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AD_HTT_031_038___AUG04_06 29/4/07 9:35 AM Page 31 How to treat w w w. a u s t r a l i a n d o c t o r. c o m . a u Pull-out section Earn CPD points on page 38 Complete How to Treat quizzes online (www.australiandoctor.com.au/cpd) or in every issue. inside Causes of wheeze Diagnosis and management of asthma Managing acute exacerbations Interval management of childhood asthma Asthma prevention The authors Background WHEEZE is an extremely common symptom in children, with up to 40% of children reported as having at least one episode of wheeze during childhood. Wheezing is most common in infancy and decreases in incidence as children age. Wheeze may have many causes (see table 1, page 33). The most common is asthma, so it is important to distinguish asthma from other conditions that may also cause wheeze. This article discusses risk factors for developing asthma, particularly progression from infant wheeze to childhood asthma, and the patterns of asthma in children and their management. What is wheeze and how is it generated? Wheeze can be a difficult symptom to ascertain. Many parents erroneously use the term to describe a cont’d page 33 DR JOHN MASSIE, consultant respiratory physician, department of respiratory medicine, Royal Children’s Hospital, Parkville, Victoria. WHEEZE DR JO HARRISON, clinical research fellow, department of respiratory medicine, Royal Children’s Hospital, Parkville, Victoria. in childhood BEFORE PRESCRIBING, PLEASE REVIEW PRODUCT INFORMATION AND PBS INFORMATION IN THE PRIMARY ADVERTISEMENT IN THIS PUBLICATION. APPROVED PRODUCT INFORMATION CAN BE FOUND VIA THE ADVERTISERS’ INDEX OR IS AVAILABLE ON REQUEST FROM MERCK SHARP & DOHME. Merck Sharp & Dohme (Australia) Pty Limited, Sydney TMTrademark of Merck & Co., Inc., Whitehouse Station, N.J., U.S.A. MER0771AD/CJB 06-07-FSP-06-AUS-443-J www.australiandoctor.com.au 4 August 2006 | Australian Doctor | 31 AD_HTT_031_038___AUG04_06 29/4/07 9:36 AM Page 33 from page 31 variety of noises originating from the airways, including stridor, snoring or rattling of upper airway secretions. When taking a history from families whose first language is not English it is important to remember that some languages do not include a word with exact equivalence to wheeze. Considering the significance of wheeze in research and epidemiological classification, there is little information about its acoustic characteristics. Wheezes are continuous adventitious lung sounds with a ‘musical’ quality, mainly heard during expiration. The American Thoracic Society committee on pulmonary nomenclature defines wheezes as high-pitched continuous sounds with a domi- Table 1: Causes of wheeze Small airways disease Large airways disease Asthma Congenital structural airway disease (eg, tracheomalacia, bronchomalacia, congenital tracheal stenosis, vascular ring) Transient infant wheeze Mediastinal mass (eg, lymphoma) Acute viral bronchiolitis Foreign-body aspiration Suppurative lung disease (eg, cystic fibrosis) Gastro-oesophageal reflux Congenital heart disease Chronic neonatal lung disease nant frequency >400Hz. The pathophysiological mechanisms that generate wheeze are still not entirely clear. Its predominance as an expiratory noise indicates an intrathoracic origin (as opposed to stridor, which is predominantly inspiratory in nature and originates from the extrathoracic airway). A recently proposed model of wheeze production based on mathematical analysis of the stability of airflow through a collapsible tube indicates that wheezes are produced by the fluttering of the larger airways walls, induced by increased airflow velocity. This increased velocity may occur because of localised obstruction or dynamic compression of the trachea during expiration (caused by widespread obstruction of smaller airways). Such small airway obstruction causes expiration to become an active process and pleural pressure to become positive. Normally there is a progressive fall in pressure along the airway from alveoli to the mouth. When the pleural pressure becomes positive, the pressure outside the airway (ie, pleural pressure) at some point becomes greater than that within and the airway collapses. The linear velocity of airflow in small airways is too low to cause audible sound, even when these are significantly narrowed. Therefore the sound that is heard as wheeze originates in the large airways, even when the pathology is in the smaller airways. This point is clinically relevant, as there is a temptation to ascribe wheeze to small airway obstruction (classically asthma) and to forget the possibility of large airway obstruction. Causes of wheeze Small airway diseases children with bronchiolitis from those with asthma. However, care must be exercised with use of short-acting beta2-agonists in children with bronchiolitis, as they can worsen hypoxia by exacerbating ventilation-perfusion (V/Q) mismatching. Generally they should be avoided if the diagnosis is certain. Transient infant wheeze TRANSIENT infant wheeze mostly affects young children with smaller-calibre airways that develop either because of familial factors or maternal smoking during pregnancy. This group of children includes those previously referred to as ‘fat happy wheezers’. Risk factors for asthma, such as atopy and family history, are usually absent in these children. Typically, episodes of wheeze occur spontaneously and often increase with viral respiratory tract infections. Most children outgrow this condition by school age (six years) as the airways grow in size. Children with transient infant wheeze do not usually respond to bronchodilators, and preventive inhaled corticosteroids have been shown to have no benefit. Distinguishing between transient wheeze and asthma can be very difficult in a young child who presents with their first episode of wheeze. In some cases a therapeutic trial of inhaled bronchodilators (delivered by metered-dose inhaler [MDI] and spacer) can be helpful in making this distinction because a negative response makes asthma unlikely. However, it is important to remember that parental reporting of a bronchodilator response can be unreliable. Orally administered bronchodilators are ineffective and have no role in treatment. Generally the older the child at the time of their first episode of wheezing the greater the chance that asthma is the cause, but longitudinal studies have shown that most children with asthma develop their initial symptoms in the first year of