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Asthma in children part one: diagnosis

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Asthma as a clinical diagnosisAsthma as a pathological diseasePhenotypes of infant wheezePhenotypes of asthmaDifferential diagnosisAsthma and allergyEvaluationCase study

Professor John MassiePaediatric respiratory physician, department of respiratory medicine, Royal Children’s Hospital, and Melbourne Paediatric Specialists, Vic.

INTRODUCTIONASTHMA is a common childhood problem diagnosed and managed by GPs. One-third of children under five present to their GP with wheeze and one in nine children over five have diagnosed asthma.1

This How to Treat is part one of a two-part series. Part one considers the common difficulties faced by GPs in regard to early childhood wheeze and asthma. Early childhood wheeze is separated from asthma, as they are not necessarily the same thing. It is appro-priate for GPs to have a good concept of early childhood wheeze and under-stand how the clinical pattern merges with asthma. Even when it becomes obvious that the diagnosis is asthma, there are key differences in the way asthma is investigated and managed in childhood, and again in adolescence.

ASTHMA AS A CLINICAL DIAGNOSISASTHMA causes wheezing, short-ness of breath, chest tightness and cough that vary over time in their occurrence, frequency and intensity. These symptoms are associated with

variable expiratory airflow.1 When these symptoms occur in isolation (especially cough), or are not variable, exercise care making the diagnosis.2

Repeated response of these car-dinal symptoms to bronchodila-tor (effective dose, delivered by metered dose inhaler, with pressur-ised metered-dose inhaler [pMDI] and spacer) within the time of onset of action (1-5 minutes) and lasting 3-4 hours is a key feature.

Common triggers appear in box 1. A background of atopy and/or imme-diate family history ‘colour’ the clini-cal picture and can lend weight to the clinical diagnosis of asthma. Exacerba-tions are a common feature, classically with viral respiratory tract infections in childhood, but these are not always as clearly the precipitant in adolescents.

There is a role for some investiga-tions in the diagnosis of asthma, with spirometry the most useful (in those older than six). However, spirometry is only really helpful if it is obstructed and there is a bronchodilator response. Many children who clearly have asthma based on symptom history and response to therapy will have a nor-mal baseline spirometry. Bronchial

provocation tests are rarely used in children or adolescents. An exercise challenge (see later) is the main prov-ocation test paediatricians use. Peak flow meters are poor indicators of air-flow obstruction and have largely been consigned to the medical museum.

In children, the diagnosis of asthma is generally a clinical one and the response to therapy confirms the diagnosis. Clinical assessment of bronchodilator response is important, and may be on history or a planned field test (parents directed to try an appropriate dose by pMDI and spacer at various times of symptoms and report back). A trial of asthma preven-ter needs appropriate dosing, delivery and duration (at least 2-3 months with consistent use).

The author is sceptical about clin-ical improvement with asthma pre-venters, particularly if some of the clinical features are unclear. If the preventer appears to work, then a trial off it at some point (summer is a good time for many) is worthwhile. If symptoms reappear and disappear on reintroduction of the preventer, the diagnosis is clearer. Poor response to therapy warrants referral to a

paediatric respiratory physician.

ASTHMA AS A PATHOLOGICAL DISEASETHE clinical features of asthma are underpinned by difficulty exhaling due to bronchoconstriction (airway smooth muscle narrowing), airway wall thick-ening (inflammation) and increased mucus production.3 The typical inflam-mation is generated by a T-helper cell type 2 (TH2) pathway with interleukins IL-4, IL-5 and IL-13 prominent and air-way eosinophils predominating. Acti-vation of mast cells and leukotrienes are also important mechanisms in the inflammatory milieu (figure 1).3

The presence of regular asthma symptoms (not just exercise or acute flare-ups) suggests persistent airway narrowing with airway inflamma-tion, underpinning recommendations for daily treatment. Undertreated, inflamed airways are more likely to be reactive to asthma triggers, in particu-lar viral infections causing potentially life-threatening flare-ups.

PHENOTYPES OF INFANT WHEEZEWHEEZE and asthma are not syn-onymous. Consider the age at which wheeze began to determine if the diag-nosis is truly asthma. Be cautious with young infants presenting with wheeze, as most will outgrow it. This is in part due to growing airways, less frequent viral infections and a changing inflam-matory response to viral infections. Some do develop the eosinophilic, TH2 type inflammatory response, but this is probably uncommon in young children and explains why many older children, and adolescents who, clearly have an asthma phenotype, didn’t respond so clearly to asthma therapy as infants and young children.

Based on clinical experience, and supported by large epidemiological studies such as the Tucson Children’s Respiratory Study, the author has developed a model of early childhood wheeze that allows safe and effective management and is easy for parents to understand.4

Wheeze starting before 12 months Small airway size contributes and this is unlikely to be reversible with bronchodilators. These episodes are most commonly virally induced, with viral inflammation causing nar-rowing of the airway, as opposed to bronchoconstriction.

