A Consensus Statement Prepared for the
Academy of Medicine of Malaysia


List of Committee Members
The Need For An Asthma Consensus
        Differential diagnosis
Assessment of Severity of Asthma
Goals of Therapy
Management Of Asthma
        Patient education
        Drug therapy
Special Categories of Asthma
Inhaler Devices
Management of Acute Asthma
        Assessment of Severity
        Aims of treatment of acute asthma exacerbations
        Management of an acute attack
        Intensive care
        Other treatment
Long Term Assessment And Monitoring
Asthma Action Plans


APPENDIX 1  :  Mean FEV16 And PEF5 of Normal Malaysian Children
FIGURE 1       :   Summary of Management of Asthma
FIGURE 2       :   Algorithm For Management of Acute Asthma In Children
TABLE 1         :   Assessment of Severity In Childhood Asthma
TABLE 2         :   Useful Measures To Reduce Exposure To House Dust Mites
TABLE 3         :   Drug Dosages In Asthma
TABLE 4         :   Drug Delivery System For The Inhaled Route Recommended For Different
TABLE 5         :   Asessment of Severity of Acute Asthma
TABLE 6         :   Drug Dosages In Acute Asthma


Chairman : Professor Azizi Haji Omar FRCP (Edin.)


Dr. Lee Eng Lam FRACP.   

Dato' Dr. Jai Mohan FRCP (Lon).   

Dr. Koh Chong Tuan FRCP (Glas).   

Dr. Deng Cheng Teik M.Med. (UKM)   

Dr. Kuan Geok Lan MRCP (UK).   

Dr. Kwan Poh Woh MRCP (Ire).   

Dr. Quah Ban Seng MRCP (UK).   

Dr. Jessie de Bruyne MRCP (UK).   


Dr. Norzila Mohamed Zainudin M.Med. (UKM).  


Asthma is a common condition that gives rise to considerable morbidity and mortality. Its prevalence is increasing and a local study found 13.8% of primary school children in Kuala Lumpur to be asthmatic.1 It is under-diagnosed and often not managed optimally.2 In an ongoing surveillance of paediatric asthma deaths, 9 deaths have been reported in the past two years; and all of them have been due to inadequate assessment of the severity of the attack and hence under-treatment. There is an over reliance on symptomatic and oral therapy and an under-use of anti-inflammatory therapy leading to inadequate control and, in some cases, death.3 It is also recognised that disparities in management exist due to lack of access to appropriate information, drugs and resources.

Various national and international guidelines have been developed to address these problems. These guidelines are useful for the education of local practitioners but they do not address issues of special relevance to Malaysian patients and clinicians. The following document is a guideline for reference and is intended to help improve the management of asthma in Malaysian children.


Asthma is a condition characterised by airway inflammation leading to airway hyperresponsiveness and presenting with episodic or chronic wheeze and/or cough.


1. Presentation

The diagnosis of asthma should be considered in any child presenting with recurrent episodes of cough, wheeze and/or dyspnoea. The diagnosis of asthma is supported by symptoms of wheeze and/or cough that are episodic, nocturnal or following exercise or allergen exposure. Asthmatic symptoms may be mistaken for recurrent respiratory infections. Chronic cough is usually due to asthma although other causes need to be excluded. Some children may present only with symptoms following exercise. The presence of atopy (eczema, allergic rhinitis and conjunctivitis) in the child or family supports the diagnosis of asthma. However, the absence of these conditions does not exclude the diagnosis.

2. Differential diagnosis

If symptoms are associated with a neonatal onset, failure to thrive, focal lung or cardiovascular signs or vomiting a diagnosis other than asthma should be considered. In infancy it is important to recognise that wheezing may be due to other conditions including bronchopulmonary dysplasia, congenital malformations (tracheo-oesophageal fistula, vascular ring, congenital lobar emphysema), gastro-oesophageal reflux, bronchiolitis obliterans, immune deficiency, bronchiectasis and cystic fibrosis.4 Wheezing may be associated with foreign body inhalation or infectious disorders such as acute viral bronchiolitis, tuberculosis, Loeffler's pneumonia and filiariasis.

