Childhood asthma and recurrent wheeze

• Childhood asthma is a chronic inflammatory disease of the airways that causes reversible (or partly reversible) airflow obstruction: wheeze, cough, chest tightness and breathlessness that vary over time and with triggers. ^{[1] [5]}
• In a preschool child, wheeze is usually viral. Many wheeze once or twice and outgrow it; a smaller group (roughly one child in three wheezes in the first 3 years of life) has recurrent wheeze that persists and behaves like asthma. ^[3]
• In babies and toddlers the symptoms cannot be labelled confidently as asthma, because bronchiolitis, viral wheeze and other causes overlap. The diagnosis is confirmed or excluded once the child is old enough to have objective tests, from about age 5. ^[1]
• Stepwise inhaled corticosteroid (ICS) treatment, with a non-steroid reliever, controls symptoms in almost every school-aged child. A short-acting beta2 agonist (SABA) should never be given without an accompanying ICS. ^[1]
• Acute attacks are classified as moderate, severe or life-threatening by symptoms, oxygen saturation and peak flow. Early inhaled salbutamol plus oxygen, prednisolone and, when needed, hospital care save lives. ^[2]

By the end of this page you should be able to:

1. Tell the common preschool wheeze patterns apart, and say which are likely to become asthma.
2. Diagnose asthma by age group: under 5, 5 to 16, and adults with childhood asthma.
3. Explain the stepwise ICS-based treatment for a child of any age, and how to step up or down.
4. Assess the severity of an acute asthma attack in a child and give the first hour of treatment with correct doses.
5. Recognise a child whose wheeze needs urgent referral, specialist care, or a different diagnosis.
6. Counsel families about inhaler technique, adherence, triggers and what an asthma action plan covers.

Asthma is the most common chronic disease of childhood. It is an inflammatory disorder of the airways: the lining swells, produces mucus and becomes twitchy, so the airway narrows. The narrowing is reversible, at least partly, with treatment or between attacks. That reversibility, plus the variability of symptoms, is what separates asthma from fixed airway disease. ^{[1] [4] [5]}

This page covers the full clinical topic for a medical student: what preschool wheeze is and how it differs from asthma, how we diagnose by age, how we treat step by step at every age, and how we manage an acute attack. It uses the current international and UK guidance: the 2026 GINA strategy summary, the BTS/NICE/SIGN collaborative asthma pathway (NG244/NG245, published November 2024), and the 2019 BTS/SIGN guideline for acute asthma in children. ^{[1] [2] [4] [5]}

It uses generic drug names and international units, with regional and low-resource notes, so that it serves readers in any health system. It is written for medical students meeting the topic for the first time, but aims for consultant level completeness.

Asthma is usually defined clinically: a history of variable respiratory symptoms (wheeze, shortness of breath, chest tightness, cough) with objective evidence of variable airflow limitation, after excluding other causes. ^{[1] [5]}

In children under 5, "wheeze" is a sound, not a disease. About one third of children wheeze at least once before age 3. ^[3] The 2008 European Respiratory Society task force on preschool wheeze described phenotypes by their time course (transient, persistent, late-onset wheeze), and a simpler clinical division by trigger that is now used to guide treatment: ^[3]

• Episodic viral wheeze (EVW): wheezing only during (or immediately after) viral upper respiratory infections, with no, or few, symptoms in between. It is the commonest phenotype between 1 and 5 years of age. These children are usually non-atopic, respond to intermittent treatment at the time of symptoms, and are less likely to develop asthma later. ^[3]
• Multiple-trigger wheeze (MTW): wheezing with viral infections and between them, with exercise, crying, laughter, cold air or allergens. These children are more often atopic, may have a family history of asthma, respond to regular ICS, and are more likely to develop persistent asthma with some early loss of lung function. ^[3]

These two labels are useful but not fixed. A child can move from one to the other over months, so the classification should be reassessed at each review. ^[3]