Persistent wheeze between viral episodes may need further inves-tigation for other conditions (for example, suppurative lung disease, pulmonary aspiration, vascular ring or tracheobronchomalacia) although in the healthy, non-coughing child, it is likely to be ‘transient infant wheeze’ (previously the ‘fat happy wheezer’).

In children under 12 months, if the wheezing events occur only with viral infections, then it is safe to consider this acute viral bronchiolitis for which beta 2 agonists are not going to help. Reassurance and supportive care are generally all that is required. Bronchi-olitis was covered in detail in a How to Treat on 3 March 2017.

Recurrent wheeze 12-36 months In this group, the pattern is mostly recurrent viral wheeze, related to small airway size. At this age the

response to bronchodilators is often variable, as the phenotype varies and drug delivery is uncertain in young children, even when a spacer is used. It is unlikely that many of these chil-dren have persistent airway inflam-mation between viral infections.

Labelling this ‘asthma’ has impli-cations for childcare and pre-school and is likely to drive inappropriate therapy.

The author calls these patterns ‘recurrent viral wheeze that respond to bronchodilator’ and ‘recurrent viral wheeze that doesn’t respond to bronchodilator’. Response to bron-chodilator may be hard to assess, but if clearly present, and symptoms are frequent (less than 4-6 weekly), severe (warranting hospitalisation) or associated with wheeze between flare-ups, then a judicious trial of an asthma preventer may be warranted. Most children without a strong atopic background will grow out of this pattern.

Parents may be concerned their child has an immune deficiency because they have multiple respira-tory infections. The frequency in this age group is 12-15 per year. It is help-ful to explain that the child has a vig-orous inflammatory response to the virus, which is normal.

Wheeze persisting, or starting, after 36 months By this age, if children with recur-rent viral wheeze have not grown out of this pattern, they commonly start to follow a more typical child-hood asthma pattern, with wheeze,

shortness of breath and cough that clearly respond to bronchodilator. They have typical triggers and many will have an atopic background. Chil-dren with significant or frequent exacerbations and/or persistent symptoms are likely to have residual small airway inflammation underpin-ning their airflow obstruction.

Viral-induced hypersecretion of mucousThe childhood pattern of recurrent shortness of breath, cough, hypoxia and rare wheeze was previously labelled ‘hypersecretory asthma’. This is a misleading label that drives inappropriate and dangerous asthma therapy. These children rapidly pro-duce airway mucous in response to viral infections, and this causes air-way obstruction, coughing and V/Q mismatching (hypoxia) and does not respond to bronchodilators (which frequently exacerbate the V/Q mis-match). This condition has been renamed viral-induced hypersecre-tion of mucous (Viper) and should be recognised as a clinically distinct phe-notype of childhood viral lower res-piratory illness.5

PHENOTYPESOF ASTHMAInfrequent episodic asthmaTHESE wheezing episodes are gener-ally triggered by a viral infection. This can be managed with as needed beta 2 agonists with pMDI and spacer (see table 1).

Frequent episodic asthmaEpisodes are 4-6 weeks apart, but usually without persistent symptoms between exacerbations. Episodes are commonly triggered by viral infec-tions. Patients with severe exacer-bations may have persistent airway inflammation, but either do

29 NOVEMBER 2019 ausdoc.com.au18 HOW TO TREAT: ASTHMA IN CHILDREN PART ONE: DIAGNOSIS

Box 1. Triggers for asthma

• Viral infections• Allergens at home (eg, house

dust mite, pollens, cockroach) • Tobacco smoke• Exercise • Stress • Cold air

Figure 1. Pathology of asthma.

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Table 1. Definitions of asthma patterns in children aged six and over not taking a regular preventer

Category Pattern and intensity of symptoms (when not taking regular treatment)

Infrequent intermittent asthma

Symptom-free for at least six weeks at a time (flare-ups occur up to once every six weeks on average but no symptoms between flare-ups)

Frequent intermittent asthma

Flare-ups occur more than once every six weeks on average but no symptoms between flare-ups

Persistent asthma Mild FEV1 equal to or greater than 80% and at least one of:• Daytime symptoms more than once

per week but not every day• Night-time symptoms more than

twice a month but not every week

Moderate Any of:• FEV1 less than 80% predicted• Daytime symptoms daily• Night-time symptoms more than

once a week

Severe Any of:• FEV1 less than 60% predicted• Daytime symptoms continual• Night-time symptoms frequent• Flare-ups frequent• Symptoms frequently restrict activity

or sleep

Source: NAC Australia. Australian Asthma Handbook 20181

not experience symptoms or report them. Trial asthma preven-ters to reduce the severity and fre-quency of exacerbations, although these may not always be successful.

