Case 3 Asthma
Description of asthma
Definition
Asthma is a chronic inflammatory disease of the airways, characterised by acute exacerbations of reversible airway obstruction. The condition was formerly divided into two main types – extrinsic and intrinsic asthma. These classifications have since changed. Asthma is now separated into more specific aetiological subtypes, including, for example, allergic, exercise-induced, nocturnal, aspirin-sensitive and occupational asthma.
Epidemiology
This distressing, often disabling, and sometimes fatal disorder affects around ten per cent of the Australian population.1 A slightly higher prevalence rate is evident among adult women (eleven per cent) and among the 15–24 and 75 years and over age groups (eleven per cent). Higher rates of asthma are also observed among socially disadvantaged, unemployed and Indigenous populations.1
Aetiology and pathophysiology
The aetiology of asthma is multifactorial, with genetic and familial factors playing a major part in the pathogenesis of the disease. There is some suggestion that the growing prevalence of asthma is also due to a number of environmental contacts, such as vaccination, early introduction of foods, early exposure to antibiotics and food additives,2,3 but there are insufficient data to support these theories. Emerging evidence does indicate that exposure to infectious agents may be a risk factor; one recent longitudinal study reported significantly higher odds of asthma and respiratory wheeze among 5-year-old children who reported severe respiratory infections during infancy, particularly those with atopy.4 Other factors linked to the development of asthma are obesity, exposure to household allergens (e.g. dust mite, cockroaches, pets), omega 3 fatty acid intake and perinatal issues (e.g. lack of breastfeeding, poor maternal nutrition, young maternal age, prematurity, low birthweight).3,5 Evidence linking nutrient deficiency (e.g. vitamin C, vitamin E) with asthma is not convincing.6,7
The acute onset of asthma in susceptible individuals can be initiated by a range of allergic and non-allergic triggers, including household allergens (e.g. dust mite, cockroaches, animal dander), respiratory irritants (e.g. air pollution, cigarette smoke, perfumes, cleaning agents, sulfur dioxide), grass and tree pollens, occupational irritants (e.g. latex, solder, flour), hormonal changes, exercise, emotions (e.g. anger, anxiety, excitement), respiratory infections, cold air, aspirin and gastro-oesophageal reflux disease.3,8 It is not yet established how these factors trigger respiratory distress, although the prevailing theory suggests that heightened inflammatory activity could be a precipitating factor. The predominance of T-helper cell type 2 (Th2) activity observed in asthmatics and the subsequent increase in pro-inflammatory cytokine levels, airway eosinophilia and immunoglobulin (IgE) production, all appear to promote the development of smooth muscle hypertrophy and airway remodelling.9 These changes lead to airway hyper-responsiveness, which, upon exposure to any one of the aforementioned triggers, causes airway inflammation, submucosal oedema, increased mucus production, bronchoconstriction, mucus plugging and respiratory distress.3,9
Clinical manifestations
People with mild asthma are normally asymptomatic between exacerbations. In more severe cases of asthma, and during acute exacerbations of asthma, people typically present with dyspnoea, tachypnoea, chest tightness, cough, audible wheezing and anxiety. As airway obstruction progresses, and oxygen exchange diminishes, more serious manifestations begin to emerge, including hypoxia, cyanosis and altered consciousness, and at worst, respiratory failure and death.3,8
Clinical case
23-year-old woman with exercise-induced asthma
Rapport
Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, and the accuracy and comprehensiveness of the clinical assessment.
Medical history
Family history
Medications
Salbutamol inhaler 2 puffs as needed, eformoterol 1 inhalation daily, 1 multivitamin tablet daily.
Medical conditions
Asthma, allergic rhinitis, recurrent sinusitis (for the past 5 years, often during spring).
Lifestyle history
Alcohol consumption
Light social drinker. Consumes 1–2 × 375 mL premixed Vodka drinks per fortnight.
Illicit drug use
Diet and fluid intake | |
---|---|
Breakfast | Wholemeal toast with low-fat cream cheese, coffee. |
Morning tea | Protein bar, banana, walnuts. |
Lunch | Tossed salad or wholemeal sandwich with turkey or chicken, tomato, low-fat cheese and lettuce. |
Afternoon tea | 150 g vanilla yoghurt. |
Dinner | Egg white omelette with tomato and cheese, grilled salmon or whiting with carrots and beans, stirfry with chicken breast, carrots, capsicum and onion. |
Fluid intake | 1–2 cups of instant coffee a day, 7–8 cups of water a day. |
Food frequency | |
Fruit | 1–2 serves daily |
Vegetables | 2–3 serves daily |
Dairy | 2–3 serves daily |
Cereals | 4–5 serves daily |
Red meat | 1 serve a week |
Chicken | 6 serves a week |
Fish | 1 serve a week |
Takeaway/fast food | 0–1 times a week |
Physical examination
Auscultation
Vesicular breath sounds are heard equally over all lung fields. Mild late expiratory polyphonic wheeze is also evident across all lung fields. Bronchophony, aegophony and whispered pectoriloquy are absent.
