Asthma is a common chronic inflammatory condition of the airway which is classically characterized by:
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| Asthma most frequently occurs between the ages of 3-5 years |
- Airflow limitation which is usually reversible spontaneously or with treatment.
- Airway hyper-responsiveness to a wide range of stimuli which would cause no ill effects in the normal airways of nonasthmatic individuals.
- Inflammation of the bronchi/airway with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, smooth muscle hypertrophy, matrix deposition, mucus plugging and epithelial damage.
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| What happens during an asthma attack? |
Typical symptoms of asthma include wheeze (high pitched musical sound), cough, chest tightness and dyspnoea (breathlessness) particularly at night and/or early in the morning.
Epidemiology of asthma:
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| World map showing the prevalence of clinical asthma (proportion of population (%)). Data drawn from the European Community Respiratory Health Study (ECRHS) and the International Study of Asthma and Allergies in Childhood (ISAAC). |
Asthma is more common in more developed countries. There has been a significant increase in the incidence of asthma in the Western world over the past 3 decades. Some of the highest rates are in the UK, New Zealand and Australia, but the rates are lower in Far Eastern countries such as China and Malaysia, Africa and Central and Eastern Europe. Long-term follow-up in developing countries suggests that the disease may become more frequent as individuals adopt a more ‘westernized’ lifestyle.
In many countries the prevalence of asthma is increasing. This increase, with its accompanying allergy, is particularly in children and young adults where this disease may affect up to 15% of the population.
In many countries the prevalence of asthma is increasing. This increase, with its accompanying allergy, is particularly in children and young adults where this disease may affect up to 15% of the population.
Current estimates suggest that asthma affects 300 million people world-wide and
an additional 100 million persons will be diagnosed by 2025.
Although the development, course of disease and response to treatment are
influenced by genetic determinants, the rapid rise in the prevalence of asthma
implies that environmental factors are critically important in terms of its
expression.
Classification of asthma:
Asthma is a heterogeneous disease triggered by a variety of inciting agents,
there is no universally accepted classification. But the simplest classification of asthma is:
- Extrinsic/atopic asthma (70%) – implying a definite external cause and are due to IgE and TH2-mediated immune responses to environmental antigens
- Intrinsic/Non-atopic asthma (30%) – caused by non-immune stimuli such as aspirin; pulmonary infections, especially those caused by viruses; cold; psychological stress; exercise; and inhaled irritants.
This classification is useful from the point of pathophysiology, in clinical
practice it is not always possible to classify asthma.
Extrinsic/Atopic asthma:
This most common type of asthma usually begins in childhood. A positive family
history of atopy is common, serum IgE levels are elevated and asthmatic attacks are often preceded by allergic
rhinitis, urticaria, or eczema.
The term atopy or atopic syndrome is a genetic predisposition toward developing certain allergic hypersensitivity reactions to common environmental antigens such as pollen, house dust mite, animal dander, fungi (particularly Aspergillus: allergic bronchopulmonary aspergillosis), pets such as cats and dogs, pests such as cockroaches. This term was used by clinicians at the beginning of the twentieth century to describe a group of disorders, including asthma and hayfever, that appeared:
- to run in families
- to have characteristic wheal-and-flare skin reactions to common allergens in the environment
- to have circulating allergen-specific IgE.
Atopic individuals show positive skin-prick reactions to common inhalant allergens (examples given above). A skin test with the offending antigen results in an immediate wheal-and-flare
reaction (a classic example of the type I IgE-mediated hypersensitivity
reaction)
Positive skin-prick tests to inhalant allergens are shown in 90% of children and 70% of adults with persistent asthma. Childhood asthma is often accompanied by eczema (atopic dermatitis). A frequently overlooked cause of late-onset asthma in adults is sensitization to chemicals or biological products in the workplace.
Intrinsic/Non atopic asthma:
Intrinsic asthma often starts in middle age (‘late onset’). Nevertheless, many patients with adult-onset asthma show positive allergen skin tests and on close questioning give a history of respiratory symptoms compatible with childhood asthma. A positive family history is uncommon, serum IgE levels are normal, and there are no associated allergies.
In such cases the trigger may be a viral infections of the respiratory tract (most common) or inhaled
air pollutants such as sulfur dioxide, ozone, and nitrogen dioxide. These
agents increase airway hyper-reactivity in both normal and asthmatic subjects.
