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Atos Healthcare 
 
                              
 
 
 
 
 
 

Asthma 
 
 
 
 
 
 
Version 4 Final 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
EBM – Asthma 
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Atos Healthcare 
 
Document control 
 
Version history 
Version Date 
Comments 

Final 
10 
November 
2009 
Signed off by Medical Service Contract 
Management Team, 
4d  
23 October 2009 
Formatting  
4c 5th. August 2009 
External review comments 
4b 2nd. November 2008 
Internal review comments 
4a 8th October 2008 
Initial review changes 
3a Draft 
August 2008 
Initial Draft 
 
 
 
Changes since last version 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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Introduction 
Description 
 
Asthma has been recognised since ancient times.  The term is derived from 
the Greek word meaning “short – drawn breath” or “panting,” and was in use 
in the time of Hippocrates.   
The diagnosis of asthma is a clinical one; there is no standardised definition 
of the 
type, severity, frequency of symptoms, nor of the findings on 
investigation.  This may, in part, account for the reported variability in the 
prevalence of asthma. 
 
Central to all definitions is the presence of symptoms (more than one of 
wheeze, breathlessness, chest tightness, cough) and of variable airflow 
obstruction which are potentially reversible with treatment.  More recent 
descriptions of asthma in children and in adults have included airway hyper-
responsiveness and airway inflammation as components of the disease.1
 
The normal diurnal variation of peak expiratory flow rate (PEFR) is 
increased in people with asthma2
Prevalence 
Comprehensive information on asthma prevalence in the UK is not available3
 
Asthma prevalence is usually estimated from survey data.                        
In children and young adults, wheezing is most commonly used as an 
indicator of asthma although estimates based on wheezing will include 
trivial illness. Estimates based on wheezing alone are unreliable in older 
adults. 
 
12-15% of children suffer episodes of wheezing characteristic of asthma. 
Less than 5% suffer persistent or repeated attacks. 
 
The prevalence of asthma in children increased by about half between the 
early 1970s and mid 1980s but recent trends are less clear cut.             
The proportion of children diagnosed as having asthma increased over 
the last decade.  Childhood asthma is more common in boys.  Following 
puberty females are more often affected. 
 
15-20% of adults experience wheezing, but probably less than 5% suffer 
night time breathlessness or reversible air flow limitation characteristic of 
asthma. 
 
 
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Aetiology
 
Development of asthma is multifactorial and depends on the interactions 
between multiple susceptibility genes and environmental factors. 
 
Susceptibility genes are thought to include those for T-helper 1 and 2 
(TH1 and TH2) cells, IgE, cytokines (IL-3, -4, -5, -9, and -13), granulocyte-
monocyte colony-stimulating factor (GM-CSF), tumour necrosis factor-α 
(TNF-α), and the ADAM33 gene, which may stimulate airway smooth 
muscle and fibroblast proliferation or regulate cytokine production. 
 
Environmental factors may include the following:  
 
Allergen exposure 
 
Diet 
 
Perinatal factors 
 
Evidence clearly implicates household allergens (e.g., dust mite, cockroach, 
and pets) and other environmental allergens in disease development in older 
children and adults. Diets low in vitamins C and E and in ω–3 fatty acids 
have been linked to asthma, as has obesity. Asthma has also been linked to 
perinatal factors, such as young maternal age, poor maternal nutrition, 
prematurity, low birth weight, and lack of breastfeeding. 
 
On the other hand, endotoxin exposure early in life can induce tolerance and 
may be protective. Air pollution is not definitively linked to disease 
development, though it may trigger exacerbations. The role of childhood 
exposure to cigarette smoke is controversial, with some studies finding a 
contributory and some a protective effect. 
 
Genetic and environmental components may interact by determining the 
balance between Th1 and Th2 cell lineages. Infants may be born with a 
predisposition toward pro-allergic and pro-inflammatory Th2 immune 
responses, characterized by growth and activation of eosinophils and IgE 
production. Early childhood exposure to bacterial and viral infections and 
endotoxins may shift the body to Th1 responses, which suppresses Th2 
cells and induces tolerance. Trends in developed countries toward smaller 
families with fewer children, cleaner indoor environments, and early use of 
vaccinations and antibiotics may deprive children of these Th2-suppressing, 
tolerance-inducing exposures and may partly explain the continuous 
increase in asthma prevalence in developed countries (the hygiene 
hypothesis). 
Occupational Factors 
 
(See Section 3 for further details about Occupational Asthma.) 
Pathophysiology4 
 
Asthma involves  
 
Bronchoconstriction 
 
Airway oedema and inflammation 
 
Airway hyper-reactivity 
 
Airway remodelling 
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In patients with asthma, Th2 cells and other cell types—notably, eosinophils 
and mast cells, but also other CD4+ subtypes and neutrophils—form an 
extensive inflammatory infiltrate in the airway epithelium and smooth 
muscle, leading to airway remodelling (i.e. desquamation, sub-epithelial 
fibrosis, angiogenesis, and smooth muscle hypertrophy). Hypertrophy of 
smooth muscle narrows the airways and increases reactivity to allergens, 
infections, irritants, parasympathetic stimulation (which causes release of 
pro-inflammatory neuropeptides, such as substance P, neurokinin A, and 
calcitonin gene-related peptide), and other triggers of bronchoconstriction. 
Additional contributors to airway hyper-reactivity include loss of inhibitors of 
bronchoconstriction (epithelium-derived relaxing factor, prostaglandin E2) 
and loss of other substances called endopeptidases that metabolise 
endogenous bronchoconstrictors. Mucus plugging and peripheral blood 
eosinophilia are additional classic findings in asthma and may be a 
secondary phenomenon of airway inflammation. 
 
Triggers  
 
Common triggers of an asthma attack include  
 
Environmental and occupational allergens (numerous) 
 
Infections 
 
Exercise 
 
Inhaled irritants 
 
Emotion 
 
Aspirin and to lesser extent NSAIDs 
 
Gastroesophageal reflux 
 
Infectious triggers in young children include respiratory syncytial virus 
(RSV), rhinovirus, and para-influenza virus infection. In older children and 
adults, upper respiratory tract infections (URTIs), particularly with rhinovirus, 
and pneumonia are common infectious triggers.  
Exercise can be a trigger, especially in cold or dry environments.  
Inhaled irritants, such as air pollution, cigarette smoke, perfumes, and 
cleaning products, are often involved.  
Emotions such as anxiety, anger, and excitement sometimes trigger attacks. 
Aspirin is a trigger in up to 30% of older patients and in patients with more 
severe asthma. Aspirin -induced asthma is typically associated with nasal 
polyps with nasal and sinus congestion.  
Gastro-oesophageal reflux disease (GORD) is a common exacerbating 
factor in some patients with asthma, possibly via oesophageal acid-induced 
reflex bronchoconstriction or by micro-aspiration of acid.   
Allergic rhinitis often coexists with asthma. It is unclear whether the two are 
different manifestations of the same allergic process or whether rhinitis is a 
discrete asthma trigger. 
 
Response:  
In the presence of triggers, there is reversible airway narrowing and uneven 
lung ventilation. Relative perfusion exceeds relative ventilation in lung 
regions distal to narrowed airways, thus alveolar O2 tensions fall and 
alveolar CO2 tensions rise. Most patients can compensate by 
hyperventilating, but in severe exacerbations, diffuse bronchoconstriction 
causes severe air trapping, and the respiratory muscles are put at a marked 
mechanical disadvantage so that the work of breathing increases.  
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Under these conditions, hypoxaemia worsens and PaCO2 rises.  
Respiratory acidosis (due to increased PaCO2)  and metabolic acidosis (due 
to decreased bicarbonate concentration in extracellular fluid) may result and, 
if left untreated, cause respiratory and cardiac arrest. 
 