Asthma is the commonest chronic childhood disease worldwide. ^[4] In preschool children, recurrent wheeze is very common: about one child in three wheezes in the first 3 years of life. ^[3] Most infants who wheeze with viral infections improve and the wheeze resolves ("transient early wheeze"). A smaller group ("persistent wheeze") has wheezing that starts early, is linked to atopy and higher immunoglobulin E, and carries reduced lung function into school age. "Late-onset wheeze" begins after 3 years of age, is associated with atopy, and tends to persist. ^[3]

Boys wheeze more often in early childhood; after puberty the sex ratio evens and then reverses. Trigger exposure (tobacco smoke, indoor damp and mould, air pollution), premature birth, low birth weight and family history all modify risk. ^{[3] [4]}

Asthma risk is multifactorial. The strongest single factor is atopy: children with eczema, allergic rhinitis or food allergy wheeze more, and wheeze plus atopy sharply raises the chance of asthma. A family history of asthma or atopy is common. ^{[1] [3]}

• Early-life triggers: viral respiratory infection (especially RSV and rhinovirus), which is the trigger that most often first unmasks a wheezing tendency. ^[3]
• Environment: parental smoking, damp and mouldy housing, outdoor air pollution, and early-life lower respiratory infection. ^[1]
• Host: male sex in early childhood, preterm birth, low birth weight, and reduced early lung function. ^[3]
• Allergens: house dust mite and other aeroallergens in sensitised children. ^[1]

GINA and BTS/SIGN both note that a viral cold in the first two years often produces wheeze that does not become asthma, which is why the under-5 group is handled differently from school-aged children. ^{[3] [4]}

Asthma begins with chronic airway inflammation. Eosinophils, mast cells, T-helper 2 lymphocytes and epithelial cells release cytokines (for example, interleukin-4, -5 and -13) that:

1. Make the mucosa oedematous and infiltrated, narrowing the airway.
2. Increase mucus secretion, plugging small airways.
3. Cause bronchial hyperresponsiveness: airways constrict to stimuli (allergens, cold air, exercise, viral infection) that leave normal airways unchanged.
4. Remodel the airway over years if inflammation is untreated, with smooth muscle hypertrophy and basement membrane thickening.

Airflow obstruction in asthma is therefore reversible or partly reversible with bronchodilators and anti-inflammatory treatment, in contrast to the largely fixed obstruction of COPD. In a child, the airway is narrower to start with, so the same amount of oedema and mucus causes much more obstruction; that is why infants wheeze loudly with what looks like a small illness. ^{[1] [4]}

Parents describe a dry cough, wheeze or whistling, breathlessness, chest tightness, and disturbed sleep. Features that point to asthma:

• Variability: symptoms worse at night or early morning, seasonal, with exercise, laughing or crying, in cold air, or with allergens/viral infections. ^{[1] [5]}
• Response: relief within minutes of a bronchodilator. ^[1]
• Family/personal history: eczema, allergic rhinitis, asthma in parents or siblings. ^{[1] [3]}
• Interval symptoms: activity limitation, cough on exertion, cough at night between acute episodes. ^{[1] [3]}
• Triggers: colds, exercise, smoke, dust, pets, weather change. ^[1]

Red-flag histories: a toddler who first wheezed at 1 to 2 months, symptoms constant rather than variable, wet (productive) cough all year, vomiting with cough, or poor growth suggest a diagnosis other than asthma (see differential diagnosis). ^[1]

Often completely normal between attacks. During an attack: tachypnoea, use of accessory muscles, hyperinflation, wheeze (expiratory polyphonic), prolonged expiration, and chest recession. Signs that suggest something else: clubbing, focal chest signs, stridor, failure to thrive, or wheeze that sounds monophonic. ^{[1] [2]}

Always inspect inhaler and spacer technique; it is the commonest cause of "poor control". ^[1]

Wheeze in a child is not asthma until other causes are excluded. The key separating features:

Investigations depend on age: the younger the child, the more the diagnosis rests on history and response to treatment, and the less useful testing is.