In the latter, however, the bronchial response, manifested as spasm, is much
more severe and sustained.
Non-atopic individuals may also develop asthma in middle age from extrinsic causes such as sensitization to occupational agents such as toluene diisocyanate, intolerance to nonsteroidal anti-inflammatory drugs such as aspirin or because they were given β-adrenoceptor-blocking agents for concurrent hypertension or angina that block the protective effect of endogenous adrenergic agonists.
Extrinsic causes must be considered in all cases of asthma and, where possible, avoided.
Causes of asthma:
Asthma is a multifactorial disease, ie many factors are responsible for the development of asthma.
The major factors involved in the development of asthma are shown in the figure below:
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| Major factors responsible for the development of asthma |
1. Atopy and allergy
2. Genetic factors:
Genes, in combination with environmental factors, may turn out to play a key role in the development of asthma.
- Genes controlling the production of the cytokines IL-3, IL-4, IL-5, IL-9, IL-13 and GM-CSF – which in turn affect mast and eosinophil cell development and longevity as well as IgE production – are present in a cluster on chromosome 5q31–33 (the IL-4 gene cluster).
- Polymorphic variation in proteins along the IL-4/-13 signalling pathway is strongly associated with allergy and asthma.
- Novel asthma genes identified by positional cloning from whole genome scans are the PHF11 locus on
- chromosome 2 (that includes genes SETDB2 and RCBTB1) and transcription factors, which are implicated in IgE synthesis and associated more with atopy than asthma.
- ADAM 33 (a disintegrin and metalloproteinase) on chromosome 20p13 is more strongly associated with airway hyperresponsiveness and tissue remodelling.
- Other recently discovered genes associated with asthma are those that encode neuropeptide S receptor (GPRA or GPR154) on chromosome 7p15, HLA-G on chromosome 6p21, dipeptidyl peptidase 10 on chromosome 2q14 and most recently on chromosome 17q21 ORMDL3, a member of a gene family that encodes transmembrane proteins anchored in the endoplasmic reticulum.
3. Environmental factors:
Early childhood exposure to allergens and maternal smoking has a major influence on IgE production. Much current interest focuses on the role of intestinal bacteria and childhood infections in shaping the immune system in early life.
It has been suggested that growing up in a relatively ‘clean’ environment may predispose towards an IgE response to allergens (the ‘hygiene hypothesis’).
Conversely, growing up in a ‘dirtier’ environment may allow the immune system to avoid developing allergic responses.
Components of bacteria (e.g. lipopolysaccharide endotoxin; immunostimulatory CpG DNA sequences; flagellin), viruses (e.g. SS- and DS-RNA) and fungi (e.g. chiton, a cell wall component) are able to stimulate up to 10 different toll-like receptors (TLRs) expressed on immune and epithelial cells to direct the immune and inflammatory response away from the allergic (Th2) towards protective (Th1 and Treg) pathways. Th1 immunity is associated with antimicrobial protective immunity whereas regulatory T cells are strongly implicated in tolerance to allergens.
Thus early life exposure to inhaled and ingested products of microorganisms, as occurs in livestock farming communities and developing countries, may be critical in helping shape the subsequent risk of a child becoming allergic and/or developing asthma.
It has been suggested that growing up in a relatively ‘clean’ environment may predispose towards an IgE response to allergens (the ‘hygiene hypothesis’).
Conversely, growing up in a ‘dirtier’ environment may allow the immune system to avoid developing allergic responses.
Components of bacteria (e.g. lipopolysaccharide endotoxin; immunostimulatory CpG DNA sequences; flagellin), viruses (e.g. SS- and DS-RNA) and fungi (e.g. chiton, a cell wall component) are able to stimulate up to 10 different toll-like receptors (TLRs) expressed on immune and epithelial cells to direct the immune and inflammatory response away from the allergic (Th2) towards protective (Th1 and Treg) pathways. Th1 immunity is associated with antimicrobial protective immunity whereas regulatory T cells are strongly implicated in tolerance to allergens.
Thus early life exposure to inhaled and ingested products of microorganisms, as occurs in livestock farming communities and developing countries, may be critical in helping shape the subsequent risk of a child becoming allergic and/or developing asthma.
The allergens involved in asthma are similar to those in rhinitis although pollen exposure causes hay fever to a
greater extent than asthma.
Allergens from the faecal particles of the house-dust mite are associated with most cases of asthma world-wide.