An individual’s reaction to allergen exposure characteristically involves two 
phases..  Inhalation of an allergen may result in an early asthmatic reaction 
(type I) 20 minutes after exposure, which usually resolves after an hour.   
A late asthmatic response (type II) can develop after 3 hours, peaking at 6-
12 hours, and persisting for 12-24 hours.  This phenomenon is important 
because it may affect the choice of asthma treatment. 
Occasionally an individual experiences a late response without the early 
reaction. 
 
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Diagnosis 
The diagnosis of asthma is based on the recognition of a characteristic 
pattern of symptoms and the absence of an alternative explanation for them 
(see Table 1). The key is to take a careful clinical history. In many cases this 
will allow a reasonably certain diagnosis of asthma, or an alternative 
diagnosis, to be made.  
If asthma does appear likely, the history should also explore possible 
causes, particularly occupational.  
 
In view of the potential requirement for treatment over many years, it is 
important even in relatively clear cut cases, to try to obtain objective support 
for the diagnosis. Whether or not this should happen before starting 
treatment depends on the certainty of the initial diagnosis and the severity of 
presenting symptoms. Repeated assessment and measurement may be 
necessary before confirmatory evidence is acquired.  
 
Confirmation hinges on demonstration of airflow obstruction varying over 
short periods of time.  Spirometry, which is now becoming more widely 
available, is preferable to measurement of peak expiratory flow because it 
allows clearer identification of airflow obstruction, and the results are less 
dependent on effort. It should be the preferred test where available 
(although some training is required to obtain reliable recordings and to 
interpret the results). It is important to note that a normal spirogram (or PEF) 
obtained when the patient is not symptomatic does not exclude the 
diagnosis of asthma. 
History 
 
Family and Personal History: 
Asthma, Eczema or Hayfever 
When asthma arises in adult life, it may reflect a   
re-activation of childhood asthma.  The period of 
Childhood Asthma: 
‘remission’ may last for several years, but the 
tendency to develop asthma is always present. 
Home environment: 
Smoking and Pets. 
(See 
Occupation: 
Section 6 for further information about 
Occupational Asthma.) 
Triggers: 
Cold Air, Exercise and Emotion 
Response to a Trial of Treatment: 
Symptoms and/or Peak Flow Improve 
 
Examination 
 
Subjects with mild intermittent asthma frequently have no signs or 
symptoms. 
 
Observation may indicate exertional wheezing or wheezing at rest.   
 
Pigeon Chest is a feature of chronic severe asthma.  (Hyper-inflated.) 
 
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Accessory muscles (scalene and sternocleidomastoid muscles in the neck) 
may be seen to be used to aid breathing. 
 
Auscultation may reveal diminished air entry and diffuse bilateral wheeze 
with a prolonged expiratory phase. 
 
Table 1 Clinical features in adults that influence the probability that 
episodic respiratory symptoms are due to asthma 

 
Features that increase the probability of asthma  
 
More than one  of  the following symptoms: wheeze, 
breathlessness, chest tightness and  cough, particularly if: 
 
symptoms worse at night and in the early morning  
 
symptoms in response to exercise, allergen exposure 
and cold air  
 
symptoms after taking aspirin or beta blockers  
 
History of atopic disorder  
 
Family history of asthma and/or atopic disorder  
 
Widespread  wheeze  heard  on  auscultation of the chest 
 
Otherwise unexplained low FEV  or PEF (historical or serial 
1
readings) 
 
Otherwise unexplained peripheral blood eosinophilia  
Features that lower the probability of asthma  
 
Prominent dizziness, light-headedness, peripheral tingling 
 
Chronic  productive cough in  the absence of wheeze or 
breathlessness 
 
Repeatedly normal physical examination of chest when symptomatic 
 
Voice disturbance 
 
Symptoms with colds only 
 
Significant smoking history (i.e. >20 pack-years) 
 
Cardiac disease 
 
Normal PEF or spirometry when symptomatic*  
* A normal spirogram/spirometry when not symptomatic does not exclude the diagnosis of 
asthma. Repeated measurements of lung function are often more informative than a single 
assessment.  
 
 
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Investigation. 
Pulmonary Function Tests (See Appendix F  for a Glossary of Terms.) 
 
In an acute episode of asthma, the peak flow, FEV1 and FEV1/FVC ratio are 
all reduced.  (They may all return to normal between episodes.)  
 
In chronic asthma, TLC (Total Lung Capacity) may be increased by 
hyperinflation, and air trapping may increase RV (Residual Volume). 
 
The Recommended Technique for Measuring Peak Flow is described in 
Appendix A. 
 
The diurnal variation of peak expiratory flow rate is normally increased in 
asthmatics, where the lowest peak flow occurs in the early hours of the 
morning, ‘morning dipping’, and the highest is in the afternoon.  Patients are 
often asked to keep ‘Peak Flow Diaries’ as an aid to diagnosis and 
assessing the effectiveness of treatment. 
 
Results from spirometry are also useful where the initial history and 
examination leave genuine uncertainty about the diagnosis. In such cases, 
the differential diagnosis and approach to investigation is different in patients 
with and without airflow obstruction (see Figure 1 and Table 2). In patients 
with a normal or near-normal spirogram when symptomatic, potential 
differential diagnoses are mainly non-pulmonary. Such conditions do not 
respond to inhaled corticosteroids and bronchodilators. In contrast, in 
patients with an obstructive spirogram the question is less whether they will 
need inhaled treatment but rather exactly what form and how intensive this 
should be. 
Other tests of airflow obstruction, airway responsiveness and airway 
inflammation can also provide support for the diagnosis of asthma, but to 
what extent the results of the tests alter the probability of a diagnosis of 
asthma has not been clearly established, nor is it clear when these tests are 
best performed. 
Reversibility tests 
 
The best of three peak flow readings is recorded.  A bronchodilator is given, 
and the peak flow readings are repeated 15-20 minutes later.   
An improvement of at least 15% (or 200 mls) is suggestive of asthma. 
 
Chronic severe asthma may not show any reversibility after bronchodilator 
usage.  However, a two-week trial of corticosteroid may produce an 
improvement in peak flow.  This helps to differentiate between asthma 
(improvement likely), and COPD (improvement less likely). 
Provocation tests 
 
Exercise testing is a safe, simple and useful procedure if the diagnosis of 
asthma is in doubt.  Peak flow is measured before exercise.  The patient 
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does 6 minutes of vigorous exercise, and the peak flow is repeated 15-20 
minutes later.  A fall of 10-20% is highly suggestive of asthma.5 6  
 
If the diagnosis is still in doubt, then the exercise test can be performed in 
cold dry conditions to intensify the response.  Provocation with other agents 
such as histamine and metacholine can also be useful. 
Chest X Ray 
 
This is usually normal. 
Further investigation of patients with an intermediate probability of 
asthma  

 
Patients with airways obstruction 
 
Tests of peak expiratory flow variability, lung volumes, gas transfer, airway 
hyper-responsiveness and airway inflammation are of limited value in 
discriminating patients with established airflow obstruction due to asthma 
from those whose airflow obstruction is due to other conditions. Patients 
may have more than one cause of airflow obstruction, which complicates the 
interpretation of any test. In particular, asthma and chronic obstructive 
pulmonary disease (COPD) commonly coexist.  
 
