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ACADEMY OF MEDICINE OF MALAYSIAMALAYSIAN THORACIC SOCIETY

A JOINT STATEMENT OF THE

REVISED 2002

MINISTRY OF HEALTH MALAYSIA

CLINICAL PRACTICE GUIDELINES

FOR MANAGEMENT OFADULT ASTHMA

CLINICAL PRACTICE GUIDELINES

FOR MANAGEMENT OFADULT ASTHMA


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COMMITTEE MEMBERS:

Zainudin Md. Zin, FRCP (Chairman)

Damansara Specialist Hospital, Selangor

Aziah Ahmad Mahayiddin, FCCP

Hospital Kuala Lumpur

Abdul Wahab Sufarlan, FRCP

Ampang Puteri Specialist Hospital, Selangor

Hooi Lai Ngoh, FRCP

Hospital Pulau Pinang, Pulau Pinang

George Kutty Simon, FRCP

Hospital Alor Setar, Kedah

Kuppusamy Iyawoo, FRCP

Institute of Respiratory Medicine, Kuala Lumpur

Kwa Siew Kim, FRACGP

Academy of Family Physicians, Malaysia

Leong Kwok Chi, FRACGP

Academy of Family Physicians, Malaysia

Liam Chong Kin, FRCP

University Malaya Medical Centre, Kuala Lumpur

Roslan Harun, PhD

Hospital Universiti Kebangsaan Malaysia, Kuala Lumpur

Wong Wing Keen, MRCP

Sunway Medical Centre, Selangor


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Foreword

Asthma is a major global health problem. Its prevalence is increasing everywhere both in

children and adults. The World Health Organization (WHO) estimated in 1998 that asthmaaffected 155 million people worldwide. In Malaysia, it is estimated about 1.5-1.8 million

people are affected by the disease. The burden of asthma on economy is considerable

both in terms of direct medical costs such as hospitalization and pharmaceuticals and

indirect medical costs such as time lost from work and premature deaths. Asthma

morbidity too is considerable with many patients have symptoms that affect their quality of

life such as sleep, exercise and social activities. Asthma accounted for 0.4% of all deaths,

or 1 in 250 and many of these deaths were thought to be preventable if asthma was

managed properly or patients acted appropriately. The morbidity and economic burden of

asthma can be substantially reduced if asthma is under control and one way to achieve

that is to equip doctors with the necessary knowledge on asthma management.

Guidelines for management of adult asthma was first published by the Malaysian Thoracic

Society in 1996 with the aim of providing up-to-date information on asthma management

for doctors at all level of care. Several years have gone and many new findings and

scientific information are now available which necessitates the revision of the guidelines.

It is a privilege for me to be able to work with a group of highly dedicated and motivated

people to revise these guidelines. I wish to acknowledge the good work of the committee

members who had contributed towards the success of the revision and the contribution of

others through their comments.

The revision of the guidelines and the activities for the dissemination of the document

were conducted through educational grants from AstraZeneca, Boehringer Ingelheim,

GlaxoSmithKline and Merck Sharp & Dohme. I wish to express my gratitude and thanks to

these companies for their generous support. The committee members are however, solely

responsible for the statements and conclusions presented in this document. These

guidelines are meant to serve as guides and doctors are expected to use their best

judgement and act accordingly when treating their patients based on patients clinical

conditions, the availability of facilities and resources.

Zainudin Bin Md Zin, MD,FRCP,FCCP,FAMM

Chairman of the Committee

Guidelines for Management of Adult Asthma (Revision 2002)


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Contents

Foreword

Introduction

1. EPIDEMIOLOGY

2. DEFINITION

3. PATHOGENESIS

4. DIAGNOSING ASTHMA

5. MANAGEMENT OF CHRONIC ASTHMA

5.1 The aims of management

5.2 Approach to management

5.3 Drug treatment

5.3a Anti-inflammatory medications

5.3b Long acting bronchodilators

5.3c Short acting bronchodilators

5.4 Drug delivery

6. EDUCATION OF PATIENT AND FAMILY

7. AVOIDANCE OF PRECIPITATING FACTORS

8. ASSESSMENT OF SEVERITY AND RESPONSE TO TREATMENT

8.1 Clinical assessment

8.1a Measuring peak expiratory flow (PEF)

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Long acting beta2-agonists(i)

(ii) Sustained-release theophyllines

(iii)

Corticosteroids(i)

(ii) Cromones

Antileukotrienes

Beta2-agonists(i)

(ii) Anticholinergic drugs

(iii) Methylxanthines

(iv) Other treatment


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9. APPROACH TO DRUG THERAPY - STEPWISE APPROACH

10. RESCUE COURSE OF STEROID TABLETS

11. FOLLOW-UP AND MONITORING

12 MANAGEMENT OF ASTHMA IN PREGNANCY

12.1 Introduction

12.2 Management

12.3 Labour

12.4 Breastfeeding

13. GUIDELINES FOR THE MANAGEMENT OF ACUTE ASTHMA

IN ADULTS

13.1 Aims of management

13.2 Assessment

13.3 Features of mild asthma attack

13.4 Features of moderately severe asthma attack

13.5 Features of very severe asthma attack

13.6 Features of life-threatening asthma

14. MANAGEMENT OF ACUTE ASTHMA IN AN OUTPATIENT SETTING

(i) INITIAL PEF >75% (Mild acute asthma)

(ii) INITIAL PEF < 75% (this includes moderately severe to life-

threatening asthma)

15. SUBSEQUENT MANAGEMENT IN THE WARD

15.1 Monitoring the response to treatment

15.2 Other investigations

16. MANAGEMENT IN INTENSIVE CARE UNIT

17. DISCHARGE PLAN FOR HOSPITALISED PATIENT

18. MANAGEMENT OF ACUTE ASTHMA IN GENERAL PRACTICE

Appendix 1 Example of a written asthma management plan

Appendix 2 PEF normogram

References

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Asthma is a common disease causing significant morbidity and mortality worldwide. With

appropriate treatment and care most of this morbidity can be avoided and many deaths

attributable to asthma can be prevented. Since the last decade, clinical practice guidelineshave become an important tool to improve knowledge in the management of various

common diseases including asthma. In 1995, the Malaysian Thoracic Society set up an

expert committee to work on the guidelines for the management of asthma in adults with

the aim of providing up-to-date information on asthma management to health care

providers taking into account local practices and the availability of resources. The

guidelines were completed and published in 1996 and circulated to doctors working in the

government and private sector. Since then many new findings and advances have been

made in asthma management which necessitated the revision of the guidelines.