The lack of success of a preventer should always prompt a rethink of the diagnosis and questions about adher-ence and drug delivery. However, lack of response to a preventer may simply mean that there is no baseline airway inflammation and that when a viral infection starts, the child has a dra-matic inflammatory response that no amount of inhaled preventer will con-trol. If a preventer is tried and doesn’t work it should be stopped. Consult a paediatric respiratory physician if there is concern about the appropri-ateness of therapy.

PERSISTENT ASTHMAIn persistent asthma, the patient experiences symptoms between exac-erbations. This suggests persistent airway inflammation. Even broncho-dilator responsive symptoms once a week are enough to warrant the introduction of an asthma preventer. Ask about asthma symptoms waking the child from sleep, morning wak-ing with asthma symptoms, daytime asthma symptoms at rest and exer-cise/activity limitation. These become the goals for symptom treatment with a preventer.

The author generally separates the use of bronchodilator for exercise from at-rest use (‘rescue bronchodila-tor’) when determining if a child has persistent asthma. School missed due to asthma can be a measure of sever-ity. The number of cannisters of bron-chodilator (pMDI) used per week or month is another indication of poorly

controlled asthma. For patients old enough to do reli-

able spirometry (six years), measur-ing FEV1 becomes important when considering severity. In children with persistent asthma, also explore the frequency and severity of flare-ups and whether these are precipitated by viral infections or are unexplained.

EXERCISE-INDUCED ASTHMA This may be experienced in isola-tion or as part of the listed asthma phenotypes. Most (70-90%) chil-dren with persistent asthma will have exercise-induced bronchospasm.6

For those with persistent asthma and exercise bronchoconstriction, treatment of the underlying air-way inflammation with a preventer is likely to reduce exercise-induced bronchoconstriction.

Exercise limitation in children with asthma may have other causes, so that it is important to be clear about whether exercise induces wheeze, chest-tightness and cough. Some children with exercise-induced bronchoconstriction cough for hours after exercise, which may be a clue to asthma. Exercise limitation can also be exercise dyspnoea, poor fitness, obe-sity-related or another cardio-pulmo-nary condition.7 Response to treatment or preloading with bronchodilator is helpful in separating these. An exercise

challenge in a respiratory laboratory accredited to test children will help when symptoms are unclear.

Exercise-induced laryngeal dys-function/vocal cord dysfunction may mimic exercise-induced asthma in ado-lescents. In the author’s experience, exercise-induced laryngeal dysfunction is slightly more common in girls and often experienced by those training or competing at high level.

Exercise-induced laryngeal dys-function presents with a sensation of choking or globus, with patients usu-ally pointing to their throats, stridor and rapid resolution on ceasing hard

exercise (not inspiring so forcefully through the mouth). Patients have often tried a beta 2 agonist, which makes no difference. The mechanisms are unclear, but forceful inspiration by the mouth creating negative pressure that sucks the glottis and supraglot-tis closed is a possibility. Changes are rarely seen on laboratory exercise chal-lenge or at nasendoscopy, and this is a clinical diagnosis. Speech therapists can often help.

COUGH-VARIANT ASTHMAWhile cough is an important symptom of asthma, cough on its own (without wheeze or chest-tightness, shortness of breath) in children is rarely a symptom of asthma. The absence of a broncho-dilator response makes cough-variant

asthma unlikely. Persistent cough may overlap with asthma in that it may be more common at the same times as asthma is, for example, at night, with exercise and on exposure to cold. In children, post-infectious cough and chronic non-specific cough of child-hood (cough-receptor hypersensitivity) are common causes.8

Patients with typical asthma may also develop troublesome cough. Asthma and cough can be triggered by different mechanisms. Beware of chas-ing the cough in the absence of other asthma symptoms or a satisfactory bronchodilator response to the cough. If cough is driving asthma therapy, reconsider the diagnosis or seek help from a paediatric respiratory physician.

DIFFERENTIAL DIAGNOSISTABLE 2 provides an age-based approach to the differential diagnosis of asthma.

Premature birthThe key piece of history is oxygen dependence at 36 weeks’ corrected gestation (the definiition of chronic neonatal lung disease, formerly bron-chopulmonary dysplasia). The longer oxygen is required after that, the worse the lung disease (see figures 2A and 2B). This is a structural disorder of small airways that improves with time. Infants are at risk of recurrent viral bronchiolitis and later recurrent viral wheeze. Chronic neonatal lung disase is a risk factor for later asthma, even in the absence of atopy.9

Small-for-gestational ageVery small infants may also have structural airways disease. This is

particularly the case if there was oli-gohydramnios, remembering part of the mechanism for airway and lung growth is mechanical stretching from fetal respiration of amniotic fluid.