Cockroach allergy has been implicated in asthma in US inner-city children, while allergens from furry pets (especially cats) are increasingly common causes.
The fungal spores from Aspergillus fumigatus give rise to a complex series of lung disorders, including asthma. Many allergens, including those from Aspergillus, have intrinsic biological properties, e.g. proteolytic enzymes that facilitate their passage through the airway epithelium to increase their sensitizing capacity.
Chitins are cross-linked polysaccharides found in the exoskeleton of insects and cockroaches, fungi and in the eggs of helminths. They can be inhaled into the airways. Chitinase-family proteins may play a role in the pathogenesis of asthma as the levels in the lungs and the serum are high in asthma and correlate with disease activity.
Allergens from the faecal particles of the house-dust mite are associated with most cases of asthma world-wide.
Cockroach allergy has been implicated in asthma in US inner-city children, while allergens from furry pets (especially cats) are increasingly common causes.
The fungal spores from Aspergillus fumigatus give rise to a complex series of lung disorders, including asthma. Many allergens, including those from Aspergillus, have intrinsic biological properties, e.g. proteolytic enzymes that facilitate their passage through the airway epithelium to increase their sensitizing capacity.
Chitins are cross-linked polysaccharides found in the exoskeleton of insects and cockroaches, fungi and in the eggs of helminths. They can be inhaled into the airways. Chitinase-family proteins may play a role in the pathogenesis of asthma as the levels in the lungs and the serum are high in asthma and correlate with disease activity.
4. Increased responsiveness of the airways of the lung (airway / bronchial hyperresponsiveness):
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| Normal airway vs asthmatic airway |
Other factors likely to be important include the degree of airway narrowing and the influence of neurogenic mechanisms.
Bronchial hyperresponsiveness (BHR) is demonstrated by asking the patient to inhale gradually increasing concentrations of either histamine or methacholine (bronchial provocation tests).
5. Occupational asthma:
Over 250 materials encountered at the workplace, accounting for 15% of all asthma cases, give rise to occupational asthma. The causes are recognized occupational diseases in the UK, and patients in insurable employment are therefore eligible for statutory compensation provided they apply within 10 years of leaving the occupation in which the asthma developed.
Occupational
asthma
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Cause
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Source/Occupation
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Low molecular weight
(non-IgE related)
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Isocyanates
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Polyurethane varnishes
Industrial coatings
Spray
painting
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Colophony fumes
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Soldering/welders
Electronics industry
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Wood dust
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Drugs
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Bleaches and dyes
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Complex metal salts, e.g.nickel,
platinum, chromium
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High molecular weight
(IgE related)
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Allergens from animals and insects
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Farmers, workers in poultry and
seafood processing industry;
laboratory workers
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Antidotes
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Nurses, health industry
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Latex
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Health workers
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Proteolytic enzymes
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Manufacture (but not use) of‘biological’
washing powdes
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Complex salts of platinum
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Metal refining
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Acid anhydrides and polyamine
hardening agents
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Industrial coatings
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Table: Occupational asthma
Occupational asthma can be due to:
- high molecular weight compounds, e.g. flour, organic dusts and other large protein molecules involving specific IgE antibodies, or
- low molecular weight compounds, e.g. reactive chemicals such as isocyanates and acid anhydrides that bond chemically to epithelial cells to activate them as well as provide haptens recognized by T cells.
The risk of developing some forms of occupational asthma increases in smokers.
The proportion of employees developing occupational asthma depends primarily upon the level of exposure.
Proper enclosure of industrial processes or appropriate ventilation greatly reduces the risk.
Atopic individuals develop occupational asthma more rapidly when exposed to agents causing the development of specific IgE antibody.
The proportion of employees developing occupational asthma depends primarily upon the level of exposure.
Proper enclosure of industrial processes or appropriate ventilation greatly reduces the risk.
Atopic individuals develop occupational asthma more rapidly when exposed to agents causing the development of specific IgE antibody.
Non-atopic individuals can also develop asthma when exposed to such agents, but after a longer period of exposure.
6. Non-specific factors
The characteristic feature of BHR in asthma means that, as well as reacting to specific antigens, the airways will also respond to a wide variety of non-specific direct and indirect stimuli.
a. Cold air and exercise
Most asthmatics wheeze after prolonged exercise. Typically, the attack does not occur while exercising but afterwards.
