign of airflow obstruction) and hypoxaemia. Between attacks, examination findings may be normal, underscoring the reversible nature of asthma.

Investigation

Investigation of asthma aims to confirm variable airflow limitation, identify allergic triggers, and exclude alternative causes of respiratory symptoms. Objective lung function testing is essential to support the diagnosis and guide management.

Diagnosis Criteria (Dx)

Asthma is diagnosed based on a combination of characteristic clinical features and demonstration of variable airflow limitation. According to the Global Initiative for Asthma (GINA 2024) criteria, diagnosis requires the presence of both typical symptoms and objective evidence of reversible airflow obstruction.

• Clinical features: Recurrent episodes of wheezing, breathlessness, chest tightness, and cough, especially at night or early morning, often triggered by allergens, cold air, or exercise.
• Objective evidence of variable airflow limitation:
  • FEV1/FVC ratio < normal lower limit
  • Significant bronchodilator response: FEV1 improvement ≥12% and ≥200 mL after salbutamol
  • PEF variability >20% over 2 weeks of monitoring
  • Positive bronchial provocation test (methacholine PC20 ≤8 mg/mL)
• Supportive evidence: Eosinophilia in blood or sputum, elevated FeNO (>40 ppb), and positive allergy skin test (atopy).
• Exclusion of alternative causes: Rule out COPD, cardiac failure, bronchiectasis, and vocal cord dysfunction.

Diagnosis should always integrate clinical judgement with objective findings, as some patients may have normal spirometry between attacks. Repeat testing during symptomatic periods or after withholding bronchodilators improves diagnostic accuracy.

Differential Diagnosis (DDx)

Several conditions mimic asthma due to similar symptoms such as cough, wheezing, and dyspnoea. Accurate differentiation is essential to avoid misdiagnosis and inappropriate treatment.

Disease	Distinguishing Features	Investigations	Comments
Chronic Obstructive Pulmonary Disease (COPD)	Typically affects smokers; persistent symptoms with progressive airflow limitation; less reversibility.	Spirometry: FEV1/FVC <0.7, limited reversibility; history of smoking >10 pack-years.	Older onset, fixed obstruction, chronic cough with sputum.
Vocal Cord Dysfunction (VCD)	Episodic inspiratory stridor, throat tightness, poor response to bronchodilators.	Laryngoscopy during attack shows paradoxical vocal cord adduction.	Common in young females; often stress-related.
Heart Failure (Cardiac Asthma)	Paroxysmal nocturnal dyspnoea, orthopnoea, basal crackles.	Echocardiogram showing reduced ejection fraction; elevated BNP.	Older patients with cardiovascular disease; no bronchodilator response.
Bronchiectasis	Chronic productive cough, purulent sputum, recurrent infections.	HRCT shows dilated bronchi with thickened walls.	May coexist with asthma in some cases; requires airway clearance therapy.
Allergic Bronchopulmonary Aspergillosis (ABPA)	Asthma with recurrent infiltrates, elevated IgE, eosinophilia.	Chest CT: central bronchiectasis; Aspergillus skin test positive.	Occurs in known asthmatics; needs corticosteroid and antifungal therapy.
Foreign Body Aspiration	Sudden onset wheeze or cough after choking episode.	Bronchoscopy: visible foreign object.	Common in children; unilateral wheeze on examination.

In clinical practice, spirometry with bronchodilator reversibility and history of episodic symptoms remain the most reliable differentiating tools. A multidisciplinary approach may be required in complex or overlapping cases, particularly between asthma and COPD (Asthma–COPD overlap syndrome, ACOS).

Treatment

Asthma management focuses on controlling chronic airway inflammation, relieving symptoms, and preventing exacerbations. The cornerstone of treatment is inhaled therapy, which delivers medication directly to the lungs for rapid and effective action. Pharmacologic treatment is combined with patient education, trigger avoidance, and monitoring of lung function. The therapeutic approach follows a stepwise regimen according to the Global Initiative for Asthma (GINA 2024) guidelines, which categorise management into reliever therapy (for acute symptoms) and controller therapy (for long-term control).

Reliever medications, mainly short-acting β2-agonists (SABA) such as salbutamol, provide rapid bronchodilation and symptom relief during acute attacks. Inhaled corticosteroids (ICS) are the mainstay of controller therapy, targeting airway inflammation and reducing hyperresponsiveness. For moderate to severe disease, combination therapy with ICS and long-acting β2-agonists (LABA) — e.g., budesonide/formoterol — is recommended to maintain control and prevent exacerbations. Additional agents such as leukotriene receptor antagonists (LTRAs), long-acting muscarinic antagonists (LAMAs), or biologic therapies may be used in resistant cases.