Congenital structural airway diseaseThis is generally a problem seen in infants and children under 36 months. The key clinical feature is persistent wheeze, even without a viral infection. If the airway obstruc-tion is in the proximal trachea, there may be inspiratory stridor as much as there is wheeze. Trouble swallowing solids may be a clue to a vascular ring, most of which encircle the oesopha-gus as well as the trachea.

Primary tracheobronchomala-cia will just have prominent wheeze and perhaps shortness of breath. There are a variety of other congeni-tal pathologies, such as complete tra-cheal rings and congenital lesions, that narrow the airway. An H-type tracheo-oesophageal fistula is a rare condition, which may present with wheeze after feeding. Referral to a paediatric respiratory physician for consideration of bronchoscopy or CT angiogram is indicated.

Suppurative lung diseaseProtracted bacterial bronchitis is a common childhood illness, char-acterised by a productive sounding ‘wet’ cough (children under 6-8 rarely expectorate sputum), which improves with antibiotic therapy. For most it is idiopathic, but may relate to imma-ture immune function, especially for encapsulated organisms such as Hae-mophilus influenzae and Streptococ-cus pneumoniae.10 Some children may

29 NOVEMBER 2019 ausdoc.com.au20 HOW TO TREAT: ASTHMA IN CHILDREN PART ONE: DIAGNOSIS

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Figure 2A. X-ray of infant respiratory distress syndrome.

A

The lack of success of a preventer should always prompt a rethink of the diagnosis and questions about adherence and drug delivery.

Figure 2B. Lateral view X-ray of infant respiratory distress syndrome.

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HOW TO TREAT 21ausdoc.com.au 29 NOVEMBER 2019

wheeze because of mucous obstruc-tion of the airway.

The well-defined causes of sup-purative lung disease are cystic fibro-sis (CF), primary ciliary dyskinesia/immotile cilia syndrome and immune deficiencies. The suppurative process starts in the small airways, hence the prominence of wheeze in the clini-cal picture, but the hallmark is still a prominent wet sounding cough. Some children with CF will be missed by newborn screening and present with cough and wheeze. These chil-dren tend not to be well between viral exacerbations. A referral to paediatric respiratory physician is indicated if suppurative lung disease is suspected as the cause of persistent wheeze.

Inhaled foreign bodyThis can be a cause of wheeze and cough. The hallmark is the sud-den onset, as opposed to the grad-ual build-up of wheeze and cough with viral infections. The classic age is from 12 months (pincer grip devel-ops) until about three years (when mouthing objects stops), but can occur at any age. A definite history of witnessed aspiration may not be reported (up to 50%).11

Unilateral, fixed wheeze is a clue. A lack of bronchodilator response and lack of history of wheeze with viral infections should raise suspicion. The author assumes every child has a snotty nose so suggests not to attrib-ute this as a cause of the wheeze.

If there is suspicion, a chest X-ray taken with the history in mind is helpful, remembering most foreign bodies (for example, peanut, biscuit, carrot, plastic toys) are not radio-opaque. Order an AP and two lateral

decubitus films (that is, left side up and right side up) in children under three looking for normal lung to deflate when dependent, but a for-eign body to cause a ball-valve effect with inflation (or hyper-inflation) maintained (see figure 3).11

Children over three can usu-ally hold their breath for a stand-ard inspiratory and expiratory chest X-ray, again looking for unilateral hyper-inflation. Make sure the X-ray includes the neck so the trachea can be visualised.

A combination of history, exami-nation and chest X-ray findings will guide the need for bronchoscopy. If

there is any doubt, urgently refer the patient to the local ED or a paediatric respiratory physician.

Sometimes foreign bodies have been missed and may then present with a suppurative picture and ate-lectasis that does not resolve with appropriate antibiotic treatment. Again, referral to a paediatric respira-tory physician is indicated.

Primary pulmonary aspirationThis is surprisingly common, even in developmentally normal infants. The key is a history of wheeze and cough during feeding, so ask the patient to have a bottle in your rooms. Some infants have a bottle while lying down in bed at night (The author

calls this the ‘astronaut’ bottle) pre-disposing the infant to aspiration. Children with developmental delay (low Apgar scores might be a clue) are particularly vulnerable. They may wheeze just like in asthma and have a hyper-inflated chest X-ray. A lack of bronchodilator response and a coarse interstitial pattern on X-ray may dif-ferentiate this from asthma. Speech therapy swallowing assessment usu-ally helps.

