Section 1: Epidemiology and aetiology
Asthma is a disease of the conducting airways, which in response to a wide range of exogenous and endogenous stimuli contract too much and too easily.
Interactions between multiple factors, including early allergen exposure, infections, diet, genetic predispositions, tobacco smoke exposure and pollution, result in airway inflammation, which limits airflow and leads to functional and structural changes in the airways in the form of bronchospasm, mucus hypersecretion, mucus plugs, mucosal oedema and smooth muscle contraction.1
Asthma is the most common chronic childhood disease in most industrialised countries. On average there are two asthmatic children in each UK classroom.1 The International Study of Asthma and Allergy in Childhood (ISAAC) found that the UK had among the highest prevalence, with 15% of children affected.
Sequential asthma studies have detected an increase in asthma over the past 25 years, although phase III of ISAAC has shown a fall in the prevalence.2 Higher prevalence exists with family history of atopy. The clear genetic component is inherited more strongly from the mother than the father. A child's risk of asthma is approximately double with one asthmatic parent.1
A child is admitted to a UK hospital with asthma symptoms every 17 minutes.1 An Australian study showed a 5% risk of death over 10 years post-intubation for asthma.3 Asthma UK, the Royal College of Physicians, and other bodies commenced the National Review of Asthma Deaths in February 2012 to gain an understanding of asthma deaths and assist prevention.1
Save this article and add notes with your free online CPD organiser at gponline.com/cpd
Take clinical tests and claim certificates for CPD at myCME.com/gp
Airway inflammation in asthma is a multicellular process involving eosinophils, neutrophils, T helper 2 (Th2)-type CD4 lymphocytes and mast cells. This results in recruitment and activation of inflammatory cells in the respiratory mucosa following upregulation of endothelial adhesion molecules.
Asthma is classically driven by enhanced activity of Th2 cells, which induce IgE production, and promote eosinophilic airway inflammation and airway hyperresponsiveness.4 The relative contribution of these varies between children and between asthma episodes in the same child.
X-ray of a seven-year-old with asthma, showing hyperinflated lung fields (Photograph: Author image)
Asthma is a complicated disorder and evidence suggests that different patterns of illness have different underlying pathogenesis.
Viral associated wheeze: 30-50% of preschool children have at least one episode. Some children with atopic asthma start with a pattern of episodic viral wheeze; however, most of those with pure episodic viral wheeze outgrow their symptoms.4
Cough variant asthma: up to 5-10% of preand early school-aged children have had chronic cough without wheeze.4 Cough variant asthma associated with bronchial hyperresponsiveness or reversible airways obstruction does exist, but is rare. Isolated chronic cough without typical features of asthma suggests another diagnosis.4
Atopic asthma commonly presents as the school-aged child who complains of episodic wheeze, cough and shortness of breath, often with identifiable triggers and other signs of atopy. Up to 85% of school-aged children with asthma are atopic, classically associated with airway eosinophilia and mast cells.4,5
Section 2: Making the diagnosis
The first aim of the history and examination should be to try to establish whether the symptoms are consistent with asthma.5,6 The individual case history should focus on the frequency and severity of symptoms, including wheeze, nocturnal cough, exercise-induced symptoms and persistence of cough with colds, atopy and exposure to environmental factors, including allergens and tobacco smoke.
Symptom patterns in the past six months should be discussed, with a focus on details of the past four weeks.
The presence of wheeze consistently points to a diagnosis of asthma.5 Beware, however, parental reports of wheeze as interpretation of this clinical sign can vary from a change in respiratory rate to cough.5,6
In most children, diagnosis of asthma can be made by history and examination. A simple assessment of the extent of symptoms and variability of lung function using home peak expiratory flow rate (PEFR) recordings and symptom diaries over a month or so can be helpful.5,6
If the child does not respond to initial treatment or needs high doses of inhaled corticosteroids, some specific specialised tests may help to confirm the diagnosis and assess severity more objectively.
When the diagnosis is in doubt or where severe asthma persists despite treatments, referral to a specialist paediatric respiratory clinic is needed. A few patients need specialised lung function tests, bronchoscopy, pH study or CT scanning to rule out other conditions.
|When to consider alternative diagnoses6|
In the absence of
Section 3: Managing the condition
Management of asthma should include asthma education for patients and caregivers, avoidance of airborne allergens and irritant triggers, appropriate pharmacotherapy and acute asthma management plans.6
Therapy is based on treatment combinations to relax smooth muscle and to reduce airway inflammation.
The British Thoracic Society/Scottish Intercollegiate Guidelines Network (BTS/SIGN) guidelines have clearly defined age-appropriate pharmacological management of atopic asthma following a stepwise approach according to persistence, severity and frequency of symptoms, until control is achieved. Regular monitoring allows therapy to be stepped up or down to ensure the lowest level of treatment is used to control symptoms.6
Airway inflammation is a key component of asthma and inhaled glucocorticoids are the most effective anti-inflammatory treatments available. Considerable benefit for all major clinical outcome measures is seen with low and moderate doses (beclometasone to 400 microgram/day or fluticasone to 200 microgram/day). Beyond this, the dose-response curve is relatively flat.5,6
Although side-effects are unlikely at 400 microgram/day beclometasone or equivalent, they can occur at higher doses.