Objective testing is required before confirming asthma. ^{[1] [5]}

1. FeNO (fractional exhaled nitric oxide): raised in eosinophilic airway inflammation. Diagnose if FeNO is 35 parts per billion (ppb) or more. ^[1]
2. Bronchodilator reversibility (BDR) with spirometry: if FeNO is not raised or testing is unavailable. Diagnose if FEV1 rises by 12% or more from baseline (or by 10% or more of the predicted FEV1). ^[1]
3. Peak expiratory flow (PEF): if spirometry is unavailable, measure twice daily for 2 weeks. Diagnose if PEF variability is 20% or more (amplitude percentage mean). ^[1]
4. If still suspected but not confirmed: skin-prick testing to house dust mite, or total IgE plus blood eosinophil count. Exclude asthma if no sensitisation and total IgE not raised. Diagnose if there is sensitisation or a raised IgE with an eosinophil count above 0.5 x 10^9 per litre. ^[1]
5. If still in doubt: refer to a paediatric respiratory specialist; bronchial challenge testing may be needed. ^[1]

Objective tests are rarely possible or reliable. Treat a child with recurrent wheeze, interval symptoms or severe episodes with an ICS trial and reassess: if there is no response, check inhaler technique, adherence and environment, and reconsider the diagnosis. Refer any preschool child with a hospital admission, or 2 or more emergency department admissions with wheeze in a 12-month period, to a specialist respiratory paediatrician. ^[1]

• Peak flow, spirometry and FeNO as above.
• Chest radiograph is not routine; use it if chronic symptoms, focal signs or failure to thrive, to exclude foreign body, malformation or chronic infection.
• Full blood count / eosinophils helps the allergy assessment in older children.
• Allergy testing (skin prick or specific IgE) identifies triggers for counselling and environmental advice.

There is no single test that proves asthma in this age group. The diagnosis rests on a pattern (recurrent wheeze, cough at night, interval symptoms, atopy, response to ICS) plus, usually, an ICS trial and reassessment. When the child reaches 5, do objective tests; if they cannot perform them, repeat every 6 to 12 months. ^[1]

Diagnosis is confirmed by objective testing as above. Never confirm asthma on history alone. ^{[1] [5]}

Severity is judged on the worst feature present. ^[2]

Life-threatening features are: SpO2 under 92% together with any of exhaustion, hypotension, cyanosis, silent chest, poor respiratory effort or confusion. A fall in heart rate in life-threatening asthma is pre-terminal. ^[2]

Recognition and speed matter more than any drug choice. Assessment of severity is described above. ^[2]

• Calm the child and family; give reassurance. ^[2]
• Oxygen: give high-flow oxygen to children with life-threatening asthma or SpO2 under 94%, aiming for normal saturations of 94% to 98%. ^[2]
• Inhaled SABA first-line: salbutamol via pMDI plus spacer is preferred for mild to moderate attacks. ^{[2] [3]}
• Steroids early: oral prednisolone for every acute attack. ^[2]
• Discontinue LABA while SABA is needed more often than 4-hourly. ^[2]