3. Investigation

The diagnosis of asthma is based on a good history and physical examination. Usually investigations are not necessary. Response to bronchodilator therapy, that is, symptomatic improvement in the younger child or improvement in peak expiratory flow (PEF) or forced expiratory volume in one second (FEV1 ) of greater than 15% in the older child is usually diagnostic. Peak flow readings may also show considerable diurnal variability.

In atypical cases, investigations may be necessary to exclude other conditions. These investigations include chest and sinus X-rays, reflux studies, Mantoux test, immune function studies, sweat electrolytes, bronchoscopy and pulmonary function tests. PEF and FEV1 measurements should be based on standards for local children.5,6 (Appendix I).


Asthma is a chronic disease and accurate assessment of severity is essential for optimal management of asthma. Asthma may be categorised as mild, moderate or severe based on frequency, chronicity and severity of symptoms (Table 1). These groups are arbitrary and may merge one into another. Pulmonary function testing (usually PEF monitoring) allows more objective assessment.


Although asthma is a chronic disorder, there should not be unnecessary pessimism about the outcome of the disease. Treatment is aimed at not only symptomatic relief but also achieving a complete and durable remission. The goals of therapy include :

These are realistic objectives that can be attained in all but a small group of children with recalcitrant asthma.


Inflammation of the airway,7 which is the hallmark of asthma, is precipitated in genetically susceptible children by a variety of factors viz. respiratory infections, environmental irritants and allergens. The relative importance of each factor varies in different children and thus management plans must be individualised. The role of the doctor is to explore these variables and then initiate, implement and modify treatment as dictated by the needs of the child and the family.

In order to ensure success in management, the parents and the child must be involved in decisions on treatment options. Treatment strategy includes educating the parents and the child in all pertinent aspects of the disease, preventing debilitating effects of the disease and the use of pharmacological agents to modify the disease process. A comprehensive management programme requires the involvement of doctors, specialists, nurses, pharmacists, physiotherapists, school teachers, asthma societies and patient support groups. It is the duty of the doctor to facilitate patient's access to these professionals and services as and when appropriate.

1. Patient education

At the outset it is important to convey to the parents an understanding of the nature of the disease and to clearly indicate that asthma is a chronic disease with a relapsing course. Treatment is likely to be a prolonged process. They need to recognise the associated signs and symptoms of asthma and to be aware of possible aggravating factors. Parents should have a knowledge of the medications being used and should understand the role that each medication plays in the control of asthma. There should be precise instructions and demonstrations on their proper administration and potential adverse effects should be discussed. The essential components of an effective patient education programme consists of 8 :

Education should be a continuous and evolving process. With repeated counselling parents should eventually be confident enough to assume responsibility in the home management of most asthmatic attacks without immediate recourse to a doctor. However, there should be clear guidelines on when and where to seek emergency help (See Asthma Action Plans). Children should be encouraged to progressively assume responsibility as they approach adolescence.

Resource materials are now available in the form of books, pamphlets, comics, audio-visual tapes and posters for exhibition. Doctors are encouraged to participate in educating the public through the media, schools and lay societies. Doctors should themselves keep abreast of new developments in the understanding and management of asthma. Time spent on education is time well invested.

2. Prevention

While the predisposition to asthma is probably genetically determined, environmental factors appear to be important in triggering and perpetuating disease activity.  