life. Given that most young children with wheeze do not have asthma, how can we distinguish between asthma and transient wheeze in the young child presenting with wheeze? Population-based longitudi- Orally administered bronchodilators are ineffective and have no role in treatment [of children with transient infant wheeze]. nal studies in children have allowed the development of clinical indices to define asthma risk in young children. The chance of the subsequent development of asthma in a wheezing child is increased by up to 5.5 times if there is: ■ A personal history of eczema or ■ A history of parental asthma or ■ Two of three risk factors — personal history of allergic rhinitis, wheezing that is not associated with colds and eosinophilia. If wheezing episodes are frequent (ie, more than four episodes a year) asthma is up to 9.8 times more likely to be the cause. Importantly, 95% of children who do not have these risk factors do not develop subsequent asthma. Measuring eosinophil levels requires a blood test and is therefore not usually a useful predictor in the setting of a GP’s surgery. Acute viral bronchiolitis Acute viral bronchiolitis is a common cause of wheeze in infants. It occurs most often in children under 12 months of age but can occur in those aged up to 24 months. The greatest overlap between this condition and asthma occurs between 12 and 24 months. Acute viral bronchiolitis is caused by respiratory syncytial virus in about 70% of cases, but other causes include parainfluenza, influenza and adenovirus. Seasonal epidemics occur with the highest incidence between late autumn and early spring. The infant usually presents with fever, coryza and cough and, in some cases, increasing respiratory difficulty. Auscultation shows widespread crackles and/or wheeze. The diagnosis is usually clinical, but the causative virus can be demonstrated by immunofluorescence of a nasopharyngeal aspirate. Proof of viral infection is usually reserved for hospitalised infants, epidemiological purposes and only occasionally for diagnosis. Only 1% of infants with respiratory syncytial virus infection need hospitalisation. It is important to distinguish bronchiolitis from asthma because the only effective therapy for bronchiolitis is supportive: provision of rest, supplemental oxygen (if arterial oxygen saturation [SaO2] is less than 92%) and adequate fluid intake. A trial of bronchodilators is rarely worthwhile in children under 12 months of age. However, it may be worth considering for the infant who is close to 12 months, has had recurrent episodes of wheezing and has strong risk factors for asthma (such as eczema and close family history of asthma). Between 12 and 24 months it may only be a response to bronchodilators that separates www.australiandoctor.com.au Suppurative lung disease Most suppurative lung disease in children begins in the small airways. It can present as recurrent or persistent wheeze and is often associated with a moist cough (which may be most pronounced in the morning, when secretions accumulated overnight need clearing) or increased wheeze and a moist cough during viral RTIs that only improve with antibiotics. In many cases children with suppurative lung disease have been treated for asthma with bronchodilators and inhaled corticosteroids despite no apparent benefit, because their symptoms include wheeze and they were wrongly diagnosed with asthma. This can result in the diagnosis being delayed for several years. The presence of digital clubbing or crackles on physical examination (outside of an acute exacerbation of wheeze) can help distinguish suppurative lung disease from asthma. Referral to a paediatric respiratory specialist is indicated to confirm the diagnosis and supervise treatment. In some cases, causes such as cystic fibrosis (remembering that newborn screening misses 5-10% of cases and not everyone with cystic fibrosis has pancreatic insufficiency), immunodeficiency and primary ciliary dyskinesia (formerly called immotile cilia syndrome) may be identified. Most children are not found to have bronchiectasis when investigated with CT. In many cases the cause is unknown and the children are given the diagnosis of chronic suppurative bronchitis. Response to treatment with antibiotics and chest physiotherapy is usually good, although some children need long-term treatment. We suspect that, if left untreated, this condition would lead to bronchiectasis. Gastro-oesophageal reflux and primary pulmonary aspiration Gastro-oesophageal reflux (GOR) may cause wheeze by several mechanisms, including: ■ Direct aspiration into the airways and lungs, causing inflammation. ■ Induction of bronchospasm by irritation of upper airways. ■ Induction of vagally-mediated reflex bronchospasm by oesophageal irritation. Typically, wheeze occurs at night (when lying down to sleep) and may be accompanied by vomiting in younger children and heartburn in older children. In some cases, wheezing is the only symptom. Children with developmental delay (eg, Down syndrome, cerebral palsy) are at significantly higher risk of aspiration, either directly during feeds (primary pulmonary aspiration) or via GOR. Wheeze in such patients should prompt a consideration of GOR and/or aspiration as the cause. However, it is notoriously difficult to confidently link wheeze to GOR or direct aspiration and referral to a paediatric respiratory specialist is usually needed. Congenital heart disease Congenital heart disease can also cause wheeze when pulmonary oedema is present (socalled ‘cardiac asthma’). Distinguishing between cardiac failure and respiratory disease is likely to be most difficult in infants whose major symptoms from cardiac failure are tachypnoea and poor feeding. Generally, physical examination should reveal additional features of heart disease such as tachycardia, a heart cont’d next page 4 August 2006 | Australian Doctor | 33 AD_HTT_031_038___AUG04_06 29/4/07 9:36 AM Page 34 How to treat – wheeze in childhood asthma management, which is probably best shared with a paediatric respiratory specialist. from previous page murmur and hepatomegaly. notoriously difficult. Prominent veins in the distribution of the superior vena cava can be one additional clinical sign. Spirometry may show ‘flattening’ of the flowvolume loops, and a chest X-ray usually confirms a mediastinal mass compressing the large airways. Chronic neonatal lung disease Chronic neonatal lung disease refers to a condition in infants born prematurely (typically <30 weeks’ gestational age) who continue to require supplemental oxygen at 36 weeks. It affects about 30% of babies born weighing less than 1000g. These children have abnormal airway and pulmonary parenchymal architecture that predisposes them to wheeze. Wheezing may be spontaneous and reflect the altered small airways, or occur mostly with viral RTIs and acute viral bronchiolitis, which can be more severe in this group. Although most infants with chronic neonatal lung disease improve with time, many will be shown (when they are old enough to perform adequate spirometry) to have altered pulmonary function tests that generally show an obstructive pattern. They may show improvement with bronchodilator even though they lack significant risk factors for asthma, and often benefit from ‘standard’ Large airway diseases Structural airway diseases This group of diseases includes tracheomalacia, bronchomalacia (sometimes concurrent), congenital tracheal stenosis and vascular rings (when various arrangements of the great vessels press on, or surround, the airway). Symptoms such as increased work of breathing, poor feeding and wheeze usually occur from birth or within a few weeks of birth. Depending on the level of large airway obstruction, there may be associated inspiratory stridor, suggesting an extrathoracic component to the compressing lesion. Diagnosing and managing these conditions is difficult, and referral to a paediatric respiratory physician is warranted. Mediastinal mass A mediastinal mass compressing the large airways can present with wheeze and shortness of breath, masquerading as asthma. Rarely the Foreign-body aspiration mass is a congenital lesion, such as a bronchogenic cyst, but more often it is a malignancy, such as a lymphoma or leukaemia. Reduced exercise capacity over a few days to weeks suggests the latter, but when growth of the lesion is rapid, symptoms may present more acutely. Stridor suggests extrathoracic airway compression and requires urgent intervention, as the airway can be critically narrowed. Making the diagnosis early is Wheeze due to foreign-body aspiration is typically acute in onset and unilateral in distribution. There may be a clear history of sudden onset of choking while eating or playing with small toys in some cases, but in up to 50% of foreign-body inhalations in small children no such history is elucidated and the event goes unwitnessed. Typically, children who inhale foreign bodies are in the toddler age range, but inhalation can also occur in older children. Boys are more commonly involved than girls, and the most frequently inhaled objects are peanuts, closely followed by small plastic toys. In the cooler months many children have coexistent viral URTIs and it can be tempting to attribute wheezing to causes such as a viral infection or an acute exacerbation of asthma. The history of sudden onset, the unilateral nature of the wheeze or reduced air entry, and the lack of risk factors for asthma should prompt a rethink of these diagnoses. When foreign-body aspiration is suspected, a chest X-ray, taken on inspiration and expiration, is required to help confirm the diagnosis. The X-ray should include the upper airway. Most foreign bodies are not radio-opaque, but the expiratory film may demonstrate air trapping on the affected side, due to a ballvalve effect of the foreign body. However, the X-ray may be inconclusive, partly due to the difficulty of capturing images in the correct phase of respiration in an infant. If the history is suggestive of foreign-body aspiration and the child has ongoing symptoms (classically cough) or signs (eg, wheeze) or a suggestive X-ray, urgent referral is needed for rigid bronchoscopy (see Authors’ case study, A two-yearold with a foreign body, page 36). Diagnosis and management of asthma Clinical features PERSISTENT wheeze is much more likely to be due to asthma if it continues to school age and if there are other risk factors such as atopy in the child or immediate family. A thorough history is crucial for diagnosing asthma in children. Investigations (discussed below) are often not possible in young children and may be normal in older children with asthma. Classically, children with asthma develop a combination of wheeze, shortness of breath, chest tightness and cough after exposure to known triggers. The reported or observed response to bronchodilators is a helpful part of the history. In children, viral infections are the most common triggers, precipitating attacks in up to 90% of cases. Most children with asthma also have symptoms during or after exercise — especially on colder days when the air is drier. As children get older, allergies play an increasing role in triggering symptoms. A history of eczema and other allergic manifestations in the child and immediate family provide supportive evidence for the diagnosis of asthma. Type of asthma Pattern Infrequent episodic asthma (75% of children) Episodes more than six weeks apart Symptoms rare between attacks Attacks are not usually severe Normal examination and lung function between attacks Frequent Episodes less than six weeks apart episodic asthma Increasing frequency of symptoms (20% of children) between attacks Attacks are more problematic Normal examination and lung function between attacks Persistent asthma Episodes less than six weeks apart (5% of children) Daytime symptoms on more than two days a week Nocturnal symptoms on more than one night a week May have abnormal lung function between episodes Multiple emergency department visits or hospital admissions Allergy tests *From the Asthma Management Handbook 2002 (see Online resources, page 36) Establishing the pattern of asthma in children The pattern of asthma in children distinguishes it from asthma in adults and forms the basis for treatment and prognosis. The history enables the clinician to establish the pattern of asthma (table 2). Specific questions to ask 34 The most commonly used challenge is exercise (with a standardised protocol) although challenges with hypertonic saline and, more recently, dry powder mannitol are gaining favour. Histamine and methacholine challenges are rarely used in clinical situations. Table 2: Patterns of asthma in children* | Australian Doctor | 4 August 2006 should include frequency of: ■ Exacerbations. ■ Sleep disturbance due to asthma. ■ Early morning symptoms. ■ Symptoms in relation to exercise or activity. ■ Bronchodilator use. Investigations for diagnosing asthma in children Tests of pulmonary function In school-aged