• Salbutamol via pMDI + spacer: 2 to 4 puffs (100 micrograms per puff) may be enough for a mild attack; up to 10 puffs for more severe attacks, given one puff at a time with 5 tidal breaths after each. If a child at home is not controlled by up to 10 puffs, urgent medical attention is needed. ^[2]
• Salbutamol nebulised: for severe or life-threatening asthma with SpO2 under 92%, 2.5 to 5 mg, driven by oxygen. Doses can be repeated every 20 to 30 minutes. ^[2]
• Ipratropium bromide: add 250 micrograms per dose mixed with the nebulised salbutamol if symptoms are refractory to the initial beta2-agonist; repeat every 20 to 30 minutes for the first few hours. ^[2]
• Oral prednisolone: 10 mg for children under 2 years, 20 mg for 2 to 5 years, 30 to 40 mg for over 5 years. Children already on maintenance steroid tablets receive 2 mg per kg up to 60 mg. A course of up to 3 days is usually enough; tapering is unnecessary unless treatment exceeds 14 days. ^[2]
• Intravenous steroids: hydrocortisone 4 mg per kg every 4 hours, for the severely affected child who cannot retain oral medication. ^[2]
• Magnesium sulphate: add 150 mg to each nebulised salbutamol and ipratropium in the first hour in children with a short-duration severe attack and SpO2 under 92%. Not recommended for mild to moderate attacks. ^[2]
• Antibiotics are not given routinely; most attacks are viral. ^{[2] [3]}
• Inhaled corticosteroids are not used instead of oral steroids in the acute attack, but the child's usual ICS is continued. ^[2]

High-flow oxygen: in severe or life-threatening asthma, deliver through a tight-fitting mask or nasal cannula at sufficient flow to achieve 94 to 98% saturation. ^[2]

Children with severe or life-threatening attacks, or any attack not improving after initial salbutamol, need hospital assessment. Paramedics transfer such children with nebulised salbutamol, driven by oxygen if symptoms are severe. ^[2] Admission is considered for any child with SpO2 under 92% in air after initial bronchodilator. ^[2] Chest radiography is reserved for suspected pneumothorax, lobar collapse/consolidation or life-threatening asthma not responding to treatment; blood gases for life-threatening features. ^[2]

The principle: every child with asthma should be on an ICS-containing regimen (no SABA without an ICS), and treatment is stepped up to the lowest level that controls symptoms, then reviewed. ^{[1] [5]}

Stepwise treatment by age:

Notes:

• ICS doses are paediatric low, moderate and high according to the guideline dose tables; always consult the local formulary. ^[1]
• In school-aged children, if asthma is not controlled on paediatric low-dose ICS plus SABA, MART (maintenance and reliever with ICS/formoterol) or an ICS/LABA maintenance combination plus SABA are the next steps. Review response in 8 to 12 weeks. ^[1]
• In children aged 5 to 11, only one budesonide/formoterol dry powder inhaler (100 micrograms/6 micrograms) is licensed for MART in children aged 6 to 11, so other use is off-label. ^[1]
• In children under 5, no MART regimen is used. If symptoms resolve on the ICS trial, stop after 8 to 12 weeks and review at 3 months; restart if they return or if there is an acute episode needing oral steroids or hospital. ^[1]
• Montelukast is MHRA-black-box cautioned for neuropsychiatric reactions; warn families. ^[1]

For a child under 5 with recurrent wheeze, the decision to start a controller is driven by symptoms and exacerbations. ^[3]

• Start a daily low-dose ICS controller when there is persistent or recurrent wheeze, interval symptoms, nocturnal awakenings, SABA use 3 or more times per week, or severe exacerbations. ^[3]
• GINA-style intermittent strategy: high-dose ICS for 7 to 10 days at the first sign of a respiratory infection can be used for episodic viral wheeze that is not persistent. ^[3]
• ICS is first choice over montelukast as a controller, but montelukast is reasonable if cooperation with inhalers is poor. Continue any controller for at least 3 months before deciding. ^[3]
• Oral corticosteroids are not routinely recommended in preschool wheeze; reserve them for severe exacerbations requiring emergency or hospital care. ^[3]
• Antibiotics, ipratropium nebulisation and LTRA are not recommended for acute preschool wheeze attacks. ^[3]
• SABA remains first-line for acute symptoms, delivered by pMDI with spacer (preferred over nebulisation in children under 2); nebulisation driven by oxygen is reserved for severe attacks. ^[3]

Evidence for intermittent high-dose ICS comes from regimens such as budesonide 1 mg twice daily for 7 days, or fluticasone 750 micrograms twice daily for up to 10 days. ^[3]

