Background It would be helpful if patients with asthma who require admission to hospital for an acute attack could be identified. Methods The relation between the severity of an attack of asthma as determined by admission assessment and the eventual outcome was studied in 52 asthmatic patients aged 14 to 44 years and admitted to an asthma emergency room. The patient's history, including medication and previous admissions to hospital, was recorded and a clinical assessment, including a full inspiratory and expiratory flow-volume loop, was performed on four occasions: on admission, at two hours and at 12-18 hours after the start of a standardised treatment, and two weeks later on an outpatient basis. Patients who were discharged and who had an uneventful follow up at the two week assessment were defined as good responders. Patients who had to be admitted to hospital after 12 to 18 hours or were readmitted during the two weeks, or both, were defined as poor responders. Results Thirty eight patients were good responders and 14 were poor responders (seven admitted at 12 to 18 hours, seven returned to hospital). All four patients with a raised arterial carbon dioxide tension (Paco2) ( > 6 kPa) and the three with cyanosis were in the poor responder group, and this group had lower peak expiratory flow (PEF) values (21% v 30% predicted) on admission. There was, however, considerable overlap in PEF between the two groups and no clinical measure was able to distinguish between the good and the poor responders reliably. Poor

Inhaled and oral salbutamol were compared in 12 asthmatic patients for prophylaxis in antigen-induced asthma. The patients were pretreated with 0.2- and 1.0-mg doses of inhaled salbutamol and with the standard oral 4- and 8-mg slow-release (SR) salbutamol preparations. Bronchodilatation was monitored over the ensuing 3 h and protection against antigen challenge at the end of the period. On each study day the degree of baseline airway hyperreactivity was determined by histamine challenge. Precautions were taken during the antigen challenge to ensure a reproducible response. Blood levels of salbutamol were monitored at hourly intervals for the 3 h after treatment and during the asthmatic reaction subsequent to challenge. Both the 0.2- and 1.0-mg inhalations caused immediate bronchodilatation as compared to a placebo (p < 0.05), but only the 1.0-mg dose protected subjects against antigen challenge (p < 0.05). In comparison to the placebo, no bronchodilatation was achieved with the standard 4-mg oral preparation in spite of measurable blood levels, nor were the patients protected against antigen challenge at 3 h after pretreatment. However, the 8-mg SR salbutamol caused significant bronchodilatation within 2 h and suppressed antigen challenge responses as compared to placebo (p < 0.05). It can be concluded that doses of inhaled salbutamol higher than the conventional 0.2- or the standard 4-mg oral preparations are required to protect asthmatics against inadvertent antigen exposure. In patients who are unable to use inhalers effectively, the SR preparation can be considered as an alternative