Asthma is a disease involving airway inflammation. It is characterised by airway hyperresponsiveness and attacks of reversible airway obstruction.
The best-defined and most commonly identified cause of this inflammation is inhalation of allergens. Sometimes, the relationship of these foreign proteins to the symptoms of asthma may be obvious to the patient (eg, when wheezing or coughing starts within 10 minutes of entering a house that has a cat in it). On the other hand, many patients who are allergic to house dust mites are not aware of the association between exposure and their symptoms. By contrast, most patients with asthma are well aware that their lungs vary in tightness and that many non-specific stimuli such as exercise, cold air, or passive smoking can trigger attacks. These responses to otherwise "trivial" stimuli such as cold air are referred to as bronchial hyperresponsiveness.
Classification of Asthma
Infants: In the first 2 years of life, wheezing and bronchiolitis are indistinguishable, and the commonest cause of these episodes is infection with the respiratory syncytial virus (RSV)
Older Children & Young Adults: By far the most commonly identified cause of asthma is sensitisation to one of the common inhalant allergens, particularly indoor allergens. Other important risk factors include a family history of asthma, infection with common cold viruses and housing conditions.
Asthma presenting after the age of 20: For this age group there is a wider differential diagnosis. Therefore, persistent symptoms require investigations. Major causes include simple allergic asthma in adults, intrinsic asthma associated with sinusitis, allergic bronchopulmonary aspergillosis (ABPA), and chronic obstructive lung disease.
Risk factors for Asthma
Sensitisation to: House dust mite – Cats – Alternaria mould
Family history of asthma
Cigarette smoke in infancy
High allergen load in infancy.
Evidence for indoor Allergens as Cause of Asthma
There is a strong association between sensitisation to indoor allergens and asthma.
The observations about allergens in houses, sensitisation of asthmatics and the association with asthma have been made in many different countries
The association is only with asthma, not with other lung disease
Bronchial challenge with allergens can reproduce many of the findings of asthma
Reducing exposure to dust mites in a sanatorium or in the home is an effective treatment for asthma
The mechanism by which allergen exposure causes sensitisation and subsequent disease is biologically plausible.
Other evidence for the role of allergy in asthma
There is a statistical correlation between serum IgE levels and the prevalence of asthma later.
Immunotherapy can be shown to reduce bronchial hyperresponsiveness as indicated by increased histamine PD20
Clinical features of Asthma
Cough is a common presentation, especially nocturnal cough, which often starts as soon as the child goes to bed. Another common presentation is wheezing in association with viral infections, sometimes called wheezy bronchitis. Before the age of 2 it can be difficult to diagnose asthma. A family history of atopy & positive skin prick test or associated food allergy will favour allergic asthma. It is the sensitisation to indoor allergens (cat, dogs, dust mites and moulds) that is strongly associated with asthma and not grass or other pollens.
Asthma in adults
Among adults with asthma, 30 70% are allergic, depending on the population studied. Among adults aged over 40 years who develop asthma for the first time, almost 50% may have intrinsic asthma, although these patients do not represent more than 10% of the total population.
Defined in 1947 as asthmatics presenting in adult life who showed:
Negative skin tests to common allergens
No family history of atopy
A severe course (often requiring oral steroids)
No improvement when admitted to hospital
In a random sample of adults presenting with asthma to an emergency room, almost 30% have extensive sinusitis on CT scan.
Late-onset asthma, which is frequently not associated with atopy, may be linked to the workplace. Occupational exposure to sensitising chemicals (eg, isocyanates) is an important cause of asthma as the timely removal from exposure can cure the disease or at least prevent progression.
Extrinsic (or Allergic Asthma) refers to inhaled allergen-driven cross-linking of the IgE molecules present on airway mast cells, resulting in degranulation, mediator release, and the beginning of the inflammatory cascade described below. This type of asthma typically appears before the fourth decade of life and represents the most commonly encountered asthma in clinical practise. In order to diagnose extrinsic asthma there must be:
A clear temporal relationship between exposure to the putative aeroallergen and the development of airway symptoms (either early phase, late phase, or both) to the inhaled trigger; and
Demonstrable skin test reactivity to the inhaled trigger.
A seasonal variation in the frequency or severity of asthma provides the clue to the diagnosis of extrinsic asthma.
In most cases the asthma symptoms will be accompanied by symptoms of allergic rhinitis (rhinorrhea, sneezing, ocular burning), making the diagnosis easier to recognize. An appreciation of the perennial nature of certain aeroallergens (e.g., dust mites) will ensure the diagnosis is not missed.
Occupational asthma refers to the development of asthma symptoms (changes in air flow) triggered by exposure to inhaled compounds in the workplace. It may or may not be IgE-mediated. It is important to differentiate this type of asthma from exposure to irritants (chemicals, gases, metals, and so on), infectious agents or other coincidental adult-onset asthma unrelated to occupational exposure.
It is estimated that occupational asthma represents approximately 5% of all cases of asthma. Typically features of occupational asthma include a latency period of up to several years prior to onset of symptoms, worsening of symptoms shortly at the end of the shift or at night, and improvement in asthma symptoms on the weekends.
Some frequently noted causes of occupational asthma include:
Toluene diisocynate (TDI) in plastic workers
Flour contaminants (mould or insect) among bakers, and
Plicatic acid from western red cedar wood dust in lumber workers.
Exercise-induced asthma or more accurately, exercise-induced bronchospasm (EIB), is used to describe asthmatic symptoms present only in association with exercise. This differentiate it from exercise intolerance, a condition noted in many chronic asthmatics, that often prematurely terminates exercise sessions. This differentiation is important, since the clinician must be aware of the dual-phase (early and late) response that accompanies EIB and treat appropriately. Moreover, a unique feature of EIB is the lack of increased airway hyperresponsiveness or inflammation seen with other triggers of asthma. Bronchoconstriction in EIB starts 5-10 minutes after exercise. Resolution occurs within 1 h, a late-phase response 4-6 hour later rarely occurs.
Diagnosis of Asthma
History is important in eliciting classical symptoms, in determining severity and stability of asthma, the presence of other atopic diseases, and possible triggers.
Historical Cues in Workup of the Asthmatic Patient
Frequency of symptoms (twice daily, weekly, monthly, and so on)
Severity of symptoms (hospitalisations, ER visits, workdays missed)
Temporal symptoms (perennial vs seasonal)
Timing of symptoms (e.g. nocturnal symptoms)
Known precipitants (i.e. strong odours, temperature or weather changes)
Family history of allergic diseases
Previous therapy and efficacy.
There are two simple methods, peak expiratory flow rate (PEFR) using a peak flow meter, or spirometry which indicates forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1). Reversibility of airways obstruction is demonstrated by repeating the test 15 minutes after inhalation of a beta 2 agonist, such as salbutamol.
An increased FEV1 greater than 15%, or 20% in PEFR, or if the PEFR varies more than 20% a day on more than one day, is diagnostic of asthma.