In one of its council meetings, the Malaysian Thoracic Society decided to invite all the

previous expert committee members to once again sit in the new committee to revise the

guidelines. In addition, a few new members including two representatives from the

Academy of Family Physicians of Malaysia were invited to ensure views of family

physicians were given due consideration. The committee held four meetings, each for

duration of one and a half days on 4 weekends from early 2000. The committee was

divided into 4 groups and each group was responsible to revise its assigned section.

Group 1 covered epidemiology, definition, pathogenesis and diagnosis; group 2 covered

non-pharmacological management, assessment of severity and asthma in pregnancy;

group 3 covered pharmacotherapy and drug treatment of chronic asthma; and group 4

covered management of acute asthma.

Unlike the first guidelines, in which treatment recommendations were mainly by

consensus, the present guidelines emphasised recommendations based on scientific

evidence as far as possible. Members had agreed to assign levels of evidence tostatements based on the system developed by the National Heart, Lung and Blood

Institute, Maryland, USA (Table A). The draft of the guidelines was circulated to members

of the Malaysian Thoracic Society and selected physicians for their comments. The

guidelines were also discussed at a Clinical Practice Guidelines Workshop jointly

organised by the Ministry of Health and the Academy of Medicine of Malaysia on October

12, 2002. The revised draft was circulated again to the expert committee after all the

comments from the reviewers were deliberated before the document was sent to Health

Technology Assessment Unit, Medical Development Division, Ministry of Health for

approval for adoption as national policy prior to publication and distribution.

The committee realised that an effective mechanism for dissemination of the guidelines is

important to ensure that the guidelines reach as many practitioners as possible and a

follow up study is needed to determine its effectiveness.

Introduction

i


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ii

Table A: Description of Level of Evidence

Sources of EvidenceEvidence

CategoryDefinition

Randomised controlled trials(RCTs). Rich body of data.

A Evidence is from endpoints of welldesigned RCTs that provide a consistentpattern of findings in the population forwhich the recommendation is made.Category A requires substantial numbersof studies involving substantial numbers ofparticipants.

Randomised controlled trials

(RCTs). Limited body of data.B Evidence is from endpoints of

intervention studies that include only

limited number patients, post hoc or

subgroup analysis of RCTs, or meta-

analysis of RCTs. In general, category

B pertains when few randomised trials

exist, they are small in size, they were

undertaken in a population that differs

from the target population of the

recommendation, or the results are

somewhat inconsistent.

Nonrandomised trials.

Observational studies.C Evidence is from outcomes of

uncontrolled or nonrandomised trials or

from observational studies.

Panel consensus judgement.D This category is used only in caseswhere the provision of some guidance

was deemed valuable but the clinical

literature addressing the subject was

insufficient to justify placement in one of

the other categories. The panel

consensus isbasedonclinicalexperience or knowledge that does not

meet the above-listed criteria.


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mucosal oedema and increased

vascular permeability

1. EPIDEMIOLOGY

Asthma is a common disease with unacceptably high morbidity and mortality. Asthma

prevalence is increasing worldwide and it is commonly under diagnosed and under-

treated. In a large survey of asthmatics in 8 areas in the Asia Pacific region, only 13.6% of

respondents were on inhaled corticosteroids despite almost half of them having symptoms

of persistent asthma1. Many asthma deaths and morbidity have been associated with

inadequate treatment, under-use of objective measurement of severity and inadequate

supervision2-4.

In Malaysia, the prevalence of asthma in primary school children is reported as 13.8%5

and in children aged 13-14 years is 9.6%6 . The prevalence of self-reported asthma in

adults as reported in a Ministry of Health Second National Health and Morbidity Survey is

4.1%7. In the same study, the Chinese recorded significantly lower prevalence of asthma

(2.4%) than other races (5.6%). This survey and other studies also confirmed under-

diagnosis of the disease, inappropriate treatment and under-use of peak flow

measurements8,9. Only 36.1% of adult asthmatics ever had their peak flow measured.

The survey also reported that the prevalence of asthma was higher in rural (4.5%) than in

urban areas (4.0%)7. There was a higher prevalence of asthma in those with lower

educational status (5.6%) and lower income (4.7%). The majority of patients (87.3%) had

mild asthma; 9.9% had moderate asthma and 2.7% had severe asthma. Among the

severe asthmatics, only 19.4% were on inhaled corticosteroids. The duration of days ill

due to asthma was 4.2 days per episode while days off work or school were 2.4 days per

episode, indicating significant morbidity and socio-economic impact of the disease.

2. DEFINITION

Asthma, irrespective of severity, is a chronic inflammatory disorder of the airways10. This

has implication in the diagnosis, management and prevention of the disease. Insusceptible individuals, this inflammation causes recurrent episodes of wheezing,

breathlessness, chest tightness and cough particularly at night and in the early morning.

These episodes are usually associated with widespread but variable airflow obstruction

that is often reversible either spontaneously or with treatment.

