Acute Severe Asthma in Adults
Acute Severe Asthma in Adults
Acute Severe Asthma in Adults
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Colin Robertson
Investigations
Assessment of oxygenation and ventilation pulse oximetry is
commonly available in and out of hospital and provides a simple,
non-invasive estimate of tissue oxygen saturation. An SaO2 of 92%
or less indicates a life-threatening attack. Arterial blood analysis
is required in all patients with any life-threatening feature (Figure
2) and in any patient with SaO2 less than 92%. Normal arterial
partial pressure of carbon dioxide (PaCO2, 4.66.0 kPa) implies a
life-threatening episode. Raised PaCO2 or respiratory acidaemia is
particularly ominous.
Other investigations no individual laboratory marker at a
single point in time is useful for prognosis. A full blood count
is commonly performed, but a raised WBC count is common in
acute asthma even in the absence of infection. Urea and electrolyte
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ADULT ASTHMA
Management
Patients should be seen and treated immediately in a highdependency or resuscitation area of the A&E department or receiving unit. ECG, SaO2 and non-invasive blood pressure recordings are the minimum monitoring requirements.
Oxygen therapy hypoxaemia is almost invariably present in
patients with acute severe asthma. All patients should be given
oxygen at a high inspired concentration, using a mask that can
deliver an FiO2 of 4060%. The aim is to maintain SaO2 above 92%.
Nebulizers should be oxygen-driven whenever possible. Concerns
that hypercapnoea may be induced by high-flow oxygen, as may
occur in some patients with chronic obstructive pulmonary disease
(COPD), are unfounded. Hypercapnoea in the context of acute
severe asthma indicates a near-fatal event and mandates immediate involvement of senior specialist/anaesthetic staff.
2-agonists are first-line agents and should be given immediately. Salbutamol, 5 mg, and terbutaline, 10 mg, are equally ef-
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Risk factors
Exposure to tobacco smoke cigarette smoking is the most
important risk factor for COPD. In general, the greater the exposure
to tobacco, the greater the risk, though there is wide variation in
susceptibility (Figure 1). The commonly cited statement that only
1020% of smokers appear to be susceptible and develop clinically
significant COPD is probably an underestimate, because COPD is
under-diagnosed.
Passive exposure to cigarette smoke may also contribute to
respiratory symptoms and to COPD. Smoking during pregnancy
may increase the risk of COPD by affecting fetal lung growth.
Recurrent bronchopulmonary infections the British hypothesis suggests that persistent airflow obstruction may be the end
result of damage caused by repeated bronchopulmonary infections.
A history of severe childhood infections has been associated with
reduced lung function and increased respiratory symptoms in
FURTHER READING
British Thoracic Society, Scottish Intercollegiate Guidelines Network.
British guideline on asthma management: a national clinical
guideline. Thorax 2003; 58: (Suppl. 1): i194.
(Essential reading for all clinicians involved in the care of asthma
patients.)
Cates C J, Rowe B H, Bara A. Holding chambers vs nebulisers for
beta-agonist treatment of acute severe asthma. The Cochrane Library
2001; 3.
Parameswaran K, Belda J, Rowe B H. Addition of intravenous
aminophylline to beta2 agonists in adults with acute asthma.
The Cochrane Library 2001; 3.
Rowe B H, Bretzlaff J A, Bourdon C et al. Magnesium sulphate for treating
exacerbations of acute asthma in the emergency department.
The Cochrane Library 2001; 2.
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