Practically, if a child seems to need higher doses of inhaled corticosteroid than those recommended by the manufacturer, questions that need to be considered are:5,6
- Correct diagnosis?
- Severity correctly reflected?
- Avoidable triggers present?
- Compliant and good technique?
- Using steroid-sparing treatment?
Long-acting beta-2 agonists in asthma
For fiveto 12-year-old children, BTS/SIGN guidance advocates a trial of long-acting beta-2 agonists before increasing inhaled corticosteroids at a dose greater than 400 microgram/day.
These should be stopped if no benefit is achieved.6
Leukotriene receptor antagonists
Leukotriene receptor antagonists may provide improvement in lung function, a decrease in exacerbations and an improvement in symptoms.6
Anti-IgE monoclonal antibody (omalizumab)
NICE recommends omalizumab for patients over 12 years of age, within its licensed indication, as an option for the treatment of severe and unstable persistent allergic asthma.7
It should be commenced by physicians experienced in both allergy and respiratory medicine in a specialist centre. History and skin testing should confirm the IgE-mediated allergic nature of the condition.5,6
Smoking and asthma
Tobacco smoke is one of the strongest environmental risk factors for developing recurrent cough/wheezing or asthma. Maternal smoking during pregnancy results in impaired lung growth in the developing fetus.
Management of difficult to treat asthma in children
Therapy-resistant asthma with frequent use of short-acting beta-2 agonists and high steroid doses needs comprehensive assessment and meticulous exclusion of other causes of asthma-like symptoms. Lack of compliance and unrecognised adverse environmental influences should always be considered. The most common cause of poor response is non-compliance.
|When to refer to a respiratory paediatrician|
Section 4: Prognosis and follow up
|Example checklist for follow up in primary care|
|Areas for discussion||√||Details|
|Symptom score – for example, Childhood Asthma Control Test|
|Adherence to medicine|
|Review prescription refill frequency|
|Check inhaler technique|
|Possession of individualised management plan|
|Use of management plan|
|Update/creation of management plan|
|Ensure adequate understanding of child and carer|
|Growth and height check and plotting|
|Smoking review and cessation advice|
| Assessment of triggers
| Other atopy
|Change to management plan|
|Agreed review date|
Section 5: Case study
A 12-year-old with height and weight on the 25th centile, appropriate for mid-parental height, presented to clinic with increased asthma symptoms over recent months. His asthma control test score was nine out of 25. His PEFR was reduced and his recent lung function tests were suboptimal.
His activity levels were limited most of the time by his asthma and he was missing one day of school on average every two weeks, with symptoms occurring more than once per day. He was being woken from sleep feeling short of breath two to three times per week and required salbutamol one to two times per day.
He was using beclometasone regularly with good inhaler technique at a dose of 800 microgram/day. A previous montelukast trial had failed to give symptomatic improvement.
Initial diagnosis was at five years of age. He also has eczema and allergic rhinitis, and experiences worsening of his asthma-related symptoms on exposure to dust and cold. He and his family are non-smokers.
In the past month, he had attended A&E once after following his acute management plan at home appropriately. He required nebulised treatment and an oral course of steroids but was not admitted to the ward.
The management plan
As per the BTS/SIGN guidance, long-acting beta-2 agonists were added. This was done in combination with an inhaled steroid. A review date was set for one month's time.
On review, things were much improved, he no longer had limitation of activity, his attendance at school had improved and he was no longer waking at night. He had used his salbutamol inhaler twice since collecting the combination inhaler.
Chest CT scan of an eight-year-old severely asthmatic patient with evidence of small airways disease (Photograph: Author Image)
Section 6: Evidence base
- BTS/SIGN. British guideline on the management of asthma 2008: a national clinical guideline; updated January 2012.
- Asthma UK. www.asthma.org.uk
Information resource for parents and children, including chat rooms and information on educational holidays.
- British Thoracic Society. www.brit-thoracic.org.uk
Provides a link to the updated guidelines on the management of asthma and the evidence behind the guidelines.
- Children's Asthma Control test. www.asthma.com/resources/asthma-control-test.html
This website provides a five-question quiz to determine if a treatment plan is working.
This topic falls under section 15.8 of the RCGP curriculum, Respiratory Problems.
|CPD IMPACT: EARN MORE CREDITS|
These further action points may allow you to earn more credits by increasing the time spent and the impact achieved.
1. Asthma UK. 2012. www.asthma.org.uk. Accessed 14 May 2012.
2. International Study of Asthma and Allergies in Childhood. Lancet 1998; 351: 1225-32.
3. Triasih R, Duke T, Robertson CF. Arch Dis Child 2011; 96(8): 729-34.
4. Silverman M (editor). Childhood asthma and other wheezing disorders.
Second edition. London, Hodder Arnold, 2002.
5. Townshend J, Hails S, Mckean M. BMJ 2007; 335: 198-202.
6. British Thoracic Society, Scottish Intercollegiate Guidelines Network. British guideline on the management of asthma 2008: a national clinical guideline; updated January 2012. 7. NICE. Omalizumab for severe persistent allergic asthma. TA133. London, NICE,2007. www.nice.org.uk/nicemedia/pdf/TA133Guidance.pdf