3. PATHOGENESIS

The inflammatory features of asthma include:

1

denudation of airway epithelium

collagen deposition beneath

the basement membrane

hypertrophy and hyperplasia of bronchial

smooth muscles and mucus glands


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2

inflammatory cell infiltration and activation of

Airway inflammation contributes to bronchial hyper-responsiveness, airflow limitation,

respiratory symptoms and disease chronicity. Acute inflammation causes airwayobstruction as a result of smooth muscle bronchospasm, mucosal oedema and mucus

plug formation. Persistent chronic airway inflammation may result in airway remodeling

which leads to irreversible bronchial obstruction. Atopy, the genetic predisposition for the

development of an IgE-mediated response to common allergens, is the strongest

identifiable predisposing factor for developing asthma.

4. DIAGNOSING ASTHMA

Consider asthma if any of the following signs or symptoms are present:

Wheezing high-pitched whistling sounds when breathing out (A normal chest examination does not exclude asthma).

History of any of the following:

Note: Eczema, hay fever, or a family history of asthma or atopic diseases is often associated with

asthma.

Symptoms occur or worsen at night/early morning, awakening the patient Symptoms occur or worsen in the presence of:

Reversible and variable airflow limitation-as measured by a peak expiratory flow (PEF) meter in any of the following ways:

PEF increases more than 15% 15 to 20 minutes after inhaling a short-acting

beta2-agonist, or PEF varies more than 20% from morning measurement upon arising to

measurement 12 hours later in patients who are taking a bronchodilator (more

than 10% in patients who are not taking a bronchodilator), or

PEF decreases more than 15% after 6 minutes of running or exercise

cough, worse particularly at

night/early morning

recurrent wheeze

recurrent difficulty in breathing recurrent chest tightness

neutrophils-

mast cells-

eosinophils-

T and B lymphocytes-

cytokine production

exercise respiratory tract infection

animals smoke (tobacco, wood)

pollen changes in temperature

aerosol chemicals drugs (aspirin, beta blockers)

dust mites (in mattress, pillows,

upholstered furniture, carpets)

strong emotional expression

(laughing or crying hard)


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5. MANAGEMENT OF CHRONIC ASTHMA

5.1 The aims of management are

To abolish day and night symptoms of asthma

To restore normal or best possible long term airway function To prevent most acute attacks To prevent mortality

5.2 Approach to management

In order to achieve those aims the approach to management should include:-

Educating patient and family members Identifying and avoiding trigger factors Assessing severity and monitoring response to treatment Selecting appropriate medications and using the lowest effective dose to

minimise short and long term side effects

5.3 Drug treatment

There are 3 major groups of medications to treat asthma (refer to table 1)

a) Anti-inflammatory medications

b) Long-acting bronchodilators

c) Short-acting bronchodilators

5.3a) Anti-inflammatory medications

As asthma is a chronic inflammatory condition, anti-inflammatory drugs should be

a logical treatment for most patients except for those with intermittent asthma.

Reducing the inflammation will decrease bronchial hyper-responsiveness. The

types of anti-inflammatory medications include:

(i) Corticosteroids

Corticosteroids are the main prophylactic drugs in adult asthmatics11-15

(Evidence A). They should be taken by inhalation and the dosage should be kept

to a minimum to reduce side effects (usually local side effects)16. Long-term oral

steroids may be required for severe persistent asthma.

(ii) Cromones

This group of medications is safe with no significant side effects. It is given by

inhalation (powder Spinhaler or metered dose inhaler). It is effective in the

symptomatic and prophylactic management of mild persistent asthma but less

effective than inhaled corticosteroids in more severe asthma17-20(Evidence A).

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(iii) Antileukotrienes

This new group of anti-inflammatory medication has been shown to have some

effect in controlling mild persistent asthma21(Evidence A). Compared to low

dose inhaled corticosteroids they have similar efficacy in reducing the rate of

asthma exacerbations but low dose inhaled corticosteroids appear to be more

effective in improving lung function, quality of life, reducing symptoms and the

need for rescue beta2-agonists22(Evidence A). They have also been shown to

reduce the requirement for high doses of inhaled corticosteroids23(Evidence B).

They may also be used for aspirin sensitive asthma24(Evidence A) and exercise-

induced asthma25(Evidence B).

5.3b) Long-acting bronchodilators

These medications should be used concomitantly with anti-inflammatory

medications for long-term control of symptoms. This group consists of long-

acting beta2-agonists and sustained-release theophyllines.

(i) Long-acting beta2-agonists

Long-acting beta2-agonists should be used in combination with inhaled

corticosteroids. The combination of long-acting beta2-agonists with inhaled

corticosteroids usually gives more effective control than increasing the dose of

inhaled corticosteroids alone26-31

(Evidence A).

These medications, except formoterol, are not recommended for treatment of

acute symptoms or exacerbations32.

Fixed dose combination inhaler of corticosteroid with long-acting beta2-agonists

(e.g. fluticasone/salmeterol, budesonide/formoterol) improves patient compliance

and hence control.

(ii) Sustained-release theophyllinesThis group of drugs may be used with inhaled corticosteroids for persistent

asthma when long-acting beta2-agonists are not available. Their usefulness is

limited by variable metabolism and a narrow therapeutic window. Sustained

release preparations may be used in nocturnal asthma33,34(Evidence B).

5.3c) Short-acting bronchodilators

These medications are used to relieve symptoms of acute asthma. They should

be used as required rather than regularly. This group consists of beta2-agonists,anticholinergic drugs and methylxanthines.


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(i) Beta2-agonists

These drugs are the most effective bronchodilators available. They are safe with

few side effects when taken by inhalation. The therapeutic effect is felt within a

few minutes of inhalation.

(ii) Anticholinergic drugsInhaled anticholinergics have slower onset but longer duration of action than

short-acting beta2-agonists. In asthma, they are generally weakerbronchodilators

than beta2-agonists. They have few side effects.

(iii) Methylxanthines

These drugs are available in oral and parenteral forms. Parenteral forms are

used in the management of acute severe asthma. Oral short-acting theophyllines

have limited role in the management of asthma.

NB: Inhaled beta2-agonists are the bronchodilator of choice. As far as

possible avoid using anti-cholinergics or xanthines as first line

bronchodilator drugs.