The inhalation of cold, dry air will also precipitate an attack.
Exercise-induced wheeze is driven by release of histamine, prostaglandins (PGs) and leukotrienes (LTs) from mast cells as well as stimulation of neural reflexes when the epithelial lining fluid of the bronchi becomes hyperosmolar owing to drying and cooling during exercise. The phenomenon can be shown by exercise, cold air and hypertonic (e.g. saline or mannitol) provocation tests.
The inhalation of cold, dry air will also precipitate an attack.
Exercise-induced wheeze is driven by release of histamine, prostaglandins (PGs) and leukotrienes (LTs) from mast cells as well as stimulation of neural reflexes when the epithelial lining fluid of the bronchi becomes hyperosmolar owing to drying and cooling during exercise. The phenomenon can be shown by exercise, cold air and hypertonic (e.g. saline or mannitol) provocation tests.
b. Atmospheric pollution and irritant dusts, vapours and fumes:
Many patients with asthma experience worsening of symptoms on contact with tobacco smoke, car exhaust fumes, solvents, strong perfumes or high concentrations of dust in the atmosphere.
Major epidemics have been recorded when large amounts of allergens are released into the air, e.g. soybean epidemic in Barcelona.
Asthma exacerbations increase in both summer and winter air pollution episodes associated with climatic temperature inversions. Epidemics of the disease have occurred in the presence of high concentrations
Major epidemics have been recorded when large amounts of allergens are released into the air, e.g. soybean epidemic in Barcelona.
Asthma exacerbations increase in both summer and winter air pollution episodes associated with climatic temperature inversions. Epidemics of the disease have occurred in the presence of high concentrations
of ozone, particulates and NO2 in the summer and particulates, NO2 and SO2 in the winter.
c. Diet
Increased intakes of fresh fruit and vegetables have been shown to be protective, possibly owing to the increased intake of antioxidants or other protective molecules such as flavonoids. Genetic variation in antioxidant enzymes is associated with more severe asthma.
d. Emotion
It is well known that emotional factors may influence asthma both acutely and chronically, but there is no evidence that patients with the disease are any more psychologically disturbed than their non-asthmatic peers. An asthma attack is a frightening experience, especially when of sudden and unexpected onset. Patients at special risk of life-threatening attacks are understandably anxious.
e. Drugs:
i. Non-steroid anti-inflammatory drugs (NSAIDs):
NSAIDs, particularly aspirin and propionic acid derivatives, e.g. indometacin and ibuprofen, have a role in the development and precipitation of asthma in approximately 5% of patients. NSAID intolerance is especially prevalent in those with both nasal polyps and asthma and is not infrequently associated with a triad of asthma, rhinitis and flushing on drug exposure.
NSAIDs, particularly aspirin and propionic acid derivatives, e.g. indometacin and ibuprofen, have a role in the development and precipitation of asthma in approximately 5% of patients. NSAID intolerance is especially prevalent in those with both nasal polyps and asthma and is not infrequently associated with a triad of asthma, rhinitis and flushing on drug exposure.
In susceptible subjects exposure to NSAIDs reveals an imbalance in the metabolism of arachidonic acid.
NSAIDs inhibit arachidonic acid metabolism via the cyclo-oxygenase (COX) pathway, preventing the synthesis of certain prostaglandins. In aspirin-intolerant asthma there is reduced production of PGE2 which, in a sub-proportion of genetically susceptible subjects, induces the overproduction of cysteinyl leukotrienes by eosinophils, mast cells and macrophages. In such patients there is evidence for genetic polymorphisms involving the enzymes and receptors of the leukotriene generating pathway.
Interestingly, asthma in intolerant patients is not precipitated by COX-2 inhibitors, indicating that it is blockade of the COX-1 isoenzyme that is linked to impaired PGE2 production.
ii. Beta-blockers.
The airways have a direct parasympathetic innervation that tends to produce bronchoconstriction. There is no direct sympathetic innervation of the smooth muscle of the bronchi, and antagonism of parasympathetically induced bronchoconstriction is critically dependent upon circulating epinephrine (adrenaline) acting through β2-receptors on the surface of smooth muscle cells.
Inhibition of this effect by β-adrenoceptor-blocking drugs such as propranolol leads to bronchoconstriction and airflow limitation, but only in asthmatic subjects. The so-called selective β1-adrenergicblocking drugs such as atenolol may still induce attacks of asthma; their use to treat hypertension or angina in asthmatic patients is best avoided.