• A spacer should usually be prescribed with every metered-dose inhaler, especially for children. ^[1]
• Match device types (preventer and reliever) when possible; for children under 12, consider a spare SABA pMDI plus spacer for emergencies. ^[1]
• Observe inhaler technique at every review, at every asthma-related consultation, and after any deterioration. ^[1]
• Choose devices on correct technique, preference, lowest environmental impact and presence of a dose counter. ^[1]
• Check adherence using prescription records, not just asking. ^[1]

Every child with diagnosed asthma should have a written personalised asthma action plan covering recognition of deterioration, increased ICS, when to use oral steroids and when to seek help, plus education for the family. ^[1] Review the plan at every admission, acute consultation and annual review. ^[1]

• Severe and near-fatal attacks: can occur even in children with previously mild asthma. Any child on an ICS who has had a severe attack needs specialist review. ^[2]
• Airway remodelling: untreated inflammation over years reduces lung function. ^[1]
• Poor control effects: sleep loss, school absence, reduced exercise and play, poor growth from repeated oral steroids.
• Drug side effects: high-dose ICS suppresses growth if unchecked; montelukast is linked to neuropsychiatric reactions; SABA overuse is a danger signal. ^[1]

Many children (particularly viral-wheeze preschoolers) become symptom-free by mid-childhood. ^[3] Some young wheezers remain symptomatic into school age, and children with persistent wheeze plus atopy are most likely to have lifelong asthma. ^[3] Untreated inflammation in the early years is associated with reduced lung function that persists into adulthood. ^[3]

• Trigger avoidance: no smoking in the home or car; reduce damp, mould and house dust mite exposure; consider outdoor air quality. ^[1]
• Immunisation: routine childhood vaccines; annual influenza vaccine for asthmatic children is standard practice.
• Exacerbation prevention: maintenance ICS, adherence support, a written action plan, and treating allergic rhinitis. ^[1]
• Early diagnosis of atopy allows preventive measures.

• Pregnancy in the mother of an asthmatic child: focus is on the child; keep the child's regimen optimised. ^[1]
• Adolescents: transition to adult services, ask about smoking/vaping, school/social use of inhalers, and highlight jobs that provoke asthma. ^[1]
• Children with atopic disease: asthma, eczema and rhinitis cluster; treat the nose too. ^[1]
• Children with neuromuscular or airway abnormalities: may need physiotherapy for secretion clearance in acute attacks. ^[2]

Where objective tests, spacers or ICS are scarce, prioritise what saves lives:

• Diagnose on history and examination; a trial of ICS plus follow-up replaces tests. ^[1]
• Ensure at least one spacer or home-made valve-mask spacer for every child on an MDI.
• Keep a salbutamol pMDI in schools and primary care; teach families up to 10 puffs. ^[2]
• Give oral prednisolone for attacks as above; it is cheap and effective. ^[2]
• Reserve antibiotics for proven bacterial infection. ^{[2] [3]}
• Refer early any child with hospital admission or 2+ ED attendances with wheeze, poor growth or red-flag features. ^[1]
• Prevention relies on smoke avoidance, housing, and early recognition.

Control is reviewed at every contact, not only at annual review. Ask how many days in the week the child had symptoms, how often the reliever was used, whether there were night-time awakenings, time off school, oral steroid courses, and any emergency or hospital attendance. A validated questionnaire such as the Asthma Control Test or the Childhood Asthma Control Test can be used at any review. ^{[1] [5]}

Regular peak expiratory flow monitoring is not used to assess control in routine care, although peak flow (or symptom) plans may be individualised in an asthma action plan. ^[1] FeNO monitoring is considered for adults, not children, in current guidance. ^[1] If control is suboptimal, consider adherence, technique, comorbidity, environment and stepping up before changing medicines. ^[1]