Gastro-oesophageal reflux disease This is very common in infants, and most have no associated respira-

tory symptoms. Several mechanisms may contribute in children who have wheeze (and/or cough) after feed-ing, including vagal stimulation from oesophageal dilatation, laryn-geal splashing or aspiration.12 It can be hard to correlate symptoms with gastro-oesophageal reflux disease. A therapeutic trial of a proton pump inhibitor may be useful. Referral to a paediatric respiratory physician is suggested.

Allergic bronchopulmonary aspergillosisThis is rare in children, but occa-sionally occurs in adolescents. It can be hard to distinguish from dif-ficult-to-control asthma with asper-gillus sensitisation. The wheeze may

not be bronchodilator responsive, the eosinophil count will be very high, there is elevated IgE and aspergillus specific IgE. The hallmark is the radi-ographic finding of dilated airways filled with mucous plugs. Referral to a paediatric respiratory physician is required.

ASTHMA AND ALLERGYTHERE is clearly a close link between asthma and allergy, with thunder-storm asthma (see part two) an example. Allergies — such as aller-gic rhinitis, eczema and IgE-medi-ated food allergy — occur commonly in people with asthma. Children with asthma are more commonly positive to allergens on testing.1

The airway inflammation of asthma is dominated by eosinophils. There is an increasingly better under-stood link with the TH2 (allergic) inflammatory response, in particular the cytokine profile that is different from the TH1 (infection) pathway.3 Some of the new biological agents that target specific cytokines block key parts of the allergic inflammatory cascade.

This all suggests that inhaled aller-gens cause asthma, but it is difficult clinically to isolate which one(s) and successfully modify the environment to improve asthma for many children. If patients report asthma symptoms on exposure to allergens such as ani-mals (commonly cats), cockroaches (can be hard to tell) or easily identi-fiable trees in their immediate envi-ronment, then it may be possible to remove them. Practically, most chil-dren with meaningful clinical reac-tions can identify these and parents

do not need a doctor’s recommenda-tion for removal. For most children, however, the link is less clear. Tests for house dust mites, for example, are commonly positive, but attempts to minimise house dust mite exposure and desensitisation is rarely effective for asthma.13 Generally, it is not pos-sible to influence pollen exposure, short of staying indoors on high pol-len days. The author sees very few patients whose treatment requires them to do this. There are usually other causes for poorly controlled asthma. These comments on inhaled allergens may not apply to allergic rhinitis. The author recommends sep-arating rhinitis from asthma, treating each in its own right. For example, nasal corticosteroids are a good treat-ment for allergic rhinitis, but don’t improve asthma symptoms. Similarly, allergen desensitisation helps the rhi-nitis, but not the asthma.

EVALUATIONHistoryTHE history is outlined in the sec-tion on asthma as a clinical diagno-sis. Consider the symptoms, pattern (intermittent or persistent) and clin-ical response to therapy. The picture is coloured by the atopic history. Dif-ferential diagnoses can be considered through a few strategic questions as outlined in table 2, which may lead to a more thorough exploration of an alternative diagnosis.

ExaminationThere are some specific findings on physical examination relevant to the examination of children with suspected asthma and who are not acutely unwell with a flare-up.

Most foreign bodies (for example, peanut, biscuit, carrot, plastic toys) are not radio-opaque.

Table 2. Differential diagnosis of asthma

Age group Differential diagnosis History

Infants and young children

Pre-term birth (chronic neonatal lung disease)

History of premature birth

Small for gestational age Birthweight, oligohydramnios

Structural airway disease (vascular ring, tracheobronchomalacia)

Persistent infant wheeze, difficulty swallowing solids

Inhaled foreign body (see figure 3)

Sudden onset, localised signs and often signs on imaging

Primary pulmonary aspiration

Worse with feeding

Gastro-oesophageal reflux disease

Worse after feeding, vomiting

Suppurative lung disease (CF, immune deficiency, primary ciliary dyskinesia)

Wet cough

Children Suppurative lung disease (CF, immune deficiency, primary ciliary dyskinesia)

Wet cough

Inhaled foreign body Sudden onset, localised signs and often signs on imaging

Primary pulmonary aspiration

Especially developmentally delayed children

Adolescents Suppurative lung disease (CF, immune deficiency, primary ciliary dyskinesia)

Wet cough, family history CF

Allergic bronchopulmonary aspergillosis

Laryngeal (vocal cord) dysfunction

Stridor and globus

Inhaled foreign body Sudden onset, localised signs and often signs on imaging

Figure 3. Chest X-ray of the lungs in a three-year-old child after aspiration of a peanut. The left lung is hyperinflated because of ball-valve mechanism. The mediastinum is shifted to the right.