                The presence of allergy can be demonstrated in the majority of children with
                asthma, particularly in those beyond five years of age. The common allergens
                identified include house dust mites (D. pteronyssinus and D. farinae), cat and
                other danders, insects such as cockroach, fungi and pollen. Skin allergy testing may
                be helpful in the diagnosis of allergy in asthma. Asthma is likely to be more
                protracted in the atopic child. In those children in whom asthma is difficult to
                control it is reasonable to recommend measures to reduce exposure to the
                offending allergen. Getting rid of house dust mites may be an insurmountable
                problem in many homes. However, there have been convincing trials to show that
                effective reduction in house mite population results in significant reduction of
                symptoms.The best strategy to reduce mite population is removal of their habitat.
                (Table 2) Sensitivity should be exercised before recommending the removal of a
                much loved pet from the household. It may take up to three months before dander
                disappears after removal of the source. Acquisition of soft toys and animals as pets
                are discouraged.

                Food allergy occurs in approximately one to two percent of childhood population
                and is an uncommon trigger for asthma. Therefore, there should not be unnecessary
                deprivation of food items unless there is a clear and reproducible link between
                ingestion of an offending food and precipitation of symptoms. Non IgE related food
                and drug sensitivity may serve as an additional mechanism in asthma exacerbation.
                Thus cold drinks, food additives (tartrazine dyes, metabisulphites) and certain drugs
                (apririns, NSAIDS, beta blockers and radiological dyes) may precipitate attacks
                and should be avoided in appropriate circumstances.

                Air pollution from any source has significant adverse effects on airway
                hyperresponsiveness. The case against environmental tobacco smoke has been
                demonstrated in many epidemiological studies. Tobacco smoke contains more than
                3800 chemical compounds and respirable suspended particulate matter can be two
                to three times higher in homes with smokers.10 Passive smoking harms the child in
                many ways : increased rate of lower respiratory illnesses in infancy, increased
                incidence of middle ear effusion, more severe asthma, more frequent exacerbations
                and reduced lung development.11 Several local studies have demonstrated that
                passive smoking is an important issue in this country and its avoidance may
                contribute to prevention of asthma and respiratory morbidity.12-15 Thus parents of
                asthmatics should be advised that their home and motor vehicles should be
                non-smoking zones.

                Other products of combustion such as carbon monoxide, nitrogen dioxide, sulphur
                dioxide, acid aerosols and emissions from kerosene, wood and charcoal stoves,
                and mosquito coils may be linked to respiratory morbidity although their role in
                asthma is not well established. There is evidence, however, that exposure to
                mosquito coil smoke is associated with increased risk for asthma12,14 and exposure
                to kerosene and wood stoves is associated with impairment of lung function14 in
                Malaysian children. The use of air conditioners, air filters, ionisers and fans do not
                have a clear relationship with asthma control or exacerbations.

                Viral respiratory infections are the commonest triggers of asthma attacks in
                children. These are unavoidable in most children. For the younger child with
                frequent severe attacks, temporary removal from day-care nurseries may be

                While exercise is a recognised precipitant of asthma symptoms, children should be
                encouraged to participate in normal activities including swimming. Exercise
                intolerance suggests inadequate therapeutic control which needs further

                There is evidence for a protective effect of breast feeding against asthma and other
                allergic diseases. In view of this and otherbeneficial effects of breast feeding, breast
                feeding should be encouraged.16

3. Drug therapy

As asthma is an inflammatory condition, management should emphasise anti-inflammatory therapy. Management will be affected by severity and the age of the child. Figure 1 outlines the recommended sequence of drugs. Table 3 gives the recommended doses for these drugs.

Progression to the next higher step (step up) is indicated when control cannot be achieved at the current step and provided there is assurance that medication is used correctly.

Reduction in therapy (step down) is considered when the outcome of therapy has been achieved and sustained for several weeks or even months at the current step. Reduction in therapy is also needed to identify the minimum therapy required to maintain control.

Long acting beta-agonists are mentioned in the recommendation although they are not yet registered for use in children in Malaysia. They are not indicated for relief of acute symptoms but for use if symptoms persist. Similarly, slow release theophylline and ipratropium bromide should be used in addition to inhaled steroids.