Patients with airways obstruction and intermediate probability of asthma 
should be offered a reversibility test and/or a trial of treatment for a specified 
period: 
 
If there is significant reversibility, or if a treatment trial is clearly beneficial 
treat as asthma 
 
If there is insignificant reversibility and a treatment trial is not beneficial, 
consider alternative conditions.  
 
Patients without airways obstruction 
 
In patients with a normal or near-normal spirogram it is more useful to look 
for evidence of airway hyper-responsiveness and/or airway inflammation. 
These tests are sensitive so normal results provide the strongest evidence 
against a diagnosis of asthma.  
 
Patients without evidence of airways obstruction and with an intermediate 
probability of asthma, should have further investigations before commencing 
treatment.  
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Figure 1: Presentation with suspected asthma in adults.  
 
Presentation with suspected Asthma 
Clinical assessment including spirometry (or PEF if 
spirometry not available 
INTERMEDIATE 
 
 
PROBABILITY: 
LOW PROBABILITY: 
HIGH PROBABILITY: 
diagnosis uncertain 
other diagnosis likely 
diagnosis of asthma 
likely 
FEV/FVC 
FEV/FVC
<0.7 
>0.7
Trial of 
Investigate/treat 
treatment 
other condition 
 
 
Response? 
Response? 
Yes 
No 
No 
Yes 
Assess compliance 
Continue 
and inhaler technique. 
Further investigation / 
Continue 
treatment 
 Consider further 
referral considered 
treatment 
investigation/referral 
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Differential diagnosis 
 
‘All that wheezes is not asthma, but equally all that is asthma need not 
wheeze.’ 
 
Table 2: Differential diagnosis of asthma in adults, according to the 
presence or absence of airflow obstruction (FEV1/FVC <0.7). 
 
Without airflow obstruction 
 
Chronic cough syndromes (e.g. associated with ACE inhibitors) 
 
Hyperventilation syndromes 
 
Vocal cord dysfunction 
 
Rhinitis 
 
Gastro-oesophageal reflux 
 
Heart failure 
 
Pulmonary fibrosis 
With airflow  obstruction 
 
COPD 
 
Bronchiectasis* 
 
Inhaled foreign body* 
 
Obliterative bronchiolitis 
 
Large airway stenosis 
 
Lung cancer 
 
Sarcoidosis 
*May also be associated with non-obstructive spirometry 
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Occupational Asthma7 8   
 
 
 
Asthma is one of the commonest occupational lung diseases. 
About 9-15% of adult-onset asthma is considered attributable to 
occupational exposures.  9  10      There is no indication that this figure has 
changed over the past decade.  
Approximately 1160 new cases were reported in the UK in 199911 12.  
 
Occupational Asthma is defined as: asthma, which is induced by an inhaled 
agent at work: 
 
 An 
irritant inhaled in toxic concentration, or 
 
A hypersensitivity reaction to a sensitising agent
 
It is commonest amongst: 
 
 
Paint Sprayers.  (isocyanates) 
 
Bakers.  (flour) 
 
Plastics and Chemicals Workers. (epoxy resins and                              
    azodicarbonamide) 
 
Hairdressers.  (persulphates) 
 
There are over 200 known respiratory sensitisers and more are being 
identified each year.  Atos Healthcare’s Occupational Asthma Sensitiser 
Information Service (OASIS) is able to give advice about identifying triggers 
for occupational asthma to doctors who are called upon to advise on 
Prescribed Disease D7 (Occupational Asthma) under the Industrial Injuries 
Provisions of the Social Security Contributions and Benefits Act 1982.   
 
Precautions to prevent occupational asthma are widely used.  Examples 
include enclosure or segregation of the process, exhaust ventilation and the 
provision of appropriate protective devices such as respirator masks. 
 
COSHH (Control of Substances Hazardous to Health) regulations require 
employers to institute health surveillance programmes where there is a risk 
of occupational asthma.  These include symptom enquiries, measurements 
of lung function and reviews of sickness absence13.  
 
Although they are no more likely to develop occupational asthma, it is 
prudent for asthmatics to avoid working in environments known to contain 
respiratory sensitisers.  The development of occupational asthma would be 
more difficult to detect, and the symptoms may be more severe. 
 
 
 
 
 
 
 
  
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Diagnosis 
 
A detailed, comprehensive history is one of the most crucial steps in 
reaching a diagnosis. 
 
 
The employment history must be obtained. 
 
Which sensitising agent has the patient been exposed to, and to what 
degree? 
 
Was there any protection available, and was it used? 
 
The latent period must be established,  
 
The latent period is the time between initial exposure and the onset of 
symptoms.  This period may be days or many years, typically up to two 
years. 
 
The timing of the ‘first attack’ is usually well remembered. 
 
Typically, symptoms improve away from work, such as at weekends or 
during periods of holiday, and deteriorate again on return to work.  It is 
important to remember that the patient may not have had sufficient time 
away from the stimulus for the inflammatory reaction to settle, before re-
exposure the next day. 
Symptoms and Examination 
 
The cardinal symptoms and signs of asthma are described in Sections 5.2 
and 5.3
Investigations 
 
Cases of suspected occupational asthma are usually referred to a hospital 
specialist.   
 
Investigations specific to occupational asthma normally include: 
 
  A Work Place Challenge Test.  The patient is removed from work for two 
weeks.  They then return to work under clinical supervision.  Several 
peak flow readings will have been taken before returning to work and 
further readings will be taken during the following three days at work. 
 
  The Laboratory Challenge Test is the definitive test for occupational 
asthma.  A specific agent is inhaled under laboratory conditions, and 
airway responsiveness is measured.  The patient must be supervised for 
at least 8 hours.   
 
 
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Management 
 
The most important aspect is:  
 
Immediate removal from the exposure. 
 
Removal very early in the disease process may result in complete resolution 
of the asthma14
 
Delay may allow chronic asthma to develop. 
 
About 50% of those affected by occupational asthma stay with the same 
employer 
 
Occupational asthma is a Prescribed Disease under the Industrial Injuries 
Provisions of the Social Security Contributions and Benefits Act 1982.   
Differential Diagnosis (RADS) 15 
 
It is necessary to differentiate between Occupational Asthma and Reactive 
Airways Dysfunction Syndrome (RADS). 
 
Indoor exposures to nitrogen oxide and volatile organic compounds are 
implicated in the development of RADS, a persistent asthma-like syndrome 
in people with no history of asthma.  RADS appears to be distinct from 
asthma and may be, on occasion, a form of environmental lung disease. 
However, RADS and asthma have many clinical similarities (e.g. wheezing, 
dyspnoea, cough), and both may respond to corticosteroids. 
 
The diagnosis of RADS requires: 
  The presumption of previously normal respiratory physiology, without 
bronchial hyperactivity. 
  Typical symptoms are cough, wheeze and dyspnoea.   
  It follows exposure to high concentrations of gas, smoke, fumes, or 
vapour with irritant properties. 
  There is no latent period.  The onset of symptoms is within 24 hours of 
exposure and they may persist for a period of a few days or for as long 
as 12 years. 
 