(iv) Other treatment

Anti-histamines including ketotifen have been shown to be of limited efficacy in

many clinical trials in asthma35-37. The role of hyposensitisation or allergen-

specific immunotherapy has been studied but the results are conflicting38-40. At

the moment it cannot be recommended as standard treatment.

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Table 1. Types Of Asthma Medications

Table 1a ANTI-INFLAMMATORY MEDICATIONS

Generic namesDrug class Side effects Remarks

(i) Corticosteroids Inhaled:

Beclomethasone

Budesonide

Fluticasone

Inhaled:

Oral candidiasis and

dysphonia. More than

1 mg a day may be

associated with skin

thinning, easy bruising,

adrenal suppression and

cataracts (Evidence C).

Inhaled:

Potential but small risk of

side effects is outweighed by

efficacy. Spacer devices and

mouth washing after

inhalation decreases oral

candidiasis.

(ii) CromonesSodium

cromoglycate

None or minimal May take 4-6 weeks to

achieve maximum effect.

(iii) Anti-

leukotrienes

Montelukast Possible elevation of liver

enzymes and bilirubin

Possible role as an

alternative to low dose

inhaled corticosteroids an

as add-on therapy to

inhaled corticosteroids.

Oral:

Prednisolone

Dexamethasone

Oral:

Long-term use may

lead to osteoporosis,

hypertension, diabetes,

cataracts, adrenal

suppression, obesity,

skin thinning and myopathy.

Oral:

If used long term, alternate

day morning dosing

produces less toxicity. For

short-term use, a 3 to 10

day course is effective for

gaining control.

Parenteral:

Hydrocortisone

Methylprednisolone

Parenteral:

To be used only in the

treatment of acute severe

asthma.


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Nausea, vomiting,

headache, tremor and

insomnia. Serious side

effects such as seizures

and arrhythmias can occur

especially at higher serum

concentrations.

Table 1b LONG-ACTING BRONCHODILATORS


(i) Long-acting

beta2-agonists

Inhaled:

Formoterol

Salmeterol

Inhaled:

Beta2-agonists have fewer

side effects than oral

formulations.

Inhaled:

These formulations are not

to be used to treat acute

attacks with the exception

of formoterol.

(ii) Long-acting

methylxanthines

Sustained-release

theophylline

Serum theophylline levels

should be monitored when

high doses are used and in

special circumstances,

eg. liver failure and cardiac

failure. Interactions with

other drugs such as

cimetidine,macrolides and

rifampicin can occur.

Oral:

Bambuterol

Salbutamol SR

Terbutaline SR

Clenbuterol

Oral:

Oral beta2-agonists may

cause tachycardia,

palpitations, tremors,

anxiety, headache and

hypokalaemia.

Should always be used in

combination with inhaled

corticosteroids.

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Table 1c SHORT-ACTING BRONCHODILATORS


(i) Short-acting

beta2-agonists

Salbutamol

Terbutaline

Fenoterol

Beta2-agonists may cause

tachycardia, tremor and

irritability. Inhaled beta2-

agonists have fewer side

effects than oral and

parenteral preparations.

Drugs of choice for relief of

acute bronchospasm. Inhaled

route has faster onset and is

more effective than oral route.

Parenteral salbutamol or

terbutaline may be used in

acute severe attacks.

(ii) Anti-

cholinergics

Ipratropium

bromide

Minimal mouth dryness. May provide additive effect

to beta2-agonists. Onset of

action is slower.

(iii) Short-acting

methylxanthines

Short acting

theophylline

Nausea, vomiting,

headache, tremor and

insomnia. Serious side

effects such as seizures

and arrhythmias can occur

especially at higher serum

concentrations.

May be used if beta2-agonists

are not available.

(iv) Nonselective

adrenergic

agonists

Adrenaline/

epinephrine

injection

Similar but more

significant side effects

than beta2-agonists.

Not recommended for treating

asthma attacks if beta2-

agonists are available.

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9

5.4 Drug delivery

The inhaled route is preferred for beta2-agonists and steroids as it produces the same

benefit with fewer side effects as compared to the oral route. In addition, inhaled

medications exert their effects at lower doses41,42. The pressurised metered dose inhaler

(MDI) is suitable for most patients as long as the inhalation technique is correct.

For patients with poor coordination, alternative methods for drug inhalation include spacer

devices, dry powder inhalers and breath-actuated pressurised MDI42-47.

The nebulised route is preferred in the management of acute attacks.

6. EDUCATION OF PATIENT AND FAMILY

This is an important but often neglected aspect in the management of asthma. It isessential in ensuring the patients cooperation and compliance with therapy. As far as

possible patients and their families should be encouraged and trained to actively

participate in the management of their own asthma. Patient education should include the

following information:

Nature of asthma

Preventive measures/avoidance of triggersDrugs used and their side-effects

Proper technique of using inhaled drugs

Peak flow monitoring

Knowledge of the difference between relieving and preventive medications

Recognition of features of worsening asthma (increase in brochodilator requirement,

development of nocturnal symptoms, deteriorating peak flow rates)

Self management plan (appendix 1)

The danger of non-prescribed self medication including certain traditional medicines

i.

ii.iii.

iv.

v.

vi.

vii.

viii.

ix.


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7. AVOIDANCE OF PRECIPITATING FACTORS

Exposure of asthmatic patients to irritants and allergens to which they are sensitive has

been shown to increase asthma symptoms and precipitate asthma episodes.