Long term oral steroids are seldom required. When indicated the minimum dose that will maintain control of symptoms should be given, preferrably on alternate days. This treatment should be reviewed frequently with the aim of stepping down as soon as possible.

There is evidence that adequate treatment of associated sinusitis and allergic rhinitis is helpful in the control of childhood asthma.

Ketotifen is not included in the recommendation because of the paucity of well conducted clinical trials supporting its role in the management of asthma. Mucolytics and anti-tussives have no place in the management of asthma.


1.    Intermittent severe asthma

Some children have infrequent attacks which are severe or life threatening. At the first sign of an attack the child should be treated with an inhaled beta-agonist and an oral steroid. Practitioners may want to consider prescribing oral steroids for use by patients at home at the start of the attack. Long term inhaled steroids may be of benefit. A self admission letter should be provided.

2.    Nocturnal asthma

The condition is best managed by optimising the anti-inflammatory therapy. Symptoms can be controlled by the use of sustained release theophylline or long acting beta-agonists if they persist despite adequate dosage of anti-inflammatory therapy.

3.    Exercise induced asthma

Optimisation of anti-inflammatory therapy is required. Further symptoms can be controlled by administration of inhaled sodium cromoglycate or beta-agonist 10 to 20 minutes before exercise. Warming up before exercise and nasal breathing should be encouraged.


The preferred route for drug delivery in asthma is by inhalation where possible. It is vital that the delivery system is appropriate to the child's age (Table 4). Home nebulisers are expensive and have been shown to be less efficient than spacer devices in delivering drugs to the lungs. In children aged under five years spacer devices with masks are preferred. Some children as young as six months may use these spacers effectively provided that there is a good seal of the mask on the face and the child is capable of inhaling fast enough to open the valve. In very young children the inspiratory flow rate may be too low to open the valve and, therefore, a nebuliser is the best choice. Spacers without masks may be used in four or five year olds.

Spacer devices available in the market may be too costly for some patients. Spacers that are made using plastic cups and soft drink bottles may be quite effective and may be tried until parents are able to afford a better device.

In children aged five years and older inhaled powder inhalers are suitable. If metered dose inhalers are preferred they should still be used with spacer devices. Breath actuated metered dose inhalers may be suitable for some children.


1. Assessment of Severity

The first step in the management of an acute attack is adequate assessment of the child (Table 5). Relevant history includes identifying the likely triggers of the acute attack, duration of the attack prior to presentation and prior drug treatment including dosages, delivery method, frequency of use, time of last dose and response to therapy. A history of coexistent medical conditions and other lung diseases is also important.

Altered conciousness, anxiety, restlessness, irritability, cyanosis and the presence of pulsus paradoxus indicate severe airflow obstruction. The absence of these signs does not mean that the child is free from significant obstruction. Tachycardia and tachypnoea are indicators of severe asthma, but in a patient with respiratory muscle fatigue, respiratory rate is slow and respiratory effort reduced. Auscultation may reveal reduced intensity of breath sound or a "silent chest" in severe obstruction.

PEF readings may be used in children over 5-6 years of age who are able to cooperate. If the post bronchodilator PEF is less than 60% of the child's previous best or predicted value then the attack is likely to be severe. A normal value is reassuring but low readings may reflect poor technique rather than severe airway obstruction.

Where available pulse oximetry is a useful adjunct to the assessment of severity especially in the younger child. Measurement of blood gases is indicated only in severe asthma when initial aggressive therapy has failed or the child is critically ill at the time of presentation. A chest X-ray is rarely helpful in the initial assessment unless complications such as pneumothorax, pneumonia or lung collapse are suspected.

2. Aims of treatment of acute asthma exacerbations

The aims of treatment of acute asthma exacerbations are to:

3. Management of an acute attack

Drugs that are used for the management of acute asthma are shown in the Table 6. Management of acute asthma will depend on the severity at presentation, the response to therapy, the setting in which the acute attack is managed and the experience of the attending doctor.