RADS is not a Prescribed Disease, but it can qualify as an Industrial 
Accident. 
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Treatment 
Guidelines 
 
In 1999 the British Thoracic Society (BTS) and the Scottish Intercollegiate 
Guidelines Network (SIGN) agreed to jointly produce a comprehensive new 
asthma guideline, both having previously published guidance on asthma. 
The new 2008 guideline has considered literature published up to March 
2007.  
It contains  
  a completely rewritten section on diagnosis for both adults and children.  
  a section on special situations which includes occupational asthma, 
asthma in pregnancy and the new topic of difficult asthma.  
 updated sections on pharmacological and non-pharmacological 
management.  
  amalgamated sections on patient education and compliance, and on 
organisation of care and audit.  
 
Advice for Asthmatics 
 
1. Where practical, identify and then avoid precipitating factors.   
(Not possible with widespread allergens e.g. house dust mite and 
pollen.) 
However, evidence that reducing allergen exposure can reduce 
morbidity and/or mortality in asthma is tenuous.  In uncontrolled 
studies, children and adults have derived benefit from removal to a 
low allergen environment such as occurs at high altitude, although 
the benefits seen are not necessarily attributable to allergen 
avoidance alone.16 
 
2. Stopping Smoking 
Direct or passive exposure to cigarette smoke adversely affects 
quality of life, lung function, need for rescue medications for acute 
episodes of asthma and long term control with inhaled steroids. 
There are very few trials which have assessed smoking cessation in 
relation to asthma control. Two studies have demonstrated 
decreases in childhood asthma severity when parents were able to 
stop smoking..  One study in adults with asthma suggested that 
smoking cessation improved asthma-specific quality of life, 
symptoms and drug requirements.  Intervention to reduce smoking 
has had disappointing outcomes. It is likely that more intensive 
intervention will be required to achieve meaningful outcomes.  
Uptake of smoking in teenagers increases the risks of persisting 
asthma. One study showed a doubling of risk for the development of 
asthma over six years in 14 year old children who started to smoke  
Parents with asthma should be advised about the dangers of 
smoking to themselves and their children with asthma and 
offered appropriate support to stop smoking
.  
 
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3.  Annual influenza vaccination is recommended.17  
 
4. Regular  exercise.18  19  20  (Sport, exercise and pulmonary 
rehabilitation improve respiratory function and quality of life.) 
 
 
Pharmacological management 1, 21  
 
The aim of asthma management is control of the disease.  Control of asthma 
is defined as: 
 
No daytime symptoms 
 
no night time awakening due to asthma 
 
no need for rescue medication 
 
no exacerbations 
 
no limitations on activity including exercise 
 
normal lung function (in practical terms FEV1 and/or PEF >80% 
predicted or best) with minimal side effects.  
 
In clinical practice patients may have different goals and may wish to 
balance the aims of asthma management against the potential side effects 
or inconvenience of taking medication necessary to achieve perfect control. 
 
A stepwise approach aims to abolish symptoms as soon as possible and to 
optimise peak flow by starting treatment at the level most likely to achieve 
this. Patients should start treatment at the step most appropriate to the initial 
severity of their asthma. The aim is to achieve early control and to maintain 
control by stepping up treatment as necessary and stepping down when 
control is good (see figure 2 for summary of stepwise management in 
adults 21
).   
 
Key Concept: Relievers and Preventers 
 
Bronchodilator drugs are highly effective at temporarily relieving the 
symptoms of asthma, “Relievers.”  
 
However, the aim of treatment is to eliminate asthma symptoms, so the main 
emphasis for most asthmatics should be the regular use of “Preventer” 
medication.   
Regular use of inhaled corticosteroids reduces airway inflammation and 
reactivity.  It is anticipated that this will prevent airway damage, which would 
otherwise lead to irreversible chronic airway obstruction.  Preventer 
treatment should be started very early in the treatment of asthma, and then 
used aggressively to gain quick control.   
 
 
 
 
 
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The Main Treatments for Chronic Asthma 
 
(See  Appendix B for additional details and information about less widely 
used drugs.) 
 
 
Relievers 
 
1. Short 
Acting 
2-Agonists 22  
  Salbutamol (Ventolin) is the most widely used example. 
  Rapid onset in minutes and lasts for a few hours. 
  Ideal for the rapid relief of symptoms. 
 
2. Long 
Acting 
2-Agonists. 23  
  Salmeterol (Serevent) is the most widely used example. 
  Maximum effect after 2 hours and lasts for 12 hours. 
  Particularly effective for nocturnal and exercise induced symptoms. 
 
Preventers 
 
1.  Inhaled Corticosteroids.  (“Inhaled Steroids.”) 24 
  Beclomethasone is the most widely used example 25  
  Must be taken regularly every day. 
  Excellent anti-inflammatory effects.   
 
2.  Oral Corticosteroids.  (“Oral Steroids.”) 
  Prednisolone is the drug of choice. 
  Often used in short courses to treat exacerbations. 
  Serious side effects are associated with regular long-term use.  (A 
last resort in outpatient management.) 
 
3. Leukotriene 
receptor 
antagonists. 
  Montelukast (Singulair) is an example. 
  Taken orally once each day. 
  Bronchodilator and anti-inflammatory effects. 
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Figure 2: Stepwise management in adults  
 
as needed 
Patients should start treatment at the step most appropriate to the 
control 
initial severity of their asthma. Check concordance and reconsider 
improve 
Move  up to 
diagnosis if the response to treatment is unexpectedly poor 
Use daily steroid tablet in 
lowest dose providing 
adequate control. 
step 
Consider trials of: 
controlling 
 
lowest 
  Increasing inhaled steroid 
Maintain high dose inhaled 
maintain 
and 
up to 2000mcg/day* 
steroid at 2000mcg/day* 
find 
to 
1. 
Add inhaled long acting 
Move  down  
  Adding fourth drug e.g.  
 
Beta2 agonist (LABA) 
leukotriene receptor 
Consider other treatments to 
2. Assess 
control 
of 
antagonist ,SR 
minimise the use of steroid 
Add inhaled steroid 200-
asthma: 
theophylline, Beta2 
tablets 
800mcg/day* 
  Good response to LABA 
agonist tablet 
 
 
– continue LABA 
Refer patient for specialist 
Inhaled short acting Beta 2 
400mcg is an appropriate 
  Benefit from LABA but 
care 
agonist as required 
starting dose for many 
control still 
patients 
inadequate – continue 
 
LABA and increase 
Start at dose of inhaled 
inhaled steroids to 
steroid appropriate to 
800mcg/day* (if not 
severity of the disease. 
already on this dose) 
  No response to LABA 
stop LABA and 
increase inhaled 
steroids to 
800mcg/day* if control 
still inadequate 
institute trail of other 
STEP 5 
therapies leukotriene 
receptor antagonist or 
Continuous or frequent use 
SR theophylline 
STEP 4 
of oral steroids 
STEP 3 
Persistent poor control 
STEP 2 
Initial add-on therapy 
 
Regular preventer therapy 
STEP 1 
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Monitoring and Measuring Asthma Control 
 
In General Practice, the majority of this work is performed by Practice 
Nurses who have received additional training and work to written guidelines. 
 The following information is valuable for assessing the success of asthma 
treatment, and it should be checked at each asthma review 26 27 28  
 
 
Frequency of daytime symptoms. 
(Ideally, these should be no more common than once a fortnight.) 
 
 
Frequency of nocturnal symptoms. 
(If these are present at all, the asthma is poorly controlled.) 
 
 
 
Patient’s Peak Flow Diary. 
(Diurnal variation of peak flow >20% indicates poor control.) 
 
 
Inhaler Technique. 
(This is critical, as it is often sub-optimal, and may prevent a useful 
therapeutic effect.) 
 