children (≥6 years) lung function testing may be helpful in confirming the diagnosis of asthma. Useful tests include spirometry, particularly FEV1 and the ratio of FEV1 to FVC, both of which are reduced in asthma. A significant increase in FEV1 (eg, ≥12%) after administration of a bronchodilator provides further evidence of reversible airway obstruction. Care needs to be taken in performing and interpreting spirometry in children, as they often find it difficult to understand the appropriate commands. However, it is worth persisting and letting the child get used to the technique so that reliable results can eventually be generated. It is also important to remember that spirometry may be normal if the measurement is made between episodes of bronchospasm. Thus, normal results do not exclude a diagnosis of asthma. However, if results are repeatedly normal when tested during symptoms, the diagnosis of asthma must be placed in doubt. Tests of bronchial hyperresponsiveness may be helpful in some cases when the diagnosis of asthma is in doubt. These should be performed at a laboratory experienced in testing children, and the opinion of a paediatric respiratory specialist may be warranted. www.australiandoctor.com.au Allergy tests may be helpful when seeking causal factors, and in making a general diagnosis of atopy, but the presence of allergy is not essential to the diagnosis of asthma. Allergy tests should look for sensitisation to aeroallergens such as house-dust mite, dog and cat dander and grasses. Food allergies, while helpful in defining an atopic child, are generally not causally associated with asthma. Tests include skin prick testing and the radioallergosorbent test (RAST). Chest X-ray Chest X-rays are not useful in making a diagnosis of asthma, although they may play a role in excluding other diagnoses, such as foreign-body inhalation or suppurative lung disease. They should be reserved for children who have signs or symptoms that arouse suspicion of alternative diagnoses, or for children whose symptoms do not respond to routine asthma treatment. Treating asthma in children The management of asthma in children differs from that in adults and this difference is reflected in the varying patterns of childhood asthma, suggesting that we are not dealing with an homogeneous disease process. Childhood asthma is dominated by the presence of virus-induced exacerbations, even in children with persistent (‘adult style’) disease. Furthermore, the activity levels of children are different to those in adults and may sometimes influence therapy. The goals of asthma management should be to allow children to be symptom free and able to lead as normal a life as possible, while using the lowest dose of medication possible to minimise the risk of side effects. Managing asthma includes treating exacerbations and interval symptoms. Response to treatment A therapeutic trial of appropriately delivered therapy can be helpful in confirming the diagnosis of asthma in children. To determine whether the symptoms are caused by bronchospasm, a trial of inhaled short-acting beta2 agonists is warranted, looking for a rapid response (1-3 minutes after dose) that lasts 3-4 hours. It may still be difficult to be certain about the diagnosis in some cases and a supervised trial of inhaled corticosteroids over 4-6 weeks is appropriate. During the trial it is best not to use a label of asthma, reserving this until the diagnosis is confirmed. Failure to respond to conventional treatment should prompt consideration of alternative diagnoses. It is also important to remember that apparent improvement after the introduction of inhaled corticosteroids may be coincidental. AD_HTT_031_038___AUG04_06 29/4/07 9:36 AM Page 35 Managing acute exacerbations THE standard management of acute exacerbations in children is a combination of prn short-acting inhaled beta2 agonist (bronchodilator) and oral prednisolone (Panafcortelone, Predmix, Predsolone, Redipred, Solone) (see table 3). Inhaled medication is best delivered by puffer and spacer unless the child is too ill to sit up and co-operate, in which case continuous nebulised salbutamol (Airomir, Asmol, Butamol, Epaq, Ventolin) should be used. Ipratroprium (Aeron, Atrovent, Ipratropium, Ipra- Table 3: Managing acute exacerbations of asthma in children Bronchodilator (as needed) Salbutamol (by MDI) (100µg/puff) ■ Age < six years: six puffs via small-volume spacer ■ Age ≥ six years: 12 puffs via large-volume spacer Terbutaline turbuhaler (500µg/puff) (age > eight years) ■ Age > eight years: six puffs Prednisolone ■ 1mg/kg (maximum 50mg) daily for three days trin, Ipravent) has very little role outside the setting of a severe exacerbation and in these cases may be used in conjunction with salbutamol as a repeated treatment every 20 minutes (up to three doses). Oral prednisolone has been part of the acute exacerbation paradigm for some time. Treatment duration of three days does not require weaning and has been chosen because that is the usual duration of acute symptoms. If a child continues to have significant symptoms, prednisolone can be used for a longer period of time. Side effects from short courses of prednisolone such as these are negligible: use fewer than four times a year has been shown to be safe. Parents should be taught to recognise the symptoms of an exacerbation and empowered to initiate treatment with prednisolone. There is no value in doubling the dose of inhaled corticosteroids (if the child is using them) or of introducing them acutely, as the onset of action takes weeks. Prednisolone may not be effective in younger children (<5 years) who wheeze with viral RTIs even when there has been an apparent bronchodilator response. This is probably because ‘asthma’, as we think of it, is a symptom complex, not a diagnosis. These children are simply ‘wheezing with colds’ although the phenotype is similar to ‘true asthma’. Separating the two is difficult and may rely on the presence of risk factors (atopy, family history) or simply be a matter of time for the ‘wheezers with colds’ to grow out of it. There is some emerging evidence that montelukast (Singulair), which has a relatively rapid onset of action, may shorten the duration of symptoms in this group. However, it is still too early to alter the current paradigm. Interval management of childhood asthma Infrequent episodic asthma CHILDREN with infrequent episodic asthma can be managed with reliever medication such as salbutamol 100-200µg and terbutaline (Bricanyl) on a prn basis only. Frequent episodic asthma It is worth considering a trial of daily preventer therapy for children with frequent episodic asthma in an attempt to reduce the frequency and severity of exacerbations. However, such therapy is often unsuccessful and the only approach remains to optimise management of acute events. Preventive therapy should be tried (as per the schedule for mild persistent asthma) using either low-dose inhaled corticosteroids or montelukast. Mild persistent asthma There are two choices for preventive treatment for mild persistent asthma — low-dose inhaled corticosteroid or a leukotriene-receptor antagonist such as montelukast. Despite the inclusion of sodium cromoglycate (Cromese, Intal) and nedocromil sodium (Tilade) in several national guidelines on asthma management, they have not been proven to be effective and we cannot recommended them. Inhaled corticosteroids are the preventer of choice for most children. Four drugs are available: ■ Fluticasone (Flixotide). ■ Beclomethasone (Qvar). ■ Budesonide (Pulmicort). ■ Ciclesonide (Alvesco). Although any of the above may be started, decisions about drug delivery devices (eg, MDI and spacer vs dry powder inhaler) and adherence (device, once daily vs twice daily) may be factors that determine choice of medication. It is important to remember that fluticasone, ciclesonide and beclamethasone are twice as potent as budesonide, ie,100µg fluticasone is equivalent to 200µg of budesonide. A standard starting dosage would be, for example, fluticasone 100-200µg/day. At these dosages, 80-90% of treatment effect occurs and serious side effects are rare. It is important to explain to parents that it may take up to six weeks before the maximal benefits of treatment are apparent. Table 4: Interval management of asthma in children Pattern of childhood asthma Treatment Infrequent episodic asthma As-required bronchodilators only Frequent episodic asthma Patient may benefit from preventive therapy, eg, low-dose inhaled corticosteroids or leukotriene-receptor antagonist Persistent asthma Mild Low-dose inhaled corticosteroids (fluticasone 100-200µg/day or equivalent) or a leukotriene-receptor antagonist Moderate Inhaled corticosteroids (fluticasone 200-500µg/day or equivalent) ± a LABA Severe Inhaled corticosteroids (fluticasone up to 500µg/day or equivalent) + a LABA Table 5: Route of drug delivery General tips for children with persistent asthma Age Route of administration <2 years 2-6 years 6-8 years 8 years and older MDI + large-volume spacer Yes Yes Turbuhaler Some children Yes Accuhaler Some children Yes MDI, small-volume Yes spacer + mask May drop the mask at 4 years old MDI (alone) Only for bronchodilator Autohaler Yes Oral Yes Preventive therapy should be started with inhaled corticosteroids alone. Not only is this a PBS requirement but it makes sense to gauge the effect of a single therapy before the addition of a second (eg, a longacting beta2 agonist [LABA]). Budesonide and ciclesonide can be used once daily, which may be advantageous for some patients. Montelukast is a legitimate starting medication for children with mild persistent asthma. It has PBS listing for children aged 2-14 years (authority required) for this indication, which makes the price to consumers equivalent to that of inhaled corticosteroids. The onset of action is rapid (within a few days), as it has both a bronchodilator and an anti-inflammatory action. In children with mild persistent asthma, the choice between an inhaled corticosteroid and a leukotriene-receptor antagonist is Yes Yes usually one based on the choice of drug delivery system, with the patient’s (and parents’!) choice likely to positively benefit adherence. Moderate or severe persistent asthma The starting point for children judged to have moderate or severe persistent asthma, and who have not been treated for some reason, is inhaled corticosteroids. Even modest dosages such as fluticasone 200µg/day (or equivalent) may be adequate, but it is possible to start with higher doses and back-titrate after control is achieved. When adequate control of symptoms is not achieved with inhaled corticosteroids alone, a long-acting beta2 agonist such as salmeterol (Serevent) or eformoterol (Foradile, Oxis) should be added next. The PBS requires that this is done using a separate inhaler initially. The patient should be reviewed to assess www.australiandoctor.com.au After symptoms have been well controlled for 3-6 months, consider reducing the therapy, starting with reducing the dose of inhaled corticosteroid. ■ Every time a child requires a step-up of therapy, reconsider the diagnosis of asthma, adherence to therapy and form of drug delivery. ■ If a child is poorly controlled on maximal therapy (fluticasone 500µg/day or equivalent) + a LABA, they should be referred to a paediatric respiratory physician. ■ the success of this addition before combination inhalers (Symbicort or Serevent) are used. LABAs should be discontinued if there is no response. The dose of inhaled corticosteroid (with or without a LABA) can be increased if control is poor, but dosages above 500µg/day of fluticasone (or equivalent) rarely help. There is no benefit in adding montelukast to inhaled corticosteroids for patients with poorly controlled asthma. Side effects of treatment There has been increasing concern about potential side effects of inhaled corticosteroids, such as growth retardation and osteoporosis. However, it should be remembered that under-treatment of persistent asthma is potentially associated with far greater risks than those associated with low-dose inhaled corticosteroids. We know that increasing the dosage of fluticasone above 500µg/day (or equivalent) results in minimal clinical benefit in most children but does increase the risk of side effects. Recent trials have shown that, despite an initial reduction in expected growth of about 1cm over 12 months in children treated with 400µg/day budesonide, their subsequent growth velocity was normal and they achieved expected adult height. Conversely, poorly controlled asthma results in impaired growth. Nonetheless, it is possible that some children may be susceptible to the effects of inhaled corticosteroids at lower doses and be at risk of growth retardation. Therefore all children taking inhaled steroids should have their growth monitored every 6-12 months. Another concern is the effect of inhaled corticosteroids on bone metabolism and risk of osteoporosis. To date, the evidence shows