There is no one definite way of treating acute asthma. An algorithm for the management of acute asthma is shown in Figure 2. This algorithm is only a suggested mode of therapy. The steps in the management may be modified depending on the facilities available and the experience of the medical staff managing the patient. In some settings, admission of patient to the ward may occur earlier depending on the expertise of the staff and the facilities. Patients who are in the severe category should be observed continuously and be reviewed regularly by experienced staff.

Generally principles of management are discussed below.

                A beta2-agonist administered by nebuliser is the bronchodilator of choice. The
                respiratory solution is diluted in normal saline to a total of 3-4 ml and delivered via
                a nebuliser. If there is a good immediate response to the initial dose of nebulised
                beta2-agonist the child should be kept under observation to ensure that the
                improvement is sustained. Further nebulised beta2-agonist therapy may be needed.
                If response is not sustained hospitalisation is necessary.

                In hospitalised patients nebulised beta2-agonist is required frequently and a dose of
                0.15 mg/kg (maximum 5 mg/dose) can be given every 20 minutes and then at
                longer intervals as the patient improves. If beta2-agonist is required frequently it
                should be administered together with systemic steroids and preferably oxygen at
                6-8 l/min.
                Beta2-agonists may also be delivered via continuous nebulisation or via the
                parenteral route in the more severe cases in which close monitoring is necessary.

                In moderate or severe acute asthma hypoxaemia is often present. Supplementary
                oxygen by face mask or headbox is mandatory to correct hypoxaemia and relieve

                If the attack is severe or if there is a poor response to initial treatment with
                nebulised beta2-agonist therapy a short course of a systemic corticosteroid should
                be administered. Children on doses of greater than 400 microgrammes per day of
                inhaled steroids usually require systemic steroids for the management of the acute
                episode. Early administration of systemic corticosteroids has been shown to reduce
                markedly both the rate and the duration of hospitalisation. Parenteral steroids are
                not more effective than oral steroids but are indicated if the child does not tolerate
                oral therapy.

                Ipratropium bromide has been shown to give additional bronchodilatation when
                added to nebulised beta2-agonists. Addition of ipratropium bromide may be
                considered when response to therapy with a combination of corticosteroids,
                frequent beta2-agonists and oxygen is inadequate.

                Oral theophylline is not indicated in the management of acute asthma. The role of
                intravenous aminophylline is being debated. Adverse effects of the drug may
                outweigh any additional benefits. Thus it should be used with caution in those not
                responding adequately to beta2-agonist and systemic corticosteroids or those who
                are critically ill.

4. Monitoring

Patient can be monitored using the guidelines in Table 4.

5. Intensive care

Assiated ventilation may be required for a small number of cases who are hypoxic, hypercapnoeic or exhausted.

6. Other treatment

Intravenous fluids are rarely required and are reserved for the critically ill child. Antibiotics are indicated only in patients suspected of having bacterial infection. Inhaled mucolytics and antihistamines are of no benefit. Sedatives should be avoided.

Preventive medications can be continued during the acute attack provided the child can manage to inhale the medications; otherwise they can be discontinued temporarily. Presentation with an acute attack of asthma should be used as an opportunity to reevaluate the management of the child's asthma.


The response to treatment should be monitored by regular clinical assessment. The importance of follow-up visits should be stressed to patients.

In children requiring moderate to high doses of inhaled steroids and in those with severe unstable asthma continued daily recordings of symptoms and, where possible, measurements of PEF may be useful adjuncts to clinical assessments. Growth of the children should be monitored.


Children with frequent episodic or severe asthma and their care givers should be educated to recognise early warning signs of deterioration of asthma control, for example failure to respond to usual doses of bronchodilators.

An individually written action plan is recommended. This should include instructions on recognising and dealing with an acute attack highlighting the importance of seeking medical help early in severe or unresponsive attacks.