 
 
Education and Understanding 29  
The success of asthma treatment depends on this.  Patients often have 
misconceptions about their condition and its treatment.  The provision of 
written information and written individual management plans is effective for 
improving compliance and symptom control.30  
(An example is provided in Appendix C.) 
 
An asthma diary is a useful tool for assessing control, and an example is 
attached at Appendix D.31 
Compliance with monitoring and treatment  
 
Compliance with regular monitoring using peak flow meters, even in clinical 
drug trials is poor with recorded daily use as low as 6%.  The lack of 
evidence supporting long term peak flow monitoring, however, does not 
negate the use of home charting at critical times, for example, at diagnosis 
and initial assessment, when assessing response to changes in treatment, 
or as part of a personalised action plan during exacerbations.   
Comparison should be with the patient’s best known peak flow (not the 
predicted peak flow value).  
 
Patients are more likely to under-use than over-use treatment and under-use 
should be considered when there is a failure to control asthma symptoms. 
Patient self reporting and health care professional assessment both over-
estimate regular use of prophylactic medication. 
Computer repeat-prescribing systems, widely available in general practice, 
provide a good indication of adherence with prescribed asthma regimens. 
Electronic monitoring, whilst the most accurate method, is only practical in 
clinical drug trials. 
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Prognosis 
Chronic asthma32
 
In people with mild asthma, prognosis is good, and progression to severe 
disease is rare. However, as a group, people with asthma lose lung function 
faster than those without asthma, although less quickly than people without 
asthma who smoke.  
 
People with chronic asthma can improve with treatment.  
 
However, some people (possibly up to 5%) have severe disease that 
responds poorly to treatment. These people are most at risk of morbidity and 
death from asthma.  
Acute asthma. 
 
About 10–20% of people presenting to the emergency department with 
asthma are admitted to hospital.  
Of these, fewer than 10% receive mechanical ventilation. Those who are 
ventilated are at 19-fold increased risk of ventilation for a subsequent 
episode.  
 
It is unusual for people to die unless they have suffered respiratory arrest 
before they reach hospital.  
 
One study of 939 people discharged from emergency care found that of 
those available for follow-up 17% (95% Confidence Interval of 14% - 20%) 
relapsed within 2 weeks. 
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Main Disabling Effects 
Asthma is a chronic but variable condition.  Both the baseline level of 
symptoms and their variability must be assessed to arrive at a true picture of 
a claimant’s disability. 
Assessing the Claimant 
The assessment should be made using all the information available.  This 
includes information from the claimant’s file, informal observations, medical 
history, activities of daily living, and examination. 
 
To take account of the variability of asthma, it is important to ask about the 
claimant’s illness over time.  Considering events in the last 2 years will give 
a representative impression.  There is a wide range of severity amongst 
claimants with asthma: 
 
Controlled Asthma 
Modern asthma treatment is capable of eliminating or significantly reducing 
regular asthma symptoms.  ‘Activities of Daily Living’ are unlikely to be 
significantly restricted.  The asthmatic should be able to live independently 
and continue with their usual interests and hobbies.  The claimant’s asthma 
will probably be monitored and treated in primary care. 
 
Poorly controlled/Uncontrolled Asthma 
Poorly controlled asthmatics are likely to require high doses of inhaled 
and/or regular oral steroids, regular long acting ß-agonists, and one or more 
of: theophylline, leukotriene antagonist, cromoglycate, nedocromil or 
anticholinergic bronchodilator.   
 
Poorly controlled/Uncontrolled asthmatics are likely to experience frequent 
or severe exacerbations that require additional treatment such as high dose 
oral steroids, nebulised bronchodilators or courses of antibiotics.  Some may 
have required emergency treatment from their GP or at an Accident and 
Emergency unit, and the most severe may have experienced hospital 
admission.  Their asthma may be under the supervision of a Consultant.   
 
The main effect of asthma is to impair exercise tolerance.  This is particularly 
likely to affect the activities of walking and climbing stairs.  In the most 
severe cases, even washing and dressing may become difficult. 
Considering Exemption from the IB-PCA 
Exemption from the assessment should be considered if effort tolerance is 
severely limited, or they have had to adapt their home, for example by 
installing a stair lift or converting a room downstairs for their bedroom. 
 
 
 
 
 
 
 
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Helpful Questions for Assessing Asthma Severity and Related Disability 
 
 
Are there any specific triggers for the asthma? 
  (Exercise, cold air, respiratory infections, allergen exposure, 
drugs, emotional factors.) 
 
What has been the frequency and duration of attacks over the last 2 
years? 
 
‘Bad Days’ – what, in terms of daily activities, makes them different, and 
how often do they occur? 
 
Does their asthma interfere with hobbies and interests? 
 
How do they get around, for instance for shopping or taking the children to 
school?  (Walking, car, bicycle or public transport.) 
 
Does their asthma cause any difficulty sleeping? Where do they sleep? 
 
What is the claimant doing about their asthma? 
  Do they attend their GP’s asthma clinic? 
  Do they do monitor their peak flow? 
  Do they have a management plan for their asthma? 
 
How effective is their treatment? 
  Have there been any changes to medication in the last 2 years 
and why were the changes made? 
  How many courses of oral steroids and antibiotics have they 
needed in the last 2 years?  
  Have they required the use of a nebuliser in the last 2 years? 
 
Do they attend a hospital outpatient clinic because of their asthma? 
Have they required emergency asthma treatment from their GP or at 
Casualty? 
Have they been admitted to hospital because of their asthma in the last 2 
years? 
Interpreting the Peak Flow Measurement 
 
A peak flow measurement taken in the course of a disability examination is 
only a snapshot, and may not reflect the typical experience of the claimant.  
However, it does provide an objective piece of information that can be 
weighed with all the other data obtained from the claimant’s medical history, 
treatment, examination findings and Typical Day.  All this information must 
be used to build up a picture of their asthma and any disability it may cause. 
 
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Aids to Grading the Disabling Effects of Asthma 
The Medical Research Council Breathlessness Scale33 
 
Grade  Degree of breathlessness related to activities 
1 
Not troubled by breathlessness except on strenuous exercise 
2 
Short of breath when hurrying or walking up a slight hill 
Walks slower than contemporaries on level ground because of breathlessness, or has to 
3 
stop for breath when walking at own pace 
4 
Stops for breath after walking about 100m or after a few minutes on level ground 
5 
Too breathless to leave the house, or breathless when dressing or undressing 
Percentage of Predicted Peak Flow 
 
The percentage of predicted peak flow is one way of assessing the severity 
of asthma.  It is important to remember that there is considerable variability 
between individuals, and measures of lung function do not always correlate 
with functional ability.   
The following table describes broad categories of functional impairment:  
NB.  The table is for guidance only.
 7 
  
% Predicted 
Description of 
Range of Functional Effects 
Peak Flow 
Severity 
>75% 
Mild 
Nil 
From 
Breathlessness on heavy exertion. 
50-75% Moderate 
Breathlessness walking at normal pace 
To 
on the flat. 
From 
Breathlessness on walking 100m. 
33-49% 
Severe 
Breathlessness on climbing one flight of 
To 
stairs without stopping. 
Cannot climb one flight of stairs without 
From 
stopping. 
<33% Very 
Severe 
To 
Bed-bound or chair-bound. 
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Psychological and Social Aspects  
 
When a person is suffering from a chronic illness such as asthma, 
psychological problems may result.  Emotions such as anxiety or denial may 
affect their ability to process, remember, or act upon the information they are 
given.  This may hinder their compliance with advice and treatment, and 
reduce their chances of gaining control of their illness.34   The successful 
recognition and treatment of psychological illnesses may improve quality of 
life and reduce disability. 35  
 
Research has demonstrated that the relationship between a person’s 
symptoms and the severity of their asthma is complex.  It partly depends on 
the individual’s mental and physical ability to cope with the demands of the 
condition.36  
 
Social factors such as income, marital status, alcohol consumption and 
housing have an important influence on levels of physical functioning among 
people with chronic illnesses.37  
 
There is some evidence to show that a worker with the label ‘asthmatic’ may 
face prejudicial attitudes in the workplace.38 
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Asthma in children 
Asthma in children causes recurrent respiratory symptoms of:  
 
Wheezing 
 
Cough 
 
Difficulty breathing 
 
chest tightness.  
 