Non-pharmacologic interventions include smoking cessation, vaccination (influenza, pneumococcal), and avoidance of known allergens. Pulmonary rehabilitation and patient self-monitoring (e.g., peak flow diary) are vital for long-term disease control. Severe cases may require systemic corticosteroids during exacerbations or biologic therapy targeting IgE or interleukin pathways.

Pharmacology

Pharmacologic treatment of asthma aims to control inflammation, relax airway smooth muscle, and prevent exacerbations. Drugs are broadly classified into relievers and controllers. Inhalation is the preferred route because it ensures high local effect and fewer systemic side effects.

Drug Class	Mechanism of Action	Common Drugs / Dosage	Key Adverse Effects
Short-acting β2-agonists (SABA)	Relax airway smooth muscle via β2-receptor stimulation; rapid symptom relief.	Salbutamol 100–200 µg inhaled q4–6h prn; Terbutaline 250 µg q6h.	Tremor, palpitations, tachycardia, hypokalaemia.
Inhaled corticosteroids (ICS)	Suppress airway inflammation and cytokine production; reduce eosinophil infiltration.	Budesonide 200–800 µg/day; Fluticasone 100–500 µg/day (divided doses).	Oral candidiasis, hoarseness; rinse mouth after use.
Long-acting β2-agonists (LABA)	Prolonged bronchodilation; used in combination with ICS for maintenance therapy.	Formoterol 12–24 µg/day; Salmeterol 50 µg bid.	Should not be used as monotherapy; risk of asthma-related death if used alone.
Leukotriene receptor antagonists (LTRA)	Block leukotriene-mediated bronchoconstriction and inflammation.	Montelukast 10 mg PO qhs.	Headache, rare neuropsychiatric effects (agitation, mood changes).
Long-acting muscarinic antagonists (LAMA)	Inhibit M3 receptors causing bronchodilation and mucus reduction.	Tiotropium 2.5 µg inhaled daily.	Dry mouth, urinary retention (rare).
Systemic corticosteroids	Suppress severe airway inflammation during exacerbations.	Prednisolone 30–50 mg/day PO for 5–10 days (short course).	Hyperglycaemia, weight gain, osteoporosis with chronic use.
Biologic agents	Target specific inflammatory mediators (IgE, IL-5, IL-4Rα).	Omalizumab (anti-IgE) 150–300 mg SC q2–4w; Mepolizumab (anti–IL-5) 100 mg SC q4w.	Injection site reactions, rare anaphylaxis.

Therapeutic choice depends on disease severity, phenotype (allergic or eosinophilic), and patient adherence. Step-down therapy may be considered when asthma control is maintained for at least three months to minimise medication burden.

Guideline

The management of asthma is guided by the Global Initiative for Asthma (GINA 2024) framework, which emphasises a personalised, stepwise approach aimed at achieving symptom control, preventing exacerbations, maintaining normal activity levels, and minimising treatment-related side effects. The key principle is to use the lowest effective dose of medication that maintains control, with periodic reassessment to adjust therapy up or down depending on disease activity.

Stepwise Approach to Asthma Management

Asthma treatment follows a stepwise regimen that balances symptom control with risk reduction. Each step builds upon the previous one, escalating therapy for poor control or stepping down once stability is maintained for at least 3 months.

• Step 1: For patients with infrequent symptoms (<2 times per month). Preferred therapy is as-needed low-dose ICS-formoterol (e.g., budesonide/formoterol 160/4.5 µg 1 puff PRN). This combination reduces exacerbation risk compared to short-acting β2-agonist (SABA) monotherapy.
• Step 2: Low-dose ICS daily (e.g., budesonide 200 µg BID) or as-needed low-dose ICS-formoterol. This prevents progression and reduces inflammation in mild persistent asthma.
• Step 3: Low-dose ICS/LABA combination (e.g., budesonide/formoterol 160/4.5 µg 2 puffs BID). Consider adding LTRA (montelukast 10 mg HS) in allergic or exercise-induced cases.
• Step 4: Medium-dose ICS/LABA combination. If uncontrolled, add-on LAMA (tiotropium 2.5 µg daily) or consider maintenance oral corticosteroids for short periods.
• Step 5: For severe refractory asthma, refer to a specialist. Add biologic therapy based on phenotype — e.g., omalizumab (anti-IgE 150–300 mg SC q2–4w), mepolizumab (anti–IL-5 100 mg SC q4w), or dupilumab (anti–IL-4Rα 200–300 mg SC q2w).

Non-Pharmacologic and Supportive Measures

Effective asthma control extends beyond medication. Comprehensive management includes:

• Trigger avoidance: Identify and minimise exposure to allergens (dust mites, animal dander, mould, pollen) and irritants (smoke, pollution, occupational agents).
• Vaccination: Annual influenza and pneumococcal vaccines reduce infection-triggered exacerbations.
• Patient education: Teach correct inhaler technique, adherence importance, and recognition of early warning signs.
• Asthma action plan: Provide written instructions for step-up therapy during worsening symptoms and when to seek medical attention.
• Exercise and lifestyle: Encourage physical activity and weight control, as obesity worsens asthma control.