HELLERH

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29 NOVEMBER 2019 ausdoc.com.au22 HOW TO TREAT: ASTHMA IN CHILDREN PART ONE: DIAGNOSIS

2 4 6

Vol [L]

10

8

6

4

2

0

2

4

6

8

10 Flow [L/s]

F/V in

F/V ex PrePost

Pred LLN Pre %Pred Post %Pred %Chg Z ScrLevel date 05.06.13 05.06.…Level time 02:46PM 03:03…

FEV 1 L 4.39 3.51 2.79 63.5 3.40 77.5 22.0FVC L 5.15 4.18 5.20 100.9 5.24 101.7 0.8FEV1/FVC % 85.76 74.44 53.68 62.6 64.94 75.7 21.0FEF 25-75% L/s 4.77 3.17 1.45 30.4 2.18 45.8 50.6PEF L/s 8.67 6.27 5.39 62.2 6.96 80.3 29.1

Last Name: Identification:First Name: Age:

Height:Date of Birth: Weight:Gender: BMI:Diagnosis: Technician:Ref. Physician: -- Physician:

Test performance was good with repeatable effortsobtained.

Test Comments

Interpretation

Spirometry

There is moderate obstructive lung disease.There was a significant bronchodilator response on this occasion.

(Physician 14.06.2013 10:50AM, Robinson Phil / Final: 14.06.2013 10:50AM, Robinson, Phil)

FEV1p %

59.00

64.00

69.00

74.00

79.00

Measured values

15/09/2011

15/12/2011

28/03/2012

28/06/2012

18/10/2012

20/02/2013

5/06/2013

FEV1 L

2.002.302.602.903.203.503.80

Measured values

15/09/2011

15/12/2011

28/03/2012

28/06/2012

18/10/2012

20/02/2013

5/06/2013

Respiratory Laboratory, Department of Respiratory MedicineRoyal Children's Hospital, Flemington Road

Parkville, VIC, 3052

Bronchoprovocation (EIA/EIB) Exercise TestIdentification: xx Date of Birth:Last Name: xxx Age:First Name: xxxx Height:Sex: Weight:Ref. Physician: Diagnosis:Operator:

On the day of the TestDate 10/06/10Time 11:06:59AMBaro. pressure 1026 hPaTemperature 22 °CRel. humidity 47 %

Pre Exercise 2.021-3 minutes Post Exercise 1.30Post Bronchodilator 2.29

Pre Exercise Predicted %(Pre Ex/Predicted)[L]FEV 1 2.02 2.29 88[L]FVC 2.85 2.75 104[L]VC MAX 2.88 2.80 103

[%]FEV 1 % FVC 70.68 84.52 84[L/s]MMEF 75/25 1.47 2.80 53[L/s]PEF 3.63 5.05 72

1-3 mins Post Ex -35Post Bronchodilator 14

PID:xx, xxx, xxxx 22/07/2010 09:50 PS991026:EIA 1-3MINS BD POS 1 /1

Percentage Change in FEV1 Pre & Post ExerciseChallenge & Post Bronchodilator

Actual Values FEV1 (L) Pre Exercise, PostExercise & Post Bronchodilator

Bronchodilator = 400mcg Salbutamol via MDI & Spacer

Technical Comments:

Good ex test and spirometry technique with audible wheeze and cough and SOB post ex. Target HR reached and sustained for last 4 mins of test.

Interpretation:Moderate exercise induced bronchoconstriction 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0

Vol [L]

6

4

2

0

2

4

6 Flow [L/s]

F/V in

F/V ex

123

FEV 1 [L]

-40-30-20-10

01020 relative to the first test [%]

10/062010

10/062010

10/062010

THIS TEST IS POSITIVE FOR EXERCISE INDUCED BRONCHOCONSTRICTION/ASTHMA

Respiratory Laboratory, Department of Respiratory MedicineRoyal Children's Hospital, Flemington Road

Parkville VIC 3052

FLOW-VOL CURVE

0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0

Vol [L]

10

8

6

4

2

0

2

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10 Flow [L/s]

F/V in

F/V ex

1

Predicted Actual %Pred[L]FEV 1 2.32 2.17 94[L]FVC 2.79 2.53 91[L]VC MAX 2.84 2.53 89[%]FEV 1 % FVC 84.49 85.87 102

[L/s]MMEF 75/25 2.83 2.35 83[L/s]PEF 5.11 5.14 101

[L]FVC IN 2.84 1.88 66[L/s]FIF 50 3.74

[%]FEF50 % FIF50 76.85[L/s]PIF 4.05

[L]FEV 0.5 1.70

Date 21/07/10Time 02:42:07PMBaro. pressure 1022 hPaTemperature 21 °CRel. humidity 52 %Altitude 50 m

Identification: xx Date of Birth: Age:Last Name: xxx Height: Sex:First Name: xxxx Weight: Diagnosis:Ref. Physician: Operator:

Technical Comments

Post = spirometry performed post 400mcgSalbutamol via MDI & spacer.