minimal effect when dosages of fluticasone <500µg/day or equivalent are used. There are a handful of case reports linking moderate-high dosage (fluticasone >500µg/day or equivalent) of inhaled corticosteroids with adrenal suppression in children. As a minimum, children regularly taking ≥500µg/day of fluticasone (or equivalent) should have a screening earlymorning cortisol after three months of therapy and inform medical staff of their treatment dosages in the event of a serious illness or anaesthetic. Route of drug delivery Choice of delivery route of medication is an essential component of management. Delivery systems and appropriate ages are presented in table 5. Issues to consider include: ■ Patient choice (to optimise adherence). ■ Factors affecting maximisation of drug delivery to the lower airways (use of a spacer with an MDI). ■ Minimising oropharyngeal deposition (use of a spacer with an MDI). In many cases drug delivery should be the first consideration and the choice of medication should suit the preferred form of delivery. 4 August 2006 | Australian Doctor | 35 AD_HTT_031_038___AUG04_06 29/4/07 9:36 AM Page 36 How to treat – wheeze in childhood Asthma prevention MANY parents want to know what they can do to prevent their child developing asthma, or how they can modify its severity. The most important advice relates to smoking cessation. Avoidance of tobacco smoke exposure in utero significantly reduces the risk of a child developing transient infant wheeze. Passive smoke exposure has been shown to increase the risk of asthma and respiratory symptoms in schoolchildren. Breastfeeding has a protective effect in asthma development (along with other health benefits to the child) and should be encouraged. Allergen avoidance is a controversial area and it is difficult to give dogmatic advice to parents. Obviously if a child develops wheeze after exposure to specific animals, such exposure should be avoided. Measures to reduce environmental house dust mite exposure are costly and the evidence that they improve asthma symptoms is controversial. There is some evidence that treating patients who also have chronic rhinitis with intranasal corticosteroids may improve asthma control. Allergen immunotherapy has been best proven to help patients (including children) who have allergic rhinitis, but not those with asthma. Figure 1: Asthma Action Plan the treating physician. Provide a written reminder of maintenance therapy. ■ Give information about the management of acute episodes. Patients, particularly adolescents, should be empowered to call for an ambulance in the event of a severe exacerbation. It is important that every child with asthma is reviewed regularly. Aims include: ■ Reviewing the appropriateness of the diagnosis. ■ Assessing the level of control. ■ Assessing adherence. ■ Reviewing inhaler technique. ■ Monitoring growth. ■ Reviewing the appropriateness of medications. ■ Education. The written asthma plan should be reviewed and updated regularly. It is vitally important that parents receive sufficient education about asthma. They should be provided with information on the natural history of asthma in children, the aims of treatment, the duration of treatment and the risks compared with the benefits of therapy. A better understanding of the rationale for their child’s treatment promotes adherence to prescribed therapy. ■ For: .................................................................................... Prepared by: ...................................................................... on: ........... / ....... / ............. Preventive treatment (everyday — when sick or well) Take: 1) .......................................................... ............................ ............. times a day 2) .......................................................... ............................ ............. times a day 3) .......................................................... ............................ ............. times a day Before sport or exercise take: ................................................................... When you get mild symptoms In additional to regular preventive treatment, take: ................................................ ............... puffs ............... as often as ............ hourly, as needed ............ When symptoms are more troublesome ................................................ ............... puffs ............... as often as ............ hourly, as needed ............ Always use your spacer. IF: you need to take your Ventolin/Bricanyl more often than 3-4 hourly OR you need Ventolin/Bricanyl 3-4 hourly regularly for more than 6 doses, THEN Give: prednisolone ......................mg as a single dose daily for up to 3 days If you have a very bad attack Take: ............... puffs of Ventolin/Bricanyl every 15 minutes while arranging urgent transport to hospital When to seek help from your doctor or hospital ■ ■ ■ ■ If you have a bad attack and are worried If you need Ventolin/Bricanyl more than every 2-3 hours If wheezing persists for more than 24 hours and is not settling If you get little or no relief from Ventolin/Bricanyl or symptoms worsen suddenly, then: DO NOT STAY AT HOME — SEEK MEDICAL HELP IMMEDIATELY Keep this plan readily available at all times and give copies to others involved in care of the patient. The main reason for this is that children with mildmoderate asthma can be treated effectively, safely and relatively cheaply with inhaled corticosteroids or leukotriene-receptor antagonists. In children with more severe asthma there are significant safety concerns with use of allergen immuno- therapy, as fatal reactions have been reported. Asthma management plans All children with asthma should be provided with a written asthma plan (figure 1), which should be easy to read, concise and individualised to the patient. It should: ■ Reinforce advice given by Natural history Most children with asthma improve over time. This is because most (75%) have infrequent episodic asthma, without atopy or a family history, and tend to stop having episodes by age 10. Of those with persistent asthma, many have atopy or a family history of asthma/atopy and are more likely to have persistent asthma into adulthood. However, this outcome should never be assumed and, when children are well controlled, their therapy should be weaned and, if possible, stopped. Otherwise it is not possible to know whether good control is due to treatment or natural improvement of asthma. There