Acute Exacerbation Management

• Mild to Moderate: Inhaled SABA (salbutamol 2.5 mg via nebuliser or 100–200 µg via MDI with spacer q20min × 3 doses). Add oral prednisolone 30–50 mg/day for 5–7 days if symptoms persist.
• Severe: Oxygen to maintain SpO₂ >94%, nebulised SABA plus ipratropium bromide (0.5 mg), and IV corticosteroid (methylprednisolone 40–60 mg q6–8h). Monitor for fatigue, hypercapnia, or impending respiratory failure — consider ICU admission.

Treatment Goals

• Minimal or no daytime symptoms (<2 per week).
• No nocturnal symptoms or activity limitation.
• Normal or near-normal lung function (FEV1 >80% predicted).
• Prevention of exacerbations and need for emergency care.

Monitoring and Step-Down Therapy

Patients should be reviewed every 1–3 months until good control is achieved. Spirometry or peak flow monitoring evaluates lung function trends. Once control is sustained for ≥3 months, consider step-down therapy — for instance, reducing ICS dose by 25–50% or transitioning to once-daily dosing — while monitoring for symptom recurrence. Regular reassessment helps minimise overtreatment and side effects.

Example Doctor’s Orders

Disclaimer: Example for educational purposes only, not for direct patient advice.

Prognosis

The prognosis of asthma is generally favourable when appropriate management and long-term control are achieved. Most patients experience significant improvement with inhaled corticosteroid (ICS)-based therapy, especially when adherence is consistent. In children, asthma may remit during adolescence, although a subset will continue to have symptoms into adulthood. Early initiation of controller therapy is associated with improved lung function and reduced airway remodelling.

Patients with mild or moderate asthma can expect near-normal life expectancy and quality of life if the disease is well controlled. However, poorly managed asthma or frequent exacerbations can result in chronic airflow limitation and fixed obstruction resembling COPD. Factors associated with poor prognosis include late diagnosis, smoking, obesity, poor medication adherence, and uncontrolled exposure to environmental triggers.

Severe asthma, affecting approximately 5–10% of patients, remains challenging despite high-dose ICS/LABA or biologic therapy. These patients are at higher risk of hospitalisation, corticosteroid-related adverse effects, and reduced quality of life. With modern biologic treatments targeting IgE and interleukin pathways, the long-term outcomes of severe asthma have improved significantly. Mortality is rare in well-controlled patients but remains a concern in those with poor access to care or overreliance on short-acting β2-agonists.

Prevention

Asthma prevention focuses on reducing exposure to triggers and maintaining optimal control of airway inflammation. Primary prevention strategies include avoiding tobacco smoke exposure during pregnancy and early childhood, as well as reducing exposure to indoor allergens such as dust mites and mould. Promoting breastfeeding and delaying introduction of allergenic foods in infancy may reduce atopic risk in predisposed children.

For patients with established asthma, secondary prevention aims to avoid exacerbations through trigger management, vaccination (influenza and pneumococcal), and adherence to controller medication. Occupational asthma can be prevented by reducing contact with sensitising agents such as chemicals, dust, and fumes. Educating patients on inhaler technique and having an individualised asthma action plan are critical components of tertiary prevention, helping reduce morbidity and emergency visits.

Conclusion

Quiz (USMLE OSCE)

Frequently Asked Questions (FAQ)

What is the difference between asthma and COPD?

Asthma is characterised by reversible airflow obstruction due to airway inflammation, often triggered by allergens, whereas COPD involves irreversible obstruction from chronic bronchitis or emphysema, usually in smokers. Asthma typically starts early in life, while COPD develops later and progresses steadily.

Why is inhaled corticosteroid (ICS) important in asthma management?

ICS is the cornerstone of therapy as it reduces airway inflammation, improves lung function, and prevents exacerbations. Consistent ICS use decreases the need for emergency treatment and long-term complications.

Can asthma be cured?

Asthma cannot be completely cured, but with appropriate treatment and avoidance of triggers, it can be well controlled. Many children experience symptom remission, although inflammation may persist subclinically.

What are common asthma triggers?

Triggers include allergens (dust mites, pollen, pets), infections, cold air, exercise, stress, smoke exposure, and air pollution. Identifying and avoiding triggers are key to preventing exacerbations.

When should a patient seek emergency care?

Patients should seek immediate medical attention if symptoms rapidly worsen, if rescue inhaler use exceeds every 2–3 hours, or if there is difficulty speaking or a drop in oxygen saturation. Prompt treatment with oxygen and bronchodilators can be lifesaving.