All results meet ATS/ERS 2005 Guidelinesunless otherwise stated in the "Technical

Comments" section of the report.

Figure 4A. Normal spirometry.

Figure 5. Poor spirometry technique.

Slow rise to peak flow

False start

Cough

Premature stop

There are some findings that point towards asthma: hyper-inflated chest, pectus carinatum, Harrison’s sulcus/groove, prolonged expiratory phase of respiration and wheeze. If patients are wheezy, clinical response to bron-chodilator in the examination room is a helpful finding (in addition to lung function, if the child is old enough and the facility is available). Findings such as a productive cough, failure to thrive, digital clubbing and chest crackles suggest another diagnosis, such as suppurative lung disease. These should prompt referral to a paediatric respiratory physician.

InvestigationsThese are presented in order of prac-tical utility for the diagnosis and management of asthma in children.

LUNG FUNCTIONMost children from age six can be taught to do reliable spirome-try (see figures 4A, B and C). The quality and utility of spirometry (see figure 5) depends on the skill,

clinical expertise and experience of the person doing and interpreting spirometry.

Spirometry is helpful for diagno-sis when there is evidence of airway obstruction (FEV1 less than 80% with FEV1/FVC less than 70% and 12% improvement in FEV1 after broncho-dilator, for example, 4 x 100µg/puffs salbutamol with a spacer).14 In addi-tion to grading the severity of persis-tent asthma and monitoring progress, low FEV1 predicts clinically signifi-cant flare-ups making it an impor-tant test at asthma reviews.

The pitfalls of spirometry in children are poor measurement of height (with sex, the main predic-tor of lung function) and poor tech-nique. Remember, spirometry uses forced manoeuvres so that a poor effort will result in falsely low meas-urements. Poor technique will most commonly produce a flow volume loop that does not have an early peak and appears more as a dome. This can be interpreted as show-ing restrictive lung disease

Figure 4B. Exercise induced bronchoconstriction spirometry.

PAGE 24

Figure 4C. With bronchodilator response.

(that is low FEV1 and low FVC with FEV1/FVC ratio main-tained above 80%). Many young children do not exhale all the way out to residual lung volume, giving an underestimate of FVC. There are many good office spirometers that show a flow-volume loop which is good to use to interpret effort and technique. If you use laboratory ser-vices for spirometry, ensure they are accredited for measurement of lung function in children and adolescents.

CHEST X-RAY A chest X-ray is generally recom-mended for children with persis-tent symptoms who need to start an asthma preventer.1 This may help exclude other conditions mimicking asthma. Hyperinflation (see figure 6) may be the only sign of asthma. Atelectasis and patchy infiltrates are generally confined to acute flare-ups. The exception might be right middle lobe collapse, the so called right middle lobe syndrome that is caused by retained mucous in the right middle lobe bronchus. This is not a specific finding for asthma and failure for it to resolve is an indica-tion for referral to a paediatric res-piratory physician for consideration of CT scan or bronchoscopy.

BLOOD TESTSBlood tests do not have a large role in the diagnosis and management of asthma. An FBC might reveal an elevated eosinophil count, but this could be due to atopy as much as asthma. If there is diagnostic con-cern, or severe asthma that might warrant biological agents, then an IgE and aspergillus precipitins (to

consider allergic bronchopulmonary aspergillosis) may be warranted.

SPUTUMSputum analysis for eosinophils is not usually helpful for the diagnosis of asthma in children. Most children cannot expectorate until age 6-8. If the child has a productive cough, it is more likely to represent protracted bacterial bronchitis than asthma,

in which case sputum culture is warranted.

FRACTIONAL EXHALED NITRIC OXIDE Exhaled nitrix oxideis a measure of airway inflammation. Values of frac-tional exhaled nitric oxide (FeNO) greater than 40 parts per billion are positive and may be helpful for diagnosis when there is doubt and

probably predicts a good short-term response to inhaled corticosteroid treatment. At the moment, however, measurement of FeNO are not rec-ommended in primary care to guide treatment decisions, but are increas-ingly used in specialist clinics.15

CASES STUDYBELLA, 19 months old, presents to her GP for the third time this winter

with recurrent wheezing. She was born at term with no neonatal com-plications. Her vaccinations are up to date. Her mother did not smoke in pregnancy, but her father smokes 15 cigarettes/day (mostly at work, but always outside when at home). Bella is not atopic and there is no immedi-ate family history of asthma.

The episodes of wheeze began at six months and are all in asso-ciation with viral illnesses. She is well between events (including not coughing) and had a good summer. She does not aspirate and there is no history of foreign body aspiration.

On examination, Bella is thriving, and there is no digital clubbing. She has coryza but is not working hard to breath, and has generalised wheeze. She does not respond to six puffs of salbutamol given with pMDI and spacer and mask.