• Short-acting beta2 agonist (salbutamol): rapid bronchodilator for symptom relief and acute attacks; dose by puffs via spacer. Overuse is a warning sign of poor control. ^{[1] [2]}
• Inhaled corticosteroids (beclometasone, budesonide, fluticasone and others): the basis of control; given at low, moderate or high paediatric dose depending on step. Local dose tables must be used. ^[1]
• ICS/formoterol combination (MART/AIR): provides both anti-inflammatory and long-acting bronchodilator effect with a flexible dose; in school-aged children this is off-label for some ages and devices, so local guidance applies. ^[1]
• ICS/LABA combination: twice-daily maintenance with SABA reliever, when MART is not appropriate. ^[1]
• Leukotriene receptor antagonist (montelukast): oral once-daily adjunct; useful when adherence to inhalers is difficult, but warn families about possible neuropsychiatric side effects and stop if ineffective. ^[1]
• Long-acting muscarinic antagonist: considered in adults and older adolescents as an add-on; not a standard step in young children. ^[1]
• Biological therapies: out of scope of this page; referred for specialist assessment in difficult asthma. ^[5]

Inhalers and spacers are as important as the drug: children under 4 usually need a pMDI with a spacer and face mask, actuated one puff at a time with five tidal breaths. ^[2]

• Preschool child with a hospital admission, or 2 or more emergency department admissions with wheeze, in 12 months. ^[1]
• Suspected asthma in a child under 5 that does not respond to a moderate-dose ICS trial plus an LTRA trial. ^[1]
• School-aged child uncontrolled on paediatric moderate-dose MART or ICS/LABA (with or without LTRA). ^[1]
• Diagnostic doubt after objective testing, including consideration of bronchial challenge. ^[1]
• Frequent or severe exacerbations, or any life-threatening attack. ^[2]
• Red-flag symptoms suggesting an alternative diagnosis (fixed monophonic wheeze, focal signs, poor growth, clubbing, stridor). ^[1]

• Prescribing a SABA without an ICS. Always pair a reliever with ICS control. ^[1]
• Assuming wheeze equals asthma in infants. Many wheezers do not have asthma; be willing to stop and reconsider. ^[3]
• Poor technique or no spacer. Show, observe and re-check at every visit. ^[1]
• Not stepping up (or down). Review response in 8 to 12 weeks and adjust to the lowest effective step. ^[1]
• Missing atopy and triggers. Treat allergic rhinitis and avoid tobacco smoke and mould. ^[1]
• No action plan. Every diagnosed child needs a written, understood plan. ^[1]

A 6-year-old has nocturnal cough three nights a week and breathlessness on running, with improvement after a bronchodilator. Examination is normal. FeNO is 38 ppb and spirometry shows a 14% rise in FEV1 after salbutamol. He has eczema and a parent with asthma. The diagnosis is asthma. First treatment is twice-daily paediatric low-dose ICS with a SABA via a spacer, a review in 8 to 12 weeks, a written action plan and trigger advice. ^[1]

• Infants: wheezing is rarely asthma; bronchiolitis dominates. Recurrent wheeze in the first year is often viral and may resolve. ^[3]
• Preschool (1 to 5 years): episodic wheeze with viral colds; many are well between episodes. Wheeze with exercise or laughing, night cough and atopy suggest a more persistent pattern. ^[3]
• School age (5 to 12 years): classic asthma emerges, often alongside eczema and allergic rhinitis; symptoms are variable and respond to ICS. ^{[1] [4]}
• Adolescence: symptom patterns can change; non-adherence and under-treatment are common; transition to adult services needs planning. ^[1]

Recognition that the same term "wheeze" covers different diseases at different ages is the reason the guidelines treat under-5s separately. ^{[1] [3]}

Asthma in adolescents; bronchiolitis and viral wheeze in infants; cystic fibrosis; gastro-oesophageal reflux in children; oxygen therapy and pulse oximetry; inhaled corticosteroids; leukotriene receptor antagonists; inhaler devices and spacers; allergic rhinitis; smoking and asthma.