Inhibition of this effect by β-adrenoceptor-blocking drugs such as propranolol leads to bronchoconstriction and airflow limitation, but only in asthmatic subjects. The so-called selective β1-adrenergicblocking drugs such as atenolol may still induce attacks of asthma; their use to treat hypertension or angina in asthmatic patients is best avoided.
7. Allergen-induced asthma
The experimental inhalation of allergen by atopic asthmatic individuals leads to the development of different types of reaction.
- Immediate asthma (early reaction): Airflow limitation begins within minutes of contact with the allergen, reaches its maximum in 15–20 minutes and subsides by 1 hour.
- Dual and late-phase reactions: Following an immediate reaction many asthmatics develop a more prolonged and sustained attack of airflow limitation that responds less well to inhalation of bronchodilator drugs such as salbutamol. Isolated late-phase reactions with no preceding immediate response can occur after the inhalation of some occupational sensitizers such as isocyanates. During and up to several weeks after the exposure, the airways are hyperresponsive, which may explain persisting symptoms after allergen exposure.
Pathogenesis of Asthma:
The pathogenesis of asthma is complex and not fully understood. It involves a number of cells, mediators, nerves and vascular leakage that can be activated by several different mechanisms, of which exposure to allergens is among the most significant. The varying clinical severity and chronicity of asthma is dependent on an interplay between airway inflammation and airway wall remodelling.
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| Comparison of a normal bronchiole with that in a person with asthma. Note the accumulation of mucus in the bronchial lumen resulting from an increase in the number of mucus-secreting goblet cells in the mucosa and hypertrophy of submucosal mucous glands. In addition, there is intense chronic inflammation caused by recruitment of eosinophils, macrophages, TH2 cells and other inflammatory cells. Basement membrane underlying the mucosal epithelium is thickened, and there is hypertrophy and hyperplasia of smooth muscle cells. |
Clinical features / Signs and Symptoms of Asthma:
Asthma characteristically displays a diurnal pattern, with symptoms and lung function being worse in the early morning. Particularly when poorly controlled, symptoms such as cough and wheeze disturb sleep and have led to the use of the term 'nocturnal asthma'. Cough may be the dominant symptom in some patients, and the lack of wheeze or breathlessness may lead to a delay in reaching the diagnosis of so-called 'cough-variant asthma'. |
An important minority of patients develop a particularly severe form of asthma; this appears to be more common in women. Allergic triggers are less important and airway neutrophilia predominates. |
Investigations done to diagnose asthma:
The diagnosis of asthma is predominantly clinical and based on a characteristic
history. There is no single satisfactory diagnostic test for all asthmatic patients.
1. Lung function tests:
Peak expiratory flow rate (PEFR) measurements on waking, prior to taking a bronchodilator and before bed after a bronchodilator, are particularly useful in demonstrating the variable airflow limitation that characterizes the disease. The diurnal variation in PEFR is a good measure of asthma activity and is of help in the longer-term assessment of the patient’s disease and its response to treatment. To assess possible occupational asthma, peak flows need to be measured for at least 2 weeks at work and 2 weeks off work.
Spirometry is useful, especially in assessing reversibility. Asthma can be diagnosed by demonstrating a greater than 15% improvement in FEV1 or PEFR following the inhalation of a bronchodilator. However, this degree of response may not be present if the asthma is in remission or in severe chronic asthma when little reversibility can be demonstrated or if the patient is already being treated with long-acting bronchodilators.
The carbon monoxide (CO) transfer test is normal in asthma.
2. Exercise tests
These have been widely used in the diagnosis of asthma in children. Ideally, the child should run for 6 minutes on a treadmill at a workload sufficient to increase the heart rate above 160 beats per minute. Alternative methods use cold air challenge, isocapnoeic hyperventilation (forced overbreathing with artificially maintained Paco2) or aerosol challenge with hypertonic solutions. A negative test does not automatically rule out asthma.
3. Histamine or methacholine bronchial provocation test:
This test indicates the presence of airway hyperresponsiveness, a feature found in most asthmatics, and can be particularly useful in investigating those patients whose main symptom is cough. The test should not be performed on individuals who have poor lung function (FEV1 < 1.5 L) or a history of ‘brittle’ asthma. In children, controlled exercise testing as a measure of BHR is often easier to perform.