has been much interest in attempting to halt the progression from intermittent wheeze to persistent asthma. Recent work has shown that regular inhaled corticosteroids, given prophylactically to preschool children who have recurrent wheezing and are at high risk of asthma, reduce symptoms and frequency of acute exacerbations but do not modify the natural history of asthma. Other work has shown that giving wheezy infants at high risk of asthma intermittent two-week courses of inhaled steroids during wheezing episodes had no benefit in reducing symptoms or in preventing progression to persistent wheezing. Authors’ case studies A toddler with asthma KIAN, 17 months, was taken to his GP because of his mother’s concerns about his wheezing. He had developed a fever and coryza three days before and become increasingly wheezy over the preceding 48 hours, with laboured breathing. On further questioning, his mother described recurrent episodes of wheeze since 10 months of age. These usually occurred when he had an URTI and would be accompanied by a cough and coryza. Kian had been delivered at term after an uneventful pregnancy. He had eczema as a baby, which cleared after age one. His father has asthma and his older sister has eczema. Neither parent smokes. On examination, Kian was well grown with no finger clubbing or chest deformity. He was tachypnoeic with subcostal recession and widespread expiratory wheeze on auscultation. He responded well to six inhalations of salbutamol via a smallvolume spacer and mask at the GP’s surgery. His wheeze disappeared and his respiratory distress improved markedly. The salbutamol was administered at home with instructions on its delivery. When reviewed the next day, Kian was much better. A two-year-old with a foreign body ADAM, two years, presented with a 36 | Australian Doctor | 4 August 2006 Figure 2: Chest X-rays showing unilateral hyperinflation on expiration in child with foreign body in right main bronchus 24-hour history of wheeze, which began the previous day while playing at his cousin’s house. He had never been wheezy in the past. Adam was otherwise well, with no coryza, cough or fever. He was delivered at term after an uncomplicated pregnancy. He had no past medical history of note. His parents were healthy and he had no siblings. On examination Adam looked well. He was thriving, with no finger clubbing or chest deformity. Auscultation revealed a bilateral wheeze, which was loudest on the right side. The GP gave him six inhalations www.australiandoctor.com.au of salbutamol via a small-volume spacer and mask, but the wheeze persisted. Inspiratory and expiratory chest X-ray films were ordered because of concern about the possibility of a foreign body. The X-ray showed unilateral hyperinflation on the right side, particularly obvious on expiration (figure 2). A foreign body was suspected and Adam was referred for rigid bronchoscopy. This was performed that evening and a plastic wheel from a toy car was removed from his right main bronchus. Adam remained well thereafter. Online resources National Asthma Council Australia. Asthma Management Handbook 2002. www.nationalasthma.org. au/html/management/amh n Asthma Foundations of Australia: www.asthmaaustralia. org.au n AD_HTT_031_038___AUG04_06 29/4/07 9:36 AM Page 38 How to treat – wheeze in childhood GP’s contribution Case study DR LIZ MARLES Redfern, NSW JEREMY, 12 months, is brought in by his mother for the fourth time in two weeks. She is concerned that he has a “wheeze” that is not improving. Last night he barely slept, so she gave him her elder son’s Ventolin through a spacer, but this had little effect. When seen before, Jeremy had been diagnosed with a viral illness on the basis of fever, runny nose and cough. Before this episode, he had no history of wheezing, although he did have moderate hyaline membrane disease requiring oxygen when he was born at 35 weeks’ gestation. He is still breastfeeding twice a day but has also been on solids for six months, and is crawling but not walking. Jeremy’s brother was diagnosed with mild episodic asthma a year ago at age three years, and his father also had mild asthma as a child. On examination, Jeremy is afebrile and appears happy. He is quite tachypnoeic, with some subcostal and intercostal recession, and his breathing is rattly, although there is no audible wheeze. On auscultation he has multiple upper airway transmitted sounds and there is only a mild audible expiratory wheeze. Questions for the authors Is wheezing always present in bronchiolitis? No. Although wheeze is a common finding in babies with bronchiolitis, a proportion will only have generalised crackles audible on auscultation. Very young babies can present with apnoea as the only manifestation of respiratory syncitial virus bronchiolitis. Thus the absence of wheeze does not preclude the diagnosis if the other clinical features are suggestive. Under what circumstances are How to Treat Quiz Wheeze in childhood — 4 August 2006 1. Which TWO statements about asthma in childhood are correct? ❏ a) Up to 15% of children have at least one episode of wheeze ❏ b) Even when the pathology responsible for causing wheeze occurs in the smaller airways, the sound originates in the large airways ❏ c) Most children with asthma develop their first symptoms in the third or fourth year of life ❏ d) Regular inhaled corticosteroids given prophylactically to preschool children who have recurrent wheezing and are at high risk of asthma do not modify the natural history of asthma 2. Todd brings his seven-month-old son, Jamie, to you because of wheezing. Jamie is thriving and examination is normal apart from minimal bilateral wheeze. Todd asks which factors would make asthma more likely to be causing Jamie’s wheeze. Which THREE responses are you likely to give? ❏ a) A personal history of eczema ❏ b) A history of asthma in Todd ❏ c) A history of recurrent viral URTIs in Jamie ❏ d) Wheezing episodes in Jamie not associated with colds 3. Jamie and Todd do not have risk factors for asthma and you think transient infant wheeze is more likely to be the diagnosis. Which ONE management option are you most likely to consider for Jamie at this stage? ❏ a) An oral bronchodilator ❏ b) A short course of oral steroids ❏ c) A trial of preventive inhaled corticosteroids ❏ d) Explanation about transient infant wheeze and review if Jamie’s wheeze worsens 4. Jamie’s intermittent wheeze continues over the next eight months, and a trial of inhaled bronchodilator does not