Wheezing is one of a number of respiratory noises that occur in children.  
Parents often use "wheezing" as a non-specific label to describe any 
abnormal respiratory noise.   
It is important to distinguish wheezing (a continuous, high-pitched musical 
sound coming from the chest) from other respiratory noises, such as stridor 
or rattly breathing 
  
There are many different causes of wheeze in childhood and different 
clinical patterns of wheezing can be recognised in children.  In general, 
these patterns ("phenotypes") have been assigned retrospectively.  They 
cannot reliably be distinguished when an individual child first presents with 
wheezing.  In an individual child the pattern of symptoms may change as 
they grow older 
 
The commonest clinical pattern, especially in pre-school children and 
infants, is episodes of wheezing, cough and difficulty breathing associated 
with viral upper respiratory infections (colds), with no persisting symptoms. 
Most of these children will stop having recurrent chest symptoms by school 
age. 
 
A minority of those who wheeze with viral infections in early life will go on to 
develop wheezing with other triggers so that they develop symptoms 
between acute episodes (interval symptoms) similar to older children with 
classical atopic asthma. 
  
Children who have persisting or interval symptoms are most likely to benefit 
from therapeutic interventions.  
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Initial clinical assessment  
 
The diagnosis of asthma in children is based on recognising a characteristic 
pattern of episodic respiratory symptoms and signs (see Table 1) in the 
absence of an alternative explanation for them (see Tables 2 and 3).  
 
Table 1: 
Clinical features that increase the probability of Asthma 

More than one of the following symptoms: wheeze, cough,  difficulty breathing, chest 
 tightness, particularly if these symptoms: 
 
are frequent and recurrent 
 
are worse at night and in the early morning 
 
occur in response to, or are worse after, exercise or other triggers, such as 
exposure to pets, cold or damp air, or with emotions or laughter 
 
occur apart from colds 
 
Personal history of atopic disorder 
 
Family history of atopic disorder and/or asthma 
 
Widespread wheeze heard on auscultation 
 
history of improvement in symptoms or lung function in response to adequate 
therapy 
 
 
Table 2: 
Clinical features that lower the probability of asthma 
 
Symptoms with colds only, with no interval symptoms 
 
Isolated cough in the absence of wheeze or difficulty breathing 
 
History of moist cough 
 
Prominent dizziness, light-headedness, peripheral  tingling 
 
Repeatedly normal physical examination of chest when symptomatic 
 
Normal peak expiratory flow (PEF) or spirometry when symptomatic  
 
No response to a trial of asthma therapy 
 
Clinical features pointing to alternative diagnosis (see Table 3)  
 
 
Several factors are associated with a high (or low) risk of developing 
persisting wheezing or asthma through childhood.15,20 The presence of 
these factors increases the probability that a child with respiratory symptoms 
will have asthma.  
 
 
These factors include:  
 
  Age at presentation 
The natural history of wheeze is dependent on age at first presentation. 
In general, the earlier the onset of wheeze, the better the prognosis.  
Cohort studies show a "break point" at around two years. Most children 
who present before this age become asymptomatic by mid-childhood.  
Co-existent atopy is a risk factor for persistence of wheeze independent 
of age of presentation. 
 
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  Sex  
Male sex is a risk factor for asthma in pre-pubertal children. Female sex 
is a risk factor for the persistence of asthma in the transition from 
childhood to adulthood.  Boys with asthma are more likely to "grow out" of 
their asthma during adolescence than girls.  
 
  Severity and frequency of previous wheezing episodes  
        Frequent  or  severe  episodes  of  wheezing  in  childhood  are  associated      
   with recurrent wheeze that persists into adolescence.  
 
  Coexistence of atopic disease  
A history of other atopic conditions such as eczema and rhinitis increases 
the probability of asthma.  Positive tests for atopy in a wheezing child 
also increase the likelihood of asthma.  A raised specific IgE to wheat, 
egg white, or inhalant allergens such as house dust mite and cat dander, 
predicts later childhood asthma. 
Other markers of allergic disease at presentation, such as positive skin 
prick tests and a raised blood eosinophil count, are related to the severity 
of current asthma and persistence through childhood. 
 
  Family history of atopy  
A family history of atopy is the most clearly defined risk factor for atopy 
and asthma in children.   
The strongest association is with maternal atopy, which is an important 
risk factor for the childhood onset of asthma and for recurrent wheezing 
that persists throughout childhood. 
 
  Abnormal lung function  
Persistent reductions in baseline airway function and increased airway 
responsiveness during childhood are associated with having asthma in 
adult life. 
 
 
 
 
 
 
 
 
 
 
 
Table 3: 
Clinical clues to alternative diagnoses in wheezy children (features not 
commonly found in children with asthma) 
 
Perinatal and family history 
Possible diagnosis 
Symptoms present from birth or perinatal 
Cystic fibrosis; chronic lung disease  of 
lung problem
prematurity; ciliary dyskinesia; developmental 
 
anomaly 
Family history of unusual chest disease 
Cystic fibrosis; neuromuscular disorder 
Severe upper respiratory tract disease 
Defect of host defence; ciliary dyskinesia 
 
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Table 3: 
Clinical clues to alternative diagnoses in wheezy children (features not 
commonly found in children with asthma)  
Symptom and signs  
 
Cystic fibrosis; bronchiectasis; protracted 
Persistent moist cough 
bronchitis; recurrent aspiration; host defence 
disorder; ciliary dyskinesia 
Excessive vomiting 
Gastro oesophageal reflux (± aspiration) 
Dysphagia 
Swallowing problems (± aspiration) 
Breathlessness with light-headedness and 
peripheral tingling  
Hyperventilation/panic attacks 
Inspiratory stridor 
Tracheal or laryngeal disorder 
Abnormal voice or cry 
Laryngeal problem 
Focal signs in chest 
Developmental anomaly; post-infective 
syndrome; bronchiectasis; tuberculosis 
Finger clubbing 
Cystic fibrosis; bronchiectasis 
Failure to thrive 
Cystic fibrosis; host defence disorder; gastro 
oesophageal reflux 
Investigations 
 
Developmental anomaly; cystic fibrosis;  
Focal or persistent radiological changes 
post-infective disorder; recurrent aspiration; 
inhaled foreign body; bronchiectasis; 
tuberculosis 
 
 
 
Case detection studies have used symptom questionnaires to screen for 
asthma in school-age children. A small number of questions - about current 
symptoms, their relation to exercise and their occurrence at night has been 
sufficient to detect asthma relatively efficiently.  The addition of spirometry or 
bronchial hyper-responsiveness testing to these questionnaires adds little to 
making a diagnosis of asthma in children.  
 