4. Trial of corticosteroids:
All patients who present with severe airflow limitation should undergo a formal trial of corticosteroids. Prednisolone 30 mg orally should be given daily for 2 weeks with lung function measured before and immediately after the course. A substantial improvement in FEV1 (>15%) confirms the presence of a reversible element and indicates that the administration of inhaled steroids will prove beneficial to the patient. If the trial is for 2 weeks or less, the oral corticosteroid can be withdrawn without tailing off the dose, and should be replaced by inhaled corticosteroids in those who have responded.
Exhaled nitric oxide (NO), a measure of airway inflammation and an index of corticosteroid response, is used in children as a test for the efficacy of corticosteroids.
5. Blood and sputum tests
Patients with asthma may have an increase in the number of eosinophils in peripheral blood (> 0.4 × 109/L). The presence of large numbers of eosinophils in the sputum is a more useful diagnostic tool.
6. Chest X-ray
There are no diagnostic features of asthma on the chest Xray, although overinflation is characteristic during an acute episode or in chronic severe disease. A chest X-ray may be helpful in excluding a pneumothorax, which can occur as a complication, or in detecting the pulmonary shadows associated with allergic bronchopulmonary aspergillosis.
7. Skin tests
Skin-prick tests (SPT) should be performed in all cases of asthma to help identify allergic causes. Measurement of allergen-specific IgE in the serum is also helpful if SPT facilities are not available, if the patient is taking antihistamines or if a wide range of allergens are being investigated. Asthma frequently occurs in conjunction with other atopic disorders, especially rhinitis.
8. Allergen provocation tests
Allergen challenge is not required in the clinical investigation of patients, except in cases of suspected occupational asthma. Another controversial exception is the investigation of food allergy causing asthma. This diagnosis can be difficult, although many patients are concerned about the possibility.
In the absence of any obvious allergy, e.g. peanut or milk, if the patient has asthma without any other systemic features, then food allergy is most unlikely to be the cause.
Open food challenges are unreliable and if the diagnosis is seriously entertained, blind oral challenges with the food disguised in opaque gelatine capsules are necessary to confirm or refute a causative link.
There is much speculation about food intolerance (as opposed to allergy) and asthma including the role of food additives, which occasionally can precipitate severe attacks.
In the absence of any obvious allergy, e.g. peanut or milk, if the patient has asthma without any other systemic features, then food allergy is most unlikely to be the cause.
Open food challenges are unreliable and if the diagnosis is seriously entertained, blind oral challenges with the food disguised in opaque gelatine capsules are necessary to confirm or refute a causative link.
There is much speculation about food intolerance (as opposed to allergy) and asthma including the role of food additives, which occasionally can precipitate severe attacks.
Treatment/Management of Asthma:
- abolish symptoms
- restore normal or best possible lung function
- reduce the risk of severe attacks
- enable normal growth to occur in children
- minimize absence from school or employment.
- patient and family education about asthma
- patient and family participation in treatment
- avoidance of identified causes where possible
- use of the lowest effective doses of convenient medications to minimize short-term and long-term side-effects.
Whenever possible, patients should be encouraged to take responsibility for
managing their own disease. Time should be taken to encourage an understanding
of the nature of the condition, the relationship between symptoms and
inflammation, the importance of key symptoms such as nocturnal waking, the
different types of medication, and, if appropriate, the use of PEF to guide
management decisions.
A variety of tools/questionnaires have been validated to assist in assessing asthma control. Written action plans may be helpful in developing self-management skills.
A variety of tools/questionnaires have been validated to assist in assessing asthma control. Written action plans may be helpful in developing self-management skills.
Avoidance of aggravating factors:
A stepwise approach to the management of asthma:
Step 1: Occasional use of inhaled short-acting β2-adrenoreceptor agonist bronchodilatorsFor patients with mild intermittent asthma (symptoms less than once a week for 3 months and fewer than two nocturnal episodes/month), it is usually sufficient to prescribe an inhaled short-acting β2-agonist (salbutamol or terbutaline), to be used on an as-required basis.However, many patients (and their physicians) underestimate the severity of asthma and these patients require careful supervision. A history of a severe exacerbation should lead to a step up in treatment. A variety of different inhaled devices are available and choice should be guided by patient preference and competence in using the device. The metered-dose inhaler remains the most widely prescribed.
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