change his symptoms. Which THREE findings would be consistent with suppurative lung disease as a possible cause of his symptoms? ❏ a) Lung crackles between episodes of wheezing ❏ b) Prolonged wheeze and productive cough during and after viral RTIs, which only improve with antibiotics ❏ c) A dry cough that is worse in the evenings ❏ d) Jamie’s lack of response to asthma therapy investigations warranted to preclude inhaled foreign body? Investigations should be performed in any child with a history strongly suggestive of foreign-body aspiration. This includes those where aspiration has been witnessed as well as those with acute onset of symptoms, particularly if accompanied by unilateral signs, such as wheeze and reduced air entry. Initial investigation would be inspiratory and expiratory chest X-rays. If the history suggests foreign-body aspiration and the child has ongoing symptoms (classically cough) or signs (eg, wheeze, particularly if unilateral) or a suggestive X-ray, urgent referral is needed for rigid bronchoscopy. What is the appropriate treatment for Jeremy at this stage? Jeremy’s mother has already given him a therapeutic trial of bronchodilator to which he failed to respond. As Jeremy does not appear too distressed, and presuming there is nothing to suggest hypoxia or dehy- dration, he should be managed with supportive treatment only, and his mother reassured. Are children with bronchiolitis likely to show any response to oral prednisolone? No. Oral corticosteroids have been studied in the treatment of bronchiolitis in the hope that their anti-inflammatory effect may help relieve airway swelling and reduce obstruction. However, randomised controlled trials, meta-analyses and systemic reviews have failed to show any benefit for the treatment of young children with bronchiolitis. General questions for the authors With the advent of montelukast as a preventive agent for mild persistent asthma, is there still a role for sodium cromoglycate? No, sodium cromoglycate is of no proven benefit in the treatment of asthma of any severity. How are children who experience moderate episodic asthma associated with viral infections (perhaps 3-4 times a year) and with no interval symptoms most appropriately managed? Children with this pattern of asthma are best managed by use of reliever medication (such as salbutamol 100200mg and terbutaline [Bricanyl]) as required for their symptoms, in addition to a short course (eg, three days) of oral prednisolone. If their episodes become more frequent, it would be appropriate to start a trial of daily inhaled corticosteroids. However, it must be remembered that this therapy may not prove to be beneficial, in which case it should be discontinued. At what age are spirometry and peak-flow measurements relevant in assessing childhood asthma? Spirometry can be performed in children from the age of six years in a laboratory with personnel experienced in testing children. There is no role for peakflow measurement in the management most children with asthma. INSTRUCTIONS Complete this quiz to earn 2 CPD points and/or 1 PDP point by marking the correct answer(s) with an X on this form. Fill in your contact details and return to us by fax or free post. FAX BACK Photocopy form and fax to (02) 9422 2844 FREE POST How to Treat quiz Reply Paid 60416 Chatswood DC NSW 2067 5. Which TWO circumstances would make an inhaled foreign body unlikely to be the cause of wheezing in an infant? ❏ a) Gradual onset of wheeze ❏ b) Reduced air entry in both lungs ❏ c) No history of foreign-body inhalation ❏ d) Normal chest X-ray 6. Sadie brings her five-year-old son, Garth, to see you because of increasing episodes of wheeze. Which information about Garth’s symptoms would suggest a diagnosis of asthma (choose TWO)? ❏ a) Episodes of wheeze triggered by URTIs ❏ b) Recent onset of stridor ❏ c) Episodes of recurrent tonsillitis ❏ d) Cough after exercise 7. You think Garth is likely to have asthma. Information about the frequency of which THREE of the following would help you to establish the pattern of his asthma? ❏ a) Sleep disturbance because of asthma ❏ b) Early morning symptoms ❏ c) Bronchodilator use ❏ d) Nasal symptoms such as sneezing and blockage ONLINE www.australiandoctor.com.au/cpd/ for immediate feedback 8. You perform spirometry and Garth’s results are normal. Which THREE factors may have influenced the results? ❏ a) Garth’s sex ❏ b) Tests were performed between episodes ❏ c) Incorrect diagnosis ❏ d) Garth’s age 9. Which ONE of the following tests would you order if wheezing persisted and the diagnosis of asthma was still in doubt? ❏ a) Chest X-ray ❏ b) Bronchial hyperresponsiveness ❏ c) Allergy tests ❏ d) ESR 10. Which TWO medications are most appropriate for treatment of moderately severe acute exacerbation of asthma in a child? ❏ a) Short-acting inhaled beta2-agonist via a puffer and spacer as required ❏ b) Oral prednisolone at a dose of 1mg/kg (to a maximum of 50mg daily), for three days ❏ c) Inhaled steroid at maximum dosage ❏ d) Inhaled ipratroprium bromide for three doses CONTACT DETAILS Dr: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Phone: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . E-mail: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . RACGP QA & CPD No: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .and /or ACRRM membership No: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Address: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Postcode: . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . HOW TO TREAT Editor: Dr Lynn Buglar Co-ordinator: Julian McAllan Quiz: Dr Lynn Buglar The mark required to obtain points is 80%. Please note that some questions have more than one correct answer. Your CPD activity will be updated on your RACGP records every January, April, July and October. NEXT WEEK The next How to Treat confronts the challenges faced by couples who experience stillbirth and sudden unexpected death in infancy. The authors are Dr Jacqueline M Scurlock, general paediatrician, Princess Margaret Hospital for Children, and chairman, scientific advisory committee, SIDS & Kids, WA; Belinda Jennings, perinatal loss midwife and member of the scientific advisory committee SIDS & Kids, WA; Judi Nolte, grief counsellor, SIDS & Kids, and clinical nurse, ICU, Princess Margaret Hospital, WA; and Dr Jane Freemantle, senior researcher and epidemiologist, Telethon Institute for Child Health Research, WA. 38 | Australian Doctor | 4 August 2006 www.australiandoctor.com.au