Most children under five years and some older children cannot perform 
spirometry.  These children should be offered a trial of treatment for a 
specific period.  If there is clear evidence of clinical improvement, the 
treatment should be continued and they should be regarded as having 
asthma (it may be appropriate to consider a trial of withdrawal of treatment 
at a later stage). If the treatment trial is not beneficial, then tests for 
alternative conditions should be considered and referral for specialist 
assessment arranged. 
Between 2 - 5 years of age, many children can perform several newer lung 
function tests that do not rely on their cooperation or the ability to perform a 
forced expiratory manoeuvre.  
In general, these tests have not been evaluated as diagnostic tests for 
asthma. 
 
 
 
 
 
 
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Appendix A  Peak Expiratory Flow Monitoring 
(PEF) 

Recommended Technique for Measuring Peak Flow39 
 
  Use equipment that functions correctly.  In examination centres, report 
worn-out or defective equipment to the Medical Examination Assistant 
(MEA) so that it can be replaced. 
  The type of meter used (Wright or EU) should be recorded. 
  Explain the procedure and demonstrate it to the subject. 
  Move the pointer to the bottom of the scale. 
  The subject should be sitting up straight or standing. 
  The subject should hold the peak flow meter horizontally, and the 
subject’s fingers must not impede the movement of the pointer along the 
scale. 
  Ask the subject to take a deep breath, seal their mouth around the 
mouthpiece, and blow as hard and as fast as they can.  (Like blowing out 
a candle.) Pursed lips or air leaks will invalidate the reading. 
  The result should be compared to a graph of predicted peak flow 
according to the subject’s age, sex and height.  Both the actual and the 
predicted peak flow should be recorded with a brief explanation to help 
the Decision Maker to interpret the result. 
  If the subject is not able to achieve good technique, then this must be 
noted for the benefit of the Decision Maker. 
 
PEF should be recorded as the best of three forced expiratory blows from 
total lung capacity with a maximum pause of two seconds before blowing.  
The subject can be standing or sitting. Further blows should be done if the 
largest two PEF are not within 40 l/min.  
 
PEF is best used to provide an estimate of variability of airflow from multiple 
measurements made over at least two weeks. Increased variability may be 
evident from twice daily readings. More frequent readings will result in a 
better estimate but the improved precision is likely to be achieved at the 
expense of reduced subject compliance.  
 
PEF variability is best calculated as the difference between the highest and 
lowest PEF expressed as a percentage of either the mean or highest PEF. 
 
The upper limit of the normal range for the amplitude % highest is around 
20% using four or more PEF readings per day but may be lower using twice 
daily readings. Epidemiological studies have shown sensitivities of between 
19 and 33% for identifying physician-diagnosed asthma.  
 
PEF variability can be increased in subjects with conditions commonly 
confused with asthma so the specificity of abnormal PEF variability is likely 
to be less in clinical practice than it  is in population studies
 
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PEF records from frequent readings taken at work and away from work are 
useful when considering a diagnosis of occupational asthma.  
 
Peak flow records should be interpreted with caution and with regard 
to the clinical context.  They are more useful in the monitoring of 
patients with established asthma than in making the initial diagnosis. 
 
 
 
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Appendix B  Treatments for Chronic Asthma  
Short Acting ß-Agonists 22 
 
This group refers to the selective ß2 agonists.  Salbutamol (Ventolin) and 
Terbutaline (Bricanyl) are common examples.  They are taken by inhalation, 
and have a rapid onset of action.  (The effects begin after 15 minutes, and 
last about four hours.) The ß2 agonists cause bronchodilation, and are used 
as relievers.  Possible side effects include tremor, palpitations and muscle 
cramps, although these are uncommon when the drugs are taken in inhaled 
form.   
Long Acting ß-Agonists 23 
 
Examples include Salmeterol (Serevent) and Eformoterol (Oxis).  They 
achieve their maximum effect in 2 hours and last for about 12 hours.  Thus, 
they are particularly effective for nocturnal symptoms, but they should not be 
used for the relief of acute symptoms.  The long acting ß-agonists do not 
suppress inflammation, so they should always be used with inhaled 
corticosteroids. Indeed there is evidence that given as monotherapy there is 
an increase in asthma related mortality. Inhalers which provide a 
combination of steroid and Long Acting ß-Agonist increase compliance and 
remove any concerns about only giving Long Acting ß-Agonists. This 
combination can achieve excellent symptom reduction and peak flow 
control.   
Anticholinergic Bronchodilators 
 
The commonest example is Ipratropium Bromide (Atrovent).  These drugs 
block the cholinergic bronchoconstrictor effect of the Vagus nerve. 
 
Maximum effect is achieved 30 – 60 minutes after use, and it lasts for about 
4 hours.  Anticholinergic bronchodilators are not as effective as ß-agonists in 
asthma, but can be used as an adjunct if control is incomplete, or ß-agonists 
are not tolerated.  They are particularly suitable for very young children or 
older adults.   
Theophyllines 23 
 
These drugs are effective bronchodilators.  They are taken orally as 
sustained release formulations.  The theophyllines have a narrow 
therapeutic index, with considerable individual variation in the necessary 
dose.  Therefore, it is necessary to monitor blood concentrations.  For these 
reasons, they are used much less now that long acting ß-agonists are 
available.  Common side effects include nausea and vomiting, abdominal 
discomfort, headache, malaise, tachycardia and fits.  There are numerous 
drug interactions with other common treatments such as erythromycin, 
phenytoin and cimetidine. 
Sodium Cromoglycate and Nedocromil Sodium 
 
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These drugs are sometimes known as Mast Cell Stabilisers, although this 
may not be their main mode of action in asthma.  They block 
bronchoconstriction to the stimuli of exercise and antigens.  They are 
sometimes used as first line prophylactic agents, particularly in young 
children, or as an addition to inhaled corticosteroids when control is poor.  
They are less effective than steroids in adults, and are not useful as 
relievers. 
Inhaled Corticosteroids 24 25 40 41  
 
Beclomethasone and budesonide are the most common examples. 
 
Fluticasone is a more potent drug, and is used at half the dose.  The 
majority of their benefits are seen at low to moderate doses, (up to 800 
mcgs), with relatively little additional benefit from high doses.  They are 
highly effective at reducing bronchial reactivity and inflammation and at 
controlling symptoms.  Peak effect usually occurs 3–7 days after initiation of 
treatment.  Side effects are dose-dependent, inhaler device-dependent, and 
technique-dependent.  In adults, adverse effects become more likely once a 
daily dose of 1000 mcgs of beclomethasone is reached: 
 
 Oropharyngeal 
Candidiasis. 
 
Dysphonia, Sore Throat and Cough. 
 
Purpura and Thinning of the Skin. 
 Cataracts. 
 
Large volume spacers should be used at doses above 800 mcgs to reduce 
pharyngeal deposition. 
 
Inhaled corticosteroids should be taken regularly for the prevention of 
symptoms.  Doubling the dose at the first sign of a respiratory infection is a 
frequently used tactic, and seems to reduce the risk of a severe 
exacerbation of asthma. 
 
Unfortunately, commonly discussed side effects of corticosteroids, the lack 
of an instant improvement in symptoms, and the need to take them 
regularly, at least twice a day, all conspire to make poor compliance 
extremely common. 
Oral Corticosteroids 
 
Regular long-term oral corticosteroids are the last resort in the out-patient 
management of asthma treatment.  However, short courses are very 
valuable for controlling exacerbations of asthma. 
 
Short courses of oral steroids are used in the following situations: 
 
1.  As a diagnostic test. 
2.  To gain control when starting treatment in severe cases. 
3.  When inhalers are ineffective. 
4.  During exacerbations of asthma. 
 
