Asthma is an extremely common disease producing considerable morbidity. The aim of treatment must be:
• To abolish symptoms
• To restore normal or best possible long-term airway function
• To reduce the risk of severe attacks
• To enable normal growth to occur in children
• To minimize absence from school/work This involves:
• Patient and family participation
• Avoidance of identified causes where possible
• Use of lowest effective dose of convenient medications
minimizing short-term and long-term side-effects Many asthmatics belong to self-help groups whose aim is to further their understanding of the disease and to foster self-confidence and fitness.

Control of extrinsic factors

Measures must be taken to avoid causative allergens such as the house-dust mite, pets, moulds and foods (see allergic rhinitis), particularly in childhood. voidance of the house-dust mite is now possible with effective and comfortable covers for bedding and changes to living accommodation. Active and passive smoking should be avoided as should f3-blockers both in tablet and eyedrop form.
Individuals intolerant to aspirin may benefit, though are rarely cured, by avoiding salicylates. Other agents, e.g. preservatives and colouring materials such as tartrazine, should be avoided if shown to be a causative factor. Fifty per cent of individuals sensitized to occupational agents may be cured if they are kept permanently away from exposure. The remaining 50% continue to have symptoms as severe as when exposed to materials at work. This is particularly so if they had been symptomatic for a long time before the diagnosis was made.

This underlines two points:
The importance of the rapid identification of extrinsic causes of asthma and their removal wherever possible (e.g. the family pet) 2 Once extrinsic asthma is initiated, it may become self-perpetuating.

Drug treatment

The mainstay of asthma therapy is the use of therapeutic agents delivered as aerosols or powders directly into the lungs (Practical box 12.4). The advantages of this method of administration are obvious. Drugs are delivered direct to the lung and the first-pass metabolism in the liver is avoided; both these factors mean that much lower doses are necessary and unwanted effects are slight. Both national and international guidelines have been published on the step-wise treatment of asthma (Information box 12.1) based on three important factors:
1 Asthma self-management with regular asthma monitoring using mini peak flow meters and individual treatment plans discussed with each patient.
2 The appreciation that asthma is an inflammatory disease and that anti-inflammatory therapy should be started even in mild cases
3 A diminution in the role ofbronchodilators, e.g. salbutamol since they are not anti-inflammatory and regular treatment with these drugs on their own may be associated with worsening of asthma and even asthma deaths
f32-ADRENOCEPTOR AGONISTS. The newer bronchodilator preparations contain f3-adrenoceptor agonists that, unlike isoprenaline, are selective for the f32-adrenoceptors of the respiratory tract and do not stimulate the f31-adrenoceptors of the myocardium. These drugs are potent bronchodilators in that they cause relaxation of bronchial smooth muscle. Such treatment is very effective in relieving symptoms but does little for the underlying inflammatory nature of the disease. Inhalants such as salbutarnol (IOO p.g) or terbutaline (250 p.g) should be prescribed as two puffs as required.

Inhaled therapy.
Inhaled therapy.

Salmeterol (50-100 p.g), a highly selective and potent f32-adrenoceptor agonist, is effective by inhalation for up to 12 hours, reducing the need for administration to twice daily. Only the mildest asthmatics with intermittent attacks should rely upon this treatment alone. Some patients use nebulizers at home for self-administration of salbutamol or terbutaline. Such treatment is very effective owing to the high dose delivered, but patients must not rely on repeated home administration of nebulized f32- adrenoceptor agonists for worsening asthma, and must be encouraged to seek medical advice urgently if their condition does not improve. Tablets of f32-adrenoceptor agonists are less effective than when the drug is inhaled. To help those who cannot coordinate activation of the aerosol and inhalation, new devices that are breathactivated have been developed.

The step-wise management of asthma.
The step-wise management of asthma.

ANTICHOLINERGIC BRONCHODILATORS. Muscarinic receptors are found in the respiratory tract; large airways contain mainly M3 receptors whereas the peripheral lung tissue contains M3 and Ml receptors. Non-selective muscarinic antagonists such as atropine were used for relief of bronchoconstriction. Currently ipratropium bromide 20-40 p.g three or four times daily or oxitropium bromide (200 p.g twice daily) by aerosol inhalation are used and may be additive to f3radrenoceptor stimulants. ANTI-INFLAMMATORY DRUGS. The exact mode of action of sodium cromoglycate and nedocromil sodium remains unknown but this class of drugs appears to prevent activation of inflammatory cells, possibly by blocking a specific chloride channel which in turn prevents calcium influx. These drugs are particularly effective in patients with milder asthma. Sodium cromoglycate is taken regularly either in the form of a Spincap containing 20 mg or in aerosol form from a metered-dose inhaler delivering 5 mg per puff. The dose should be two puffs four times daily from an inhaler, or one Spincap three or four times daily. Nedocromil sodium is taken as an aerosol at a dose of 4 mg (2 puffs) two to four times daily.
INHALED CORTICOSTEROIDS. All patients who have regular persisting symptoms in spite of treatment with asrequired f32-adrenoceptor agonists, sodium cromoglycate ANTIBIOTICS. There is no evidence that antibiotics are helpful in the management of patients who suffer from properly diagnosed asthma. However, wheezing frequently occurs in exacerbations of chronic bronchitis and emphysema associated with infected sputum. Yellow or green sputum containing eosinophils and bronchial epithelial cells may be coughed up in acute exacerbations of asthma. This is not due to bacterial infection and antibiotics are not required. Management of severe asthma (Emergency box 12.2) Although this condition is often called ‘status asthmaticus’, it is better considered as severe asthma that has not been controlled by the patient’s use of medication. Patients with severe asthma have:
• Inability to complete a sentence in one breath.
• Tachycardia 2: 110 beats per minute.
• Pulsus paradoxus (>10 mmHg). In very severe asthma no paradoxus is detected.
• Wheezing. Chest may be silent in severe asthma owing to insufficient airflow.
PEFR should be measured in all patients presenting with severe asthma, and if below 30% predicted or approximately 150 litre min ” (in adults), the patient should be taken to hospital and started on 40-60% oxygen. Treatment is commenced with 5 mg of nebulized salbutamol or 10 mg terbutaline with oxygen as the driving gas. A chest X-ray is taken to exclude a pneumothorax. If no improvement occurs with nebulized therapy, 250 JoLg of salbutamol or terbutaline should be administered by i.v. infusion over 10 min. Intravenous aminophylline is now not used for severe asthma because of its narrow therapeutic index. Hydrocortisone 200 mg i.v. should be administered 4-hourly for 24 hours and 60 mg of prednisolone should be given orally daily. Patients who do not respond to this regimen may require ventilation.

Treatment of severe asthma.
Treatment of severe asthma.

Patients should be kept in hospital for at least 5 days, since the majority of sudden deaths occur 2-5 days after admission. Oral corticosteroids can be reduced from 60 mg to 30 mg once improvement occurs. Further reduction should be gradual on an outpatient basis until an appropriate maintenance dose or substitution by inhaled corticosteroid aerosols can be achieved.
If the PEFR is greater than 150 litre min-I, patients may improve dramatically on nebulized therapy and may not require hospital admission. Their regular treatment should be increased, probably to include treatment for 2 weeks with 30 mg of prednisolone followed by a gradual reduction in the oral dose and substitution by an inhaled corticosteroid preparation.


Although asthma often improves in children as they reach their teens, it is now realized that the disease frequently returns in the second, third and fourth decades. Overall, in adults, there is a tendency for asthma to improve with age.

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