Children at risk of severe asthma attacks should have a prearrangement made for easy access to emergency treatment by their family doctors or at the nearest health centres or hospitals. "Fast lane" facilities should be established in all emergency departments to cater for these children. Alternatively a self-admission letter should be provided to these children. Every action plan should be reviewed after an acute attack.


1. Azizi BHO. Respiratory symptoms and asthma in primary school children in Kuala Lumpur. Acta Paediatr Japon 1990; 32: 183-7.
2. Speight ANP, Lee DA, Hey EN. Underdiagnosis and undertreatment of asthma in childhood. Br Med J 1983; 286: 1253-56.
3. Sears MR, Ros HH, Fenwick J et al. Deaths from asthma in New Zealand. Arch Dis Child 1986; 61: 6-10.
4. Norzila MZ, Azizi BHO. Cystic fibrosis in Malay children. Singapore Med J (in press).
5. Azizi BHO, Henry RL. Peak expiratory flow rate of Malaysian children. Med J Malaysia 1991; 46: 82-7.
6. Azizi BHO, Henry RL. Ethnic differences in normal spirometric lung function of Malaysian children. Respir Med 1994; 88: 349-56.
7. Beasley R, Roche WR, Roberts JA, Holgate ST. Cellular events in the bronchi in mild asthma and after bronchial provocation. Am Rev Respir Dis 1989; 139: 806-17.
8. Howell JH, Flaim T, Lung CL. Asthma patient education. Pediatric Clin North Am 1992; 39: 1343-61.
9. Taggart VS. Implementation of the guidelines: a patient's perspective. Eur Respir Rev 1995; 5: 112-5.
10. National Research Council. Environmental tobacco smoke: measuring exposures and assessing health effects. National Academy Press, Washington DC, 1986.
11. Samet JM, Marbury MC, Spengler JD. Health effects and sources of indoor air pollution. Part I. Am Rev Respir Dis 1987; 136: 1486-1508.
12. Azizi BHO, Henry RL. The effects of indoor environmental factors on respiratory illness in primary school children in Kuala Lumpur. Int J Epidemiol 1991; 20: 144-50.
13. Azizi BHO, Henry RL. The effects of indoor air pollution on lung function of primary school children in Kuala Lumpur. Pediatr Pulmonol 1990; 9: 24-9.
14. Azizi BHO, Zulkifli I, Kasim MS. Indoor air pollution and asthma in hospitalised children in a tropical environment. J Asthma 1995; 32: 413-8.
15. Chew YY, Ton SH, Azizi O, Noriah R. Urinary cotinine as a measure of tobacco smoke exposure in children with respiratory diseases. Malaysian J Lab Sc 1993; 10: 61-4.
16. Saarinen U.M., Kajosaari M. Breastfeeding as prophylaxis against atopic disease: prospective follow-up study until 17 years old. Lancet 1995; 346:1065-9.


We wish to acknowledge with thanks the support of the following companies when we were preparing the consensus :

Glaxo Wellcome (M) Sdn Bhd.
Astra Pharmaceutical (M) Sdn. Bhd.
3M Malaysia Sdn Bhd
Boehringer Ingelheim Div., Diethelm Malaysia Sdn. Bhd.
Summit Co. (M) Sdn. Bhd.
Rhone Poulenc Rorer (M) Sdn. Bhd.



Mean FEV16 And PEF5 of Normal Malaysian Children (Click here)


Summary of Management of Asthma (Click here)


Algorithm For Management of Acute Asthma In Children (Click here)


Assessment of Severity In Childhood Asthma (Click here)


Useful Measures To Reduce Exposure To House Dust Mites (Click here)


Drug Dosages In Asthma (Click here)


 Drug Delivery System For The Inhaled Route Recommended For Different Ages
(Click here)


 Asessment of Severity of Acute Asthma (Click here)


Drug Dosages In Acute Asthma (Click here)