The GP is confident she has viral-induced wheeze and is not bronchodilator responsive. The lack of wheeze between episodes reassures that a structural airway problem is unlikely. Bella has not been troubled by a wet sounding cough or required regular antibiot-ics to suggest suppurative lung dis-ease. In the absence of risk factors for asthma and her lack of symp-toms between viral episodes, the GP reassures her mother that Bella is most likely to grow out of this pat-tern of wheeze. The label of asthma is avoided.

The GP recommends influenza vaccines for Bella and her parents and invites Bella’s father to come back to discuss smoking cessation.

CONCLUSIONFOR most infants and young chil-dren, wheeze is mostly an issue with small airway size and intermit-tent exacerbations driven by viral infections. Response to bronchodi-lators is variable and preventers are less often required. Young children who do not grow out of this pattern fit more easily with the diagnosis of asthma, having variable airway narrowing, a clear bronchodilator response and, if persistent, are more likely to respond to asthma preven-ters. The diagnosis of asthma then rests on the matrix of history, sup-porting evidence of atopy, physical examination, spirometry and clini-cal response to treatment.

References on request from howtotreat@adg.com.au

29 NOVEMBER 2019 ausdoc.com.au24 HOW TO TREAT: ASTHMA IN CHILDREN PART ONE: DIAGNOSIS

1. Which THREE are cardinal symp-toms of asthma?

a Cough. b Haemoptysis. c Wheeze. d Shortness of breath.

2. Which TWO are triggers for asthma?

a Viral infections. b Dairy products. c Tobacco smoke. d Poor sleep.

3. Which THREE statements regarding infant wheeze are correct?

a Wheeze starting before 12 months is usually reversible with bronchodilators.

b Persistent wheeze between vi-ral episodes before 12 months may need further investiga-tion for other conditions.

c Labelling recurrent wheeze at 12-36 months as asthma is likely to drive inappropriate therapy.

d The condition of viral-induced hypersecretion of mucous does not respond to bronchodilators.

4. Which TWO are features of persistent asthma?

a School missed due to asthma can be a measure of severity.

b It is always mild. c Flare-ups occur more than

once every six weeks on aver-age but there are no symp-toms between flare-ups.

d The patient experiences symptoms between exacerbations.

5. Which THREE are features of exercise-induced laryngeal dysfunction?

a Inspiratory wheeze. b Stridor. c A sensation of choking. d Rapid resolution on ceasing

hard exercise.

6. Which TWO statements regard-ing the differential diagnosis of asthma are correct?

a Chronic neonatal lung disease is a risk factor for asthma only in the presence of atopy.

b The key clinical feature in congenital structural airway

disease is persistent wheeze, even without a viral infection.

c Causes of suppurative lung disease include cystic fibrosis, primary ciliary dyskinesis and immune deficiencies.

d The hallmark of allergic bronchopulmonary aspergillosis is the radiographic findings of unilateral hyperinflation.

7. Which ONE condition presents with a sudden onset, localised signs and often signs on imag-ing?

a Primary pulmonary aspiration. b Suppurative lung disease. c Inhaled foreign body. d Gastro-oesophageal reflux

disease.

8. Which TWO statements regarding asthma and allergy are correct?

a Allergic rhinitis, eczema and IgE mediated food allergy occur commonly in

people with asthma. b Nasal corticosteroids will

improve allergic rhinitis and asthma symptoms.

c Allergen desensitisation helps allergic rhinitis, but not asthma.

d All children with asthma should have allergy tests.

9. Which THREE examination find-ings point to asthma?

a Hyper-inflated chest. b Prolonged expiratory phase of

respiration and wheeze. c Harrison’s sulcus/groove. d Pes excavatum.

10. Which THREE statements regarding the investigation of asthma in children are correct?

a Right middle lobe syndrome is a specific finding for asthma.

b Spirometry is helpful for diag-nosis when there is evidence of airway obstruction and improvement after broncho-dilator.

c Blood tests do not have a large role in the diagnosis and management of asthma.

d Sputum analysis for eosinophils is not usually helpful for the diagnosis of asthma in children.

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ASTHMA IN CHILDREN PART ONE: DIAGNOSIS

• Refer children with an uncertain diagnosis, life-threatening flare-ups or difficult to control asthma to a paediatric respiratory physician.

• Infant wheeze is most often associated with small airway size and exacerbations driven by viral infections.

• From three years, children with recurrent wheeze are more likely to have asthma and respond to therapy.

• Most children from six years are able to do reliable lung function.

• Cough alone, in the absence of other asthma symptoms and without a bronchodilator response, is unlikely to be asthma.

Key points

PAGE 22Figure 6. Marked hyperinflation.