Clinical assessment tools
The asthma control scoring system (ACSS) revealed a clinical subscore of twenty per cent (a measure of symptom frequency, physical limitation and rescue medication use), a physiological subscore of eighty per cent (a measure of peak expiratory flow rate), and an inflammatory subscore of eighty per cent (a measure of airway eosinophil count).10 This provided a mean global asthma control score of 60 per cent, signifying modest asthma control and moderate asthma severity (a higher percentage score indicates better control and reduced severity).
Diagnostics
Pathology tests
Eosinophil count
This count is a useful marker of asthma activity because activated eosinophils release histamine, which triggers bronchial smooth muscle contraction and mucus production, all of which are implicated in the pathogenesis of asthma.9
Immunoglobulin E (IgE)
IgE is an antibody primarily involved in allergic reactions. When IgE is cross-linked with an antigen, it stimulates the release of vasoactive substances (e.g. histamine) from basophils and mast cells. This results in smooth muscle contraction, increased vascular permeability and inflammation,11 and the subsequent manifestation of symptoms such as wheeze and dyspnoea. Elevated levels of serum IgE are positively associated with the severity of asthma.12
Plasma or red cell fatty acid analysis
This assesses the concentration of fatty acids within the plasma or erythrocyte, including omega 3, omega 6 and omega 9 polyunsaturated fatty acids, saturated fatty acids and trans fatty acids. Given that high dietary omega 3 fatty acid intake is associated with decreased odds of developing wheeze and asthma when compared with lower omega 3 fatty acid intake,5 this test may help to determine whether poor omega 3 fatty acid consumption is a contributing factor in asthma.
Radiology tests
It is not routine practice to use medical imaging in the diagnosis of asthma. Chest X-ray and CT scans may be indicated, however, in complicated asthma, atypical presentations of asthma, and/or suspicions of more serious pathology.7
Functional tests
Pulmonary function tests (PFTs)
PFTs are often used to evaluate the presence and severity of asthma. The PFT can incorporate any number of different measures of lung volume and capacity, including total lung capacity, tidal volume, maximal mid-expiratory flow (MMEF), maximal volume ventilation (MVV), peak inspiratory flow rate (PIFR), forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and peak expiratory flow rate (PEFR). Reductions in the latter three measures are often evident in obstructive airway diseases such as asthma.11
Miscellaneous tests
Bronchial provocation tests use either direct (e.g. inhaled histamine or methacholine) or indirect (e.g. exercise, cold air hyperventilation) stimuli to trigger bronchial smooth muscle contraction in hyperresponsive airways. There is some debate as to whether the results of these tests are specific to a diagnosis of asthma.13,14
Diagnosis
Planning
Goals
Expected outcomes
Based on the degree of improvement reported in clinical studies that have used CAM interventions for the management of asthma,15,16 the following are anticipated.
Application
The range of interventions reported in the CAM literature that may be used in the treatment of asthma are appraised below.
Diet
Low-calorie diet (Level I, Strength C, Direction +)
As previously stated, there are a number of factors that elevate a person’s risk of developing asthma. A risk factor that is generally responsive to dietary change is obesity. There is, for instance, convincing evidence that high body weight at birth and/or during middle childhood increases the risk of developing asthma.17 Whether weight-reduction strategies are able to reverse this risk or improve asthma outcomes requires evidence from intervention studies. According to a Cochrane review, only one RCT has explored this hypothesis. The trial found the consumption of a low-energy diet plus education for 14 weeks to be statistically significantly superior to normal diet plus education at improving FEV1, FVC and rescue medication use in obese people with asthma.18 Given that low-calorie diets also reduce serum levels of inflammatory markers19 suggests that the low-energy diet could have improved respiratory function via an anti-inflammatory effect.
Miscellaneous diets (Level I, Strength C, Direction o)
Dietary modification is central to the overall management of asthma in many fields of CAM. While there is adequate theoretical justification to recommend many of these dietary interventions to people with asthma, such as a low-reactive or anti-inflammatory diet, there is a paucity of evidence to support these practices. A number of systematic reviews have also found insufficient or inconclusive evidence to link fish oil supplementation,20,21 dietary salt reduction22 and tartrazine avoidance23 to improvements in asthma outcomes. A recent meta-analysis of 10 observational studies also failed to find a significant correlation between dietary intake of antioxidants (including vitamin C, vitamin E and beta-carotene) and risk of asthma.6 By contrast, the consumption of whole foods (e.g. apples, pears, whole milk, butter) appears to offer some protection against asthma, according to a community-based, cross-sectional study of 1601 young adults.24 Several controlled trials have also found the dietary consumption of sulfur dioxide to exacerbate asthma in adults25 and to significantly reduce lung function in children with asthma.26 Nonetheless, these studies were small and, despite being published more than 15 years ago, have yet to be replicated using larger samples and more rigorous methodology.