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Patients prone to severe exacerbations of asthma often keep a supply of 
prednisolone tablets in reserve so that they can be used, (according to their 
individual management plans), should an exacerbation develop. 
In long-term use, a regime of alternate daily dosing is preferable.  Inhaled 
corticosteroids should be continued to keep the dose of oral steroids as low 
as possible. 
 
The prevention of osteoporosis is particularly important for patients using 
long-term steroids.  Treatments such as Hormone Replacement Therapy, 
and Bisphosphonates should be considered. 
 
The body’s immune and stress responses are blunted by regular steroid 
use.  Patients should carry ‘steroid cards’, and avoid contact with 
chickenpox or shingles. 
Leukotriene Antagonists 
 
Leukotrienes are one of the key inflammatory mediators responsible for 
bronchoconstriction.  The leukotriene antagonists are an exciting and 
relatively new class of treatment for asthma.  Examples include Montelukast 
(Singulair) and Zafirlukast (Accolate).  They are taken by mouth, once daily, 
and are generally very well tolerated.  (So, compliance is better.) They are 
useful in mild asthma or in moderate asthma in addition to inhaled steroids.  
(They are too new to feature in the BTS guidelines, but they are often 
considered for use as an alternative to long acting ß-agonists at step 3.) 
Desensitisation and Avoidance of Allergens 42 
 
Trials of these treatments have been disappointing, except where a patient 
has an obvious precipitating factor.  More common are asthmatics who are 
sensitive to a variety of ubiquitous allergens such as pollen, house dust mite, 
and fungal spores.  Unfortunately, it is impractical to entirely avoid these. 
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Appendix C  Management Plan 
Example of an Individual Management Plan for an Adult 
Asthmatic 
 
NB:  This is only an example: medication and peak flow are individual 
to each patient. 
Preventers 
 
 Take 
one puff of the becloforte in the morning and evening every day. 
 
If you get a cold, or your peak flow drops below 300, take two doses 
morning and evening. 
Relievers 
 
 Take 
two puffs of ventolin when you need it. 
 
If you need it more than five times a day, arrange an appointment at 
the surgery. 
Actions 
 
 
If your peak flow is less than 250, take six prednisolone tablets a day, 
and get an appointment at the surgery within 48 hours. 
 
If your peak flow is less than 200, take six prednisolone tablets, four 
puffs of ventolin, and ring the surgery immediately  
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Appendix D  Example Asthma diary  
Purpose: To use a diary card to keep track of a 
Citations with 
Sriram and 
patient's daily asthma symptoms. 
documentation. 
Svirbely 
01.15.02 
1998 
 
  
  
  
  
  
  
  
  
  
  
  
  
  
  
enter an "x" in the appropriate column for each question (give only 1 answer per row) 
  
  
awoken 2 or 3 
awoken once 
times or once 
during the night, 
for more than 
awake most of 
no sleep 
for less than 1 
an hour 
the night 
disturbance due 
hour, because 
because of 
because of 
  
to asthma 
of asthma 
asthma 
asthma 
  
  
Sleep disturbance 
  
  

  
Yes 

not present and 
not present but 
didn't require 
did require 
extra 
extra 
bronchodilator 
bronchodilator 
Chest tightness  
during the night 
during the night 
present 
  
  
  
on awakening  
  
  

  
Yes 

frequent but not 
most or all of 
Duration and frequency of  
none 
occasional 
all day 
the day 
  
  
daytime wheeze and 
breathlessness 
  
  

  
Yes 

moderate to 
severe; 
mild; not 
distressing 
incapacitating 
and/or had to 
Severity of daytime wheeze  
none 
or distressing 
limit activities 
  
  
  
and breathlessness 
  
  

  
Yes 

more than 
  
none 
occasional 
occasional 
  
  
  
Cough during the day 
  
  

  
Yes 

  
  
  
  
  
  
  
calculate 
result 
  
  
  
  
  
data complete? 
Yes   
  
  
  
  
asthma diary card score 
10 out of 12 
  
  
  
  
asthma severity based on 
score moderate   
  
  
  
  
  
  
  
  
  
  
  
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Appendix E  Drug Delivery Systems 
A wide variety of devices have been developed in an attempt to provide 
simple, efficient and cheap methods of administering inhaled drugs.  
Inhalation delivers the drug directly to the airways.  The necessary dose is 
smaller than for drugs given by mouth, and the incidence of side effects is 
reduced. 
Metered Dose Inhaler (MDI) 
 
This device uses compressed gas to dispense a metered dose of drug in 
aerosol form.  MDIs are very widely used, with about 400 million prescribed 
annually, worldwide.  Recently devices using CFC free gas have been 
introduced.  MDIs are cheap to produce, but they are inefficient.  Only 10% 
of the metered dose reaches the lungs (the rest is swallowed and 
metabolised by the liver), and about 25% of patients are unable to co-
ordinate the triggering of the device with the necessary intake of breath.  
MDIs work more efficiently in conjunction with a spacer device such as a 
Volumatic, and this combination is often used for young children and the 
elderly.  Because of the potential difficulties of using MDIs, it is particularly 
important to teach and then regularly check inhaler technique. 
Breath Actuated Aerosol Inhalers 
 
These inhalers do not require skilful co-ordination.  Inspiration triggers the 
device.  This makes them easier to use, especially for children.   
Dry Powder Inhalers 
These do not rely on co-ordination, and are easy to use.  The improved 
efficiency of lung deposition compared with an MDI means that the use of 
lower doses might be possible. 
Nebulisers 
 
Nebulisers are capable of delivering a high dose of bronchodilator.  These 
machines produce a fine mist of liquid medication that can be easily inhaled 
from a mask or mouthpiece.  The dose is delivered over about ten minutes.  
However, only about 12% of it reaches the lungs, as the majority escapes 
into the atmosphere, or is trapped in the nebuliser tubing. 
Tablets and Syrups 
 
This route is used for the leukotriene antagonists and the theophyllines.   
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Appendix F  Glossary of Terms 
 
 
Term Meaning 
Forced Expiratory Volume in  The amount of air that can be expelled in one second from 
the first second  (FEV1) 
a maximal inspiration using maximal effort. 
The total amount of air expired from the lung using 
Forced Vital Capacity (FVC) 
maximal effort from a maximal inspiration. 
A measure of lungpower using a simple apparatus. 
Peak Expiratory Flow (PEF) 
Useful in monitoring asthma. 
Total amount of air in the lung. 
Total Lung Capacity (TLC) 
It can only be measured by indirect means. 
A measure of the ability to transfer a respiratory gas from 
Gas Transfer Factor (DLCO) 
atmosphere to blood in a given time.  Useful in lung 
fibrosis. 
Fev1 is reduced more than FVC causing a reduced FEV1 : 
Obstructive Spirometry 
FVC ratio. 
Examples: Asthma & COPD. 
Suggests FVC is reduced.  Causes a normal or increased 
Restrictive Spirometry 
FEV1 : FVC ratio. 
Examples: chest wall abnormalities & lung fibrosis. 
 
 
FEV1 = 4 
FEV
 
1  = 1.3 
FEV1 = 2.8 
FVC = 5 
FVC = 3.1 
FVC = 3.1 
Ratio 80% 
Ratio 42% 
Ratio 90% 
Expire
a) Litres 
FEV1 
FVC 
FVC 
FVC 
FEV1
FEV1
a) Normal 
b) Obstructive
c) Restrictive       
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