Table 2. Common Asthma Triggers

Beta blockers1 Avoid using beta-blockers (Evidence C)

Tobacco smoke

(active or passive

smoking)

2 Stay away from tobacco smoke. Patients should not smoke

Air pollution3 Physical exertion should be avoided when levels of airpollution are high (Evidence C)

House dust mites4 Avoid whenever possible but current chemical and physicalmethods aimed at reducing exposure seem to be ineffectiveand cannot be recommended as prophylaxis for mitesensitive asthmatics48(Evidence A)

Allergens fromanimals with fur5

Remove animals from the home, or at least from thesleeping area (Evidence C)

Physical activity6 Do not avoid physical activity. Symptoms can be preventedby taking short or long-acting inhaled beta2-agonist atappropriate time before strenuous exercise

Aspirin and

nonsteroidalanti-inflammatory

drugs

7 Adult patients with severe persistent asthma, nasal polypsor a history of sensitivity to aspirin or nonsteroidalanti-inflammatory drugs should be counseled regarding

the risk of severe and even fatal exacerbations from usingthese drugs (Evidence C)

Other identifiedallergens e.g. food,

pollen, cockroachallergen

8 Should be avoided whenever possible (Evidence C)

Occupationalexposure

9 Change of occupation may be necessary (Evidence C)

Rhinitis, sinusitis and

gastroesophagealreflux

10 These conditions should be treated (Evidence C)

Trigger factors Recommendations


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11

8. ASSESSMENT OF SEVERITY AND RESPONSE TO TREATMENT

Assessment shouldbe done as follows:

8.1 Clinical assessment

This should include patients symptoms, sleep disturbances, disturbance ofdaily activities and the frequency of bronchodilator drug and/or rescue courses of steroid used.

Table 3. Classification of Asthma Severity

> 80% predicted

Variability 20-30%

Symptoms

CLASSIFICATION OF ASTHMA

SEVERITY

BEFORE TREATMENT

SeverePersistent

DailyFrequent exacerbationsLimitation of physical activity

Frequent < 60% predicted

Variability> 30%

Moderate

PersistentDailyDaily use of beta2-agonistExacerbations affect activityand sleep

> 1 time aweek

> 60% - < 80%predicted

Variability > 30%

MildPersistent

> 1 time a weekbut < 1 time a dayExacerbations may affectactivity and sleep

> 2 times amonth

Intermittent < 1 time a weekBrief exacerbations

Asymptomatic andnormalPEF between exacerbations

< 2 times amonth

> 80% predicted

Variability < 20%

PEF

Night time

Symptoms


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a. Measuring peak expiratory flow (PEF)

This can be measured by a peak flow meter.

PEF Measurements

(i) During periods of well-being

This allows measurement of the patients best PEF valuewhich will provide the target for

the doctor and the patient to aim for. Twicedaily measurements (morning andevening)

before any inhaled bronchodilator treatment will determine the diurnal variability of airway

calibre. This is calculated as the range divided by the highest value and expressed as a

percentage.

PEF (max) PEF (min) x 100 = _______ % PEF (max)

Good control of asthma means PEF variability is maintained at less than 10%.

(ii) During symptomatic episodes

During an attack of asthma PEF fairly accurately measures the degree of bronchospasm.

A PEF of less than50% of normal orbest suggests a very severe attack and a PEF of less

than 30% suggests a life-threatening attack. When the best PEF value is not known, a

single reading of less than 200 L/min usually indicates a severe attack.

In addition to history and physical findings the PEF helps the doctor decides on the

appropriate therapy. As far as possible patients with moderate and severe persistent

asthma should regularly measure their PEF twice a day. Comparison to local normal

values should be made49 (appendix 2). The classification of asthma severity based on

symptoms, bronchodilator usage and PEF reading is summarised in Table 3.

9. APPROACH TO DRUG THERAPY - STEPWISE APPROACH

Treatment should be carried out in a stepwise manner. Patients should be started on

treatment at the step most appropriate for the initial severity of their condition (Table 4).

Treatment would then be changed (stepped-up or stepped-down) according to their

progress.


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Table 4. Treatment of Adult Asthma

13

Long-Term Preventive Quick-Relief

Daily medications:

Inhaled corticosteroid*, 800-2000 mcg, and

Long-acting bronchodilator: eitherinhaled

long-acting beta2-agonist and/or sustained-

release theophylline, and/or oral long acting

beta2-agonist, and

Oral corticosteroid long term

Short-acting bronchodilator:

inhaled beta2-agonist as

needed for symptoms

Daily medications:

Inhaled corticosteroid*,500-1000 mcg AND,

if needed

Long-acting bronchodilator: eitherinhaled

long-acting beta2-agonist, sustained-release

theophylline, or oral long acting beta2-agonist

(Inhaled long-acting beta2-agonist may provide

more effective symptom control when added to

low-medium dose steroid compared to

increasing the steroid dose)

Consider adding anti-leukotriene, especially for

aspirin-sensitive patients and forpreventing

exercise-induced bronchospasm



needed for symptoms

Daily medications:

EitherInhaled corticosteroid*, 200-500 mcg,

or cromoglycate or sustained-release

theophylline or anti-leukotrienes



needed for symptoms

None needed Short-acting bronchodilator:


needed for symptoms, but less

than once a week

Inhaled beta2-agonist or

cromoglycate before exercise

or exposure to allergen

TREATMENT OF ADULT ASTHMA

Preferred treatments are in bold print

Patient education is essential at every step

STEP 4

Severe

Persistent

STEP 3

Moderate

Persistent

STEP 2

Mild

Persistent

STEP 1

Intermittent


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14

*Inhaled corticosteroid: Beclomethasone dipropionate (BDP) or budesonide.

Forfluticasone the equivalent dose is half of BDP/budesonide.

Step down

Patients should be reviewed regularly. When the patients condition hasbeen stable for 3-6

months, drug therapy may be stepped down gradually. The monitoring of symptoms and

peak flow rate should be continued during drug reduction.

10. RESCUE COURSE OF STEROID TABLETS

Rescue courses of oral steroids may be needed to control exacerbations of asthma at any

step. Indications include:-

(i) Symptoms and peak expiratory flow (PEF) progressively getting worse day by day

(ii) PEF falls below 60% of patients best

(iii) Sleep is frequently disturbed by asthma

(iv) Morning symptoms persist untilmidday despite usual treatment

(v) Diminishing response to inhaled bronchodilators

(vi) Emergency treatment with nebulised or injected bronchodilators is required

Method

Give 30-60 mg of prednisolone immediately. This daily dose can be tapered off overa period

of 7-14 days or stopped abruptly. It is necessary to review the adequacy of the patients

usual medications.

