Corticosteroids are not primarily bronchodilators but reduce airway wall inflammation, decrease mucus production, and have a synergistic effect with b-adrenergic agonists on bronchial smooth muscle relaxation. They are usually prescribed in severe asthma ( British Thoracic Society 1990). In some patients with chronic obstructive airways disease, corticosteroids given by either the oral or the inhaled route can hasten an improvement in pulmonary function tests ( Hudson and.M.onti. 1990). A reluctance to use steroids or failure to prescribe adequate amounts in acute asthma results in increased hospital admissions, prolonged hospital stay, and increased mortality. The route of administration seems less important than ensuring adequate dosing, and due attention must be paid when changing from intravenous to oral preparations so that equivalent doses are prescribed ( Ta.bJe.2). The advantage of intravenous administration in the acute stage is that the problems of vomiting and delayed absorption are bypassed and the amount of active drug administered is known to have reached the systemic circulation. Inhaled corticosteroids are now accepted as long-term treatment for asthmatics; the inhaled route is inadequate for an acute attack of bronchospasm.
Table 2 Equivalent anti-inflammatory doses of glucocorticoids
The onset of action depends on the route of administration and the type of steroid, but the peak effect in the asthmatic patient is likely to be 3 to 6 h after administration. Treatment should be continued for at least 7 days to suppress the inflammatory response. Side-effects include hyperglycemia, water retention, euphoria or depression, peptic ulceration, myopathy, increased susceptibility to infection, and adrenal suppression.
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