Asthma is a common chronic inflammatory disorder of the airways characterised by reversible airflow limitation, airway hyperresponsiveness and inflammation of the bronchi.
Asthma is an enormously complex condition that may present at any age. Many factors can contribute to the development of asthma, understanding these is key to effective management.
Atopy is a genetic predisposition to IgE-mediated allergen sensitivity. Atopic individuals are predisposed to the following three conditions:
The hygiene hypothesis was first developed from epidemiological data showing increased autoimmune and allergic disease in western countries.
It postulates that reduced exposure to infectious pathogens at a young age predisposes individuals to such diseases. In simple terms, this environment is thought to encourage Th2 predominant response - one that produces IgE.
A small subset of patients with asthma are affected by a sensitivity to aspirin. Ingestion is capable of triggering an attack. These patients exhibit Samter’s triad:
Around 15% of cases of asthma in adults are related to occupational exposure. Asthma may be induced or exacerbated by such exposure. Hundreds of sensitisers have been identified. They may be categorised as:
Peak expiratory flow diaries during periods of work and holiday are key to the diagnosis of occupational asthma.
In this variant asthma is triggered by strenuous physical activity. The aetiology is complex but exposure to cold air and environmental pollutants contributes.
Asthma is the result of aberrant airway inflammation and bronchospasm. Both contribute to an increase in airway resistance.
Inhalation of allergens results in an immediate (type 1) hypersensitivity reaction in the airways.
Sensitisation occurs during the allergen exposure causing the release of IgE antibodies from plasma cells. IgE bind to high affinity receptors on mast cells.
Subsequent exposure to antigens cause mast cell degranulation and histamine release. These mediators cause smooth muscle contraction and bronchoconstriction whilst inflammation contributes to airway obstruction.
The initial early phase reaction may be followed by a late response hours later. During the late phase, recruitment of a variety of inflammatory cells (e.g. PMN cells, T-cells) occurs.
The late response is more complex than the early response involving multiple additional processes. Beta-agonists do not cause complete reversal of the late response.
In response to persistent chronic inflammation, the airways lay down fibrous tissue. Over time airway remodelling occurs and manifests as fixed airway obstruction - i.e. airway narrowing that is irreversible.
There may be little in the way of signs and symptoms between attacks. Cough, shortness of breath and an expiratory wheeze are typical.
Severe asthma requires rapid recognition and treatment. Wheeze may not be present and respiratory effort is frequently depressed.
Signs of hypoxia and altered mental status may be present.
Spirometry should always be performed at the time of diagnosis to assess airway obstruction.
Spirometry measures the flow and volume of air during inhalation and exhalation:
The following changes are seen in obstructive lung disease:
Reversibility may be demonstrated by performing spirometry before and after the administration of a bronchodilator.
Asthma demonstrates characteristic variability on PEFR diaries. It usefulness in the diagnosis of asthma is limited.
It is considered non-specific as variability may be seen in other conditions. It may be used to categorise acute asthma attacks and can be key to the diagnosis of occupational asthma.
Asthma is diagnosed in the presence of indicative clinical features and the exclusion of alternate diagnoses.
BTS/SIGN guidelines advise categorisation of patients based upon the probability of asthma being the correct diagnosis. From here the choice of further investigations may be made.
Consider specialist referral and testing for alternate diagnoses. If alternate diagnosis is unlikely treat as intermediate suspicion.
Consider lung function testing, in children, consider testing for atopy:
Tests include spirometry with bronchodilator therapy to demonstrate reversibility.
Trial of treatment and reassess using lung function testing or a validated scoring system:
Asthma management is a step-wise process with advancement indicated by ongoing symptoms.
Many diagnosed in childhood will ‘grow out’ of asthma. Age of onset is a particularly good marker, those developing wheeze at less than two years of age are likely to be asymptomatic by mid-childhood.
The evidence of each therapy is variable in the different age groups asthma affects. The indications for ‘stepping up' treatment is broadly that the previous step did not achieve control of symptoms. The reality is that guidance is more nuanced, it is recommended that the BTS/SIGN guidelines are referred to (BTS/SIGN 153 British guideline on the management of asthma).
As a general rule if a therapy is ineffective it should be discontinued.
All patients should be offered a short-acting beta-2 agonists (SABAs) such as salbutamol (a reliever). Prescribed as needed (PRN), if use exceeds three times a week consider 'stepping up' therapy.
Adults should receive a regular low-dose inhaled corticosteroid (ICS, a preventer). Children receive a very low-dose ICS.
Adults receive a regular long-acting beta-2 agonist (LABAs). Children > 5 receive a LABA, those < 5 should receive a Leukotriene receptor antagonists (LTRAs).
If LABAs improve symptoms but control is inadequate ICS dose may be increased to medium-dose in adults and low-dose in children.
If there is no response to LABAs they should be stopped.
Alternative ‘add-on’ therapies may be trialled (LTRAs, SR Theophyllines, Long-acting muscarinic antagonists (LAMAs) in adults, LTRAs in children).
Increase ICS to high-dose and consider the addition of a fourth drug (Leukotriene receptor antagonists (LTRAs), SR Theophylline, Long-acting muscarinic antagonists (LAMAs), Beta-agonist tablets in adults, SR Theophylline, in children).
Involves the continuous or intermittent use of oral steroids. Specialist input is likely necessary.
A severe acute asthma attack represents a medical emergency. Prompt recognition and management is required.
The severity of an acute asthma attack is based on symptoms, observations and PEFR.
The below algorithm is based on SIGN/BTS 153 British guideline on the management of asthma. Patients not responding to first line therapies need senior clinician review and discussion with HDU/ICU/PICU.
Salbutamol nebulisers, 2.5 - 5mg (preferably driven by oxygen) should be administered in adults. They may be repeated every 15 to 30 minutes. Children may more commonly be administered salbutamol via and inhaler and spacer device with 2-10 puffs.
If there is no access to nebulisers back to back inhalers should be given. IV beta-2 agonists should be reserved for those in whom inhaled therapy is not possible.
Oxygen should be started immediately in severe attacks and is typically titrated to saturations of 94-98%.
An arterial blood gas should be obtained and repeated tests may be necessary. The development of hypercapnia indicates a near-fatal attack, specialist and anaesthetic involvement is required.
Steroids should be started. Either PO with prednisolone 40-50mg daily or IV with hydrocortisone 100mg six hourly. Children aged 2-5 receive prednisolone 20mg or hydrortisone 50mg.
They should be continued for at least five days. In cases where IV hydrocortisone has been used, switch to oral prednisolone when appropriate.
Ipratropium bromide nebulisers are given to most patients admitted with an acute asthma attack.
500mcg in adults and 250mcg in children four to six hourly can be given.
There is a body of evidence indicating magnesium sulfate has bronchodilator effects.
Discussion with senior staff is necessary, a dose of 1.2 - 2 g IV magnesium sulfate may be given over 20 minutes in adults. Children receive a dose of 40mg/kg. Children may also be given magnesium sulfate added to their initial nebulisers.
In patients still not responding B2 agonist infusions may be started.
In an acute attack, there is little evidence IV aminophylline will result in additional bronchodilation.
It is often still used and requires senior input. A 5mg/kg loading dose (over 20 minutes) is followed by a continuous infusio. Aminophylline levels should be checked daily.
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