11. FOLLOW-UP AND MONITORING

Follow-up and monitoring include review of symptoms and measurement of lung function.

PEF monitoring at every visit along with review of symptoms helps in evaluating the

patients response to therapy and adjusting treatment (step-up orstep-down) accordingly.

PEF consistently > 80% of the patient's personal best suggests good control.

Regular visits (at 1 to 6 month interval as appropriate)are essential even after control of

asthma is established. At each visit reviewthe following questions:

1) Is the asthma management plan meeting the expected goals?

2) Is the patient using inhalers, spacers or peak flow metercorrectly?

3) Is the patient compliant to the medication and avoiding triggers?

4) Does the patient have any concern?


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15

12. MANAGEMENT OF ASTHMA IN PREGNANCY

12.1 Introduction

In general, during pregnancy, asthma becomes worse in a third of women, is stable in

another third and improves in the remaining third50

. Women should be reassured that theirasthma medication carries less risk to the foetus than a severe asthma attack. Inadequately

treated asthma can cause maternal and foetal hypoxaemia, which leads to complications

during pregnancy and poorer birth outcomes. Poorly controlled asthma is associated with an

increased incidence of low birthweight and premature babies, neonatal hypoxia,

complications during labour, and perinatal and maternal mortality51-54. Hyperemesis

gravidarum, maternal haemorrhage and pre-eclampsia are more common in this group51.

12.2 Management

The management of asthma during pregnancy is similar to that at any other time: treatment

should be aggressive, with the aim of eliminating symptoms and restoring and maintaining

normal lung function. Cooperation between the respiratory physician and obstetrician is

important throughout pregnancy for women with severe asthma.

Beta2-agonists:

There is no evidence ofa teratogenic risk with the commonly used inhaled beta2-agonists

salbutamol, terbutaline and fenoterol. Delayed labour does not occur with bronchodilators

administered by metered-dose inhaler ornebulisation.

Ipratropium bromide:

It appears to be safe for use during pregnancy, as it is poorly absorbed when administered

by the inhaled route.

Salmeterol/formoterol:

These long-acting agents have not been tested extensively in pregnant women.

Theophyllines:

They may aggravate the nausea and gastroesophageal reflux suffered by some pregnant

women and can cause transient neonatal tachycardia and irritability55,56. Teratogenicity has

been shown in animals57,58 and there are occasional case reports of cardiovascular

abnormalities in humans59. However, largerhuman studies have not shown any significant

increase in foetal abnormalities60,61.

Theophylline metabolism may be altered during pregnancy leading to increased serum

levels62.


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16

Sodium cromoglycate:

This drug appears to have no adverse foetal effects.

Inhaled corticosteroids:

Inhaled corticosteroids are the mainstay of treatment in persistent asthma and appear to

have a good safety profile in pregnancy. Although beclomethasone is a known animal

teratogen, its use in pregnant women has not been associated with teratogenicity. The

largest human experience of inhaled corticosteroids is with beclomethasone and it is

therefore the inhaledsteroid of choice in pregnancy63,64.

Experience with fluticasone in pregnancy is limited.

Oral corticosteroids:

These are sometimes necessaryfor severe asthma in pregnancy but usually only forshortperiods. An increased risk of cleft palate has been reported in animals given huge doses of

oral steroids65,66. The results of animal studies should not deter the practising clinician from

using oral corticosteroids if required.

Anti-leukotrienes:

No data is available on theuse of this agent in pregnant women.

12.3 Labour

Women with very severe asthma may be advised to have an elective caesarean section at a

time when their asthma control is good. Symptoms ofasthma during labour are generally

easily controlled with standard asthma therapy.

12.4 Br eastfeeding

Breastfeeding should be continued in women with asthma. Breast milk may contain very

small amounts of the drugs used to treat asthma, but, in general, these are not known to be

harmful to the infant. Corticosteroids are about 90% protein bound in the blood and are not

secreted into breast milk in any significant quantity. Less than 1% of maternal theophylline is

transferred to the infant67.

In general, asthma medications are safe during pregnancy and lactation and the benefits

outweigh any potential risks to the foetusand baby.


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17

13. GUIDELINES FOR THE MANAGEMENT OF ACUTE ASTHMA IN ADULTS

The presentation of a patient with acute asthma requires rapid assessment of its severity so

that the appropriate treatment can be instituted.

Although an acute severe attack of asthma may occasionally develop within afew minutesor hours, it usually occurs against a background of long term poorly controlled asthma that

has been worsening for some days or weeks. The severity of acute asthma attacks is

usually underestimated by patients, theirrelatives and their doctors, mainly due to failure to

assess the condition objectively. Inadequateassessment of such attacks and inappropriate

treatment with over reliance on bronchodilators and underuse of steroids contribute to

morbidity and deaths2,3.

13.1 Aims of management

The aims of management are:

Toprevent death

To relieve symptoms

To restore the patients lung function to the best possible level as soon as possible

To prevent early relapse

13.2 Assessment

The severity of the attack should be assessed by:

History

Physical examination

PEF measurement

13.3 Features of mild asthma attack are:

persistent cough

increased chesttightness

br eathless when walking

normalspeech

pulse rate 75% of predicted orbest value

SpO2 > 95% (on room air)


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18

13.4 Features of moderately severe asthma attack are:

breathless when talking

talks in phrases

pulse rate100-120/min

respiratory rate 25-30 breaths/min loud wheeze

PEF between 50 to 75%of predicted or best value

SpO2 91-95% (on room air)

13.5 Features of very severe asthma attack are:

breathless at rest

talks in words

pulse rate> 120/min

respiratory rate > 30 breaths/min

loud wheeze

PEF


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14. MANAGEMENT OF ACUTE ASTHMA IN AN OUTPATIENT SETTING

(i) INITIAL PEF > 75% (Mild acute asthma)

Give the patients usual inhaled bronchodilatoror nebulised bronchodilator. Multiple doses

(5-20 puffs) ofinhaled bronchodilator using a large volume spacer can be given in place ofnebulised bronchodilator70-72.

Observe for 60 minutes. If the patient shows clinical improvement and PEF remains > 75%,

discharge.

Before discharge:

review adequacy ofusual treatment and step up if necessary according toguidelines fortreatment of chronic persistent asthma

ensure patient has enough supply of medications

check and correct inhaler technique

advise patient to return immediately if asthma worsens

ascertain and address precipitating factors

make sure that patient has a clinic follow-up appointment within 2 weeks

(ii) INITIAL PEF < 75% (this includes moderately severe to life-threatening asthma)

Patients with more severe degrees of acute asthma should be managed as follows:

Immediate treatment with:

a) High concentration oxygen (> 40%)

b) High doses of inhaled beta2-agonist (salbutamol 5 mg or terbutaline 5 mg orfenoterol 5

mg) in combination with anticholinergic (ipratropium bromide 0.5 mg)73-77 (Evidence A)

should be administered via nebuliser driven by oxygen. If compressed air nebuliser is

used, administration of supplemental oxygen should be continued.

Alternatively, beta2-agonists may be given by multiple actuations of a pressurised aerosol

inhaler into a large spacer device (2-5 mg, i.e. 20-50 puffs, five puffs at a time) preferably in

combination with an anticholinergic.

If there is poor response to inhaled bronchodilators, subcutaneous terbutaline or salbutamol

0.25-0.50 mg can be given.

19


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20

c) Prednisolone tablets at 30-60 mg should be commenced immediately. If patient is

unable to tolerate orally, intravenous hydrocortisone 200 mg stat or other forms of

parenteral steroids should be given.

High dose inhaled corticosteroids (2.4 mg budesonide daily in 4 divided doses) has been

shown to achieve a relapse rate similar to 40 mg prednisone daily78

. However, furtherstudies are required to document the potential benefits of inhaled corticosteroids in acute

asthma.

NB: Sedatives should not be prescribed.

Antibiotics are indicated only if there is evidence of bacterial infection. Chest

radiograph shouldbe done ifpneumothorax or pneumonia is suspected.

Assessment of response to initial treatment

The response to treatment is monitored by:

the patients symptoms

physical findings

measurement ofPEF 15-30 minutes after initiating treatment

a) Good response to initial treatment

The patient should:

be relieved of dyspnoea

have improved clinical status

have a post bronchodilator PEF which is > 75% of predicted or best value

b) Incomplete response to initial treatment

The patient has:

persistent symptoms and signs post bronchodilator PEF which is 50-75% of predicted or best value

c) Poorresponse to initial treatment

The patient has:

persistent ordeteriorating symptoms and signs

a post bronchodilator PEF < 50% of predicted orbest value

The subsequent management of patients with an initial PEF < 75% predicted or best value issummarised in Figure 1.


28/42

FIGURE 1

MANAGEMENT 30 MINUTES AFTER INITIAL TREATMENT OF ACUTE

ASTHMA WITH AN INITIAL PEF < 75% PREDICTED OR BEST

NB: Patients requiring admission should preferably be accompanied by a nurse

and/ora doctor.

Before discharge:

give prednisolone 30-60 mg daily for 7-14 days, plus regular inhaled steroids and

inhaled beta2-agonist to be taken as needed

review adequacy of usual treatment and step up if necessary according to

guidelines for treatment of chronic persistent asthma

ensure patient has enough supply ofmedications

check inhaler technique and correct if faulty

arrange for follow-up within 2 weeks

advise patients to return immediately if asthma worsens

NB: Patients should be considered for admission if there is concern over the social

circumstances such as patient staying alone and lack of transport for emergency visit

to hospital.

Good response andPEF > 75% predicted

or best value

Observe for another

60 minutes

If patient is stable or

improving and PEF

remains > 75%,

DISCHARGE

Incomplete response andPEF 50-75% predicted

or best value

Repeat nebulised beta2-

agonist and anticholinergic

1)If PEF is still < 75%, ADMIT

2)If patient improves andPEF > 75%, DISCHARGE

Observe for 60 minutes.

Poor response and PEF


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22

15. SUBSEQUENT MANAGEMENT IN THE WARD

Continue oxygen > 40%

Intravenous hydrocortisone 100-200 mg 6 hourly orprednisolone 30-60 mg daily

Nebulised beta2-agonist 2-4 hourly preferably in combination with anticholinergic (it

may be necessary to give nebulised beta2-agonist more frequently up to every 15minutes)

If patient is still not improving, commence aminophylline infusion (0.5-0.9 mg/kg/

hour); monitor blood levels (where facility is available) if aminophylline infusion is

continued for more than 24 hours. Terbutaline or salbutamol infusion at 3-20 mcg/

min after an initial intravenous bolus dose of 250 mcg over 10 minutes can be

given as an alternative

In cases where response to the above treatment is inadequate, intravenous

magnesium sulphate 2 g in 50 ml normal saline infused over 10-20 minutes may be

given79

15.1 Monitoring the response to treatment

- repeat measurement of PEF 15-30 minutes after starting treatment

- aim to maintain arterial oxygen saturation above 92%

- repeat arterial blood gas measurements if initial results are abnormal or if patient

deteriorate

- monitor PEF at least 4 times daily throughout the hospital stay

15.2 Other investigations

a) Serum electrolytes, as hypokalaemia is a recognised complication of treatment with

beta2-agonists and corticosteroids

b) Electrocardiogram if indicated

Transfer patient to the intensive care unit or prepare to intubate ifthere is:

- deteriorating PEF

- worsening hypoxaemia, or hypercapnia

- exhaustion or feeble respiration

- confusion or drowsiness

- coma or respiratory arrest


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16. MANAGEMENT IN INTENSIVE CARE UNIT

continue with oxygen supplementation

continue with intravenous hydrocortisone

if the patient is mechanically ventilated, administernebulised beta2- agonist with

anticholinergic via the endotracheal tube. This can be given up to every 15-30

minutes

Intravenous aminophylline infusion or terbutaline or salbutamol infusion should be continued

and magnesium sulphate infusion may be added.

17. DISCHARGE PLAN FOR HOSPITALISED PATIENT

Before discharge, the patient should be:

started on inhaled steroids for at least 48 hours in addition to a short course of oral

prednisolone and bronchodilators

stable on the medications he is going to take outside the hospital for at least 24

hours

having PEF of > 75% ofpredicted or best value and PEF diurnal variability of < 20%

able to use the inhalercorrectly and if necessary, alternative inhaler devices could

be prescribed

educated on the discharge medication, home peak flow monitoring and self

management plan (for selected, motivated patients), and the importance of regular

follow up

given an early follow-up appointment within 2-4 weeks for reassessment ofthe

condition and for adjustment ofthe medicines

18. MANAGEMENT OF ACUTE ASTHMA IN GENERAL PRACTICE

The clinic should preferably have facility for oxygen administration and equipment for

resuscitation.

The following are indications for immediate referral to hospital

1. Any life-threatening features

2. Any features of a severe attack that persist after initial treatment

3. PEF 15-30 minutes after nebulisation, which is < 50% of predicted or best value

Threshold forreferral to hospital should be lowered for patients80:

seen in the afternoon or evening rather than earlier in the day

with previous severe attacks, especially if the onset of the current attack was rapid

in whom there is concern over the social circumstances or relatives ability to

respond appropriately

23


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24

FIGURE 2

SUMMARY OF OUTPATIENT MANAGEMENT OF ACUTE ASTHMA

NB:Before discharge ensure that patients treatment plan is reviewed, the medicine is

adequate, the inhaler technique is correct, the appointment for review is given, and

patient is advised to return if condition deteriorates. If patient was given steroids,

continue with oral prednisolone for7-14 days81-84.

Mild acute asthma

PEF > 75% predicted/best

Moderate to severe

acute asthma

PEF < 75%

predicted/best

Give oxygen > 40%

Give nebulised beta2-agonist or

multiple puffs of MDI via a large

spacer in combination with

inhaled ipratropium

Give oral prednisolone

30-60 mg or i.v. hydrocortisone

100-200 mg stat

Give oxygen > 40%

Give nebulised beta2-agonist or

multiple puffs of MDI via a large

spacer in combination with

inhaled ipratropium

Give oral prednisolone

30-60 mg or i.v. hydrocortisone

100-200 mg stat

Life threatening acute asthma

PEF < 30% predicted/best

Give inhaled or nebulised

beta2-agonist

Observe for 60 mins.

If PEF > 75% and

clinically improved,

discharge patient

Good response

PEF > 75% and

clinically improved

Incomplete response

PEF 50-75% with

persistent symptoms

and signs

Poor response

PEF < 50% with

deteriorating or

persistent symptoms

and signs

Give i.v.

aminophylline 250

mg slowly over

20 mins or i.v

terbutaline/salbutamol 0.25 mg

over 10 mins.

AND ADMIT patient

to ICU. Do not give

bolus aminophylline

if patient is on oral

theophylline

Observe for 60 mins.

If PEF > 75%

discharge patient*

Repeat nebulised beta2-

agonist and ipratropium

Observe for 60 mins

Admit patient

PEF > 75%, discharge PEF < 75%, admit

Assess asthma severity clinically and with PEF


32/42

Example ofa written asthma managementplan

Name :

Address :

Tel Numbers

General Practitioner :

Specialist :

Ambulance :

Hospital :

Usual Medication :

1.

2.

3.

4.

Best Peak Flow Reading L/min

25

Appendix 1


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26

YOUR ASTHMA IS WELL CONTROLLED IF:

You have no wheeze, shortness of breath nor cough

You are able to do usual activities

You sleep well

You do not need yourbronchodilator more than once a day

Your peak flow is more than (80% of best)

You should continue your usual medications:

(Preventer):

(Reliever):

Keep your appointment with your doctor.

YOURASTHMA IS UNCONTROLLED IF:

You notice wheeze and difficulty in breathing more than usual during the day

Your usual activities are affected

You wake up once or twice a night with asthma

You need yourbronchodilator more than 2 times a day

Your peak flow is less than (80% of best)

You should increase the dose of

and consult your doctor as soon as possible.

YOUR ASTHMA IS SEVERE IF:

You notice wheeze and difficulty in breathing most of the day

You are unable to carry out usual activities such as talking and walking

You are awake most of the night

You need your bronchodilator more than 6 times a day

Your peak flow is less than (60% of best)

You should take 2-4 puffs of your reliever inhaler and take tablets of

prednisolone ( mg) and seek immediate medical help.


34/42

460

450

440

430

420

410

400

390

380

490

480

470

510

500

520

610

600

590

580

570

560

550

540

530

520

510

500

490

480

470

460

450

440

430

10

20

30

40

50

60

70

53

54

55

59

57

56

58

63

67

68

69

70

64

65

66

60

61

62

71

72

73

140

150

160

170

180

Male SD + 59.4

Female SD + 46.3

PEF normogram

Appendix 2

P.E.F.R.

NOMOGRAM FOR ADULT

CHINESE IN SINGAPORE

(USE HEIGHT & AGE)

Regression

Formula

Male PEF(L/min) - 72.1+9.8 H (ins) - 12 A (yrs)

Female PEF(L/min) - 159+5 H (ins) - A (yrs)

HEIGHTCM INS

FEMALEL/min

MALEL/min

27


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28

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Adult Asthma is supported by educational grants from:

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