stockley.qxp 7/8/09 3:52 pm Page 34
Chronic Obstructive Pulmonary Disease
Figure 1: Bacterial Yield versus Sputum Colour acute exacerbations.
40
Fifty per cent of the trials used parenteral
Number in Stable Chronic Obstructive Pulmonary
steroids and the remainder oral therapy with follow-up periods
Disease Patients
44
between 10 and 30 days. Steroids were found to reduce treatment
failure by 46% compared with placebo, although the method of
100 delivery had no effect. Parenteral steroids are thus usually indicated
90 only if the patient is unable to take tablets. The mean length of stay
80
was reduced by a weighted mean of 1.42 days and FEV
1
improved to
) 70
%
the greatest extent within 72 hours of starting the steroids. However,
60
there was insufficient information to determine whether steroids
50
atients (
affected mortality. Studies have also shown that there is no benefit of
P
40
giving steroids for more than two weeks.
41
GOLD
19
and National
30
Institute for Health and Clinical Excellence (NICE)
17
guidelines
20
recommend starting steroids as soon as possible when a patient has
10
an exacerbation at a dose of 30–40mg for seven tp 14 days, and the
0
1234 5
therapy can be stopped abruptly for treatment limited to this duration.
Mucoid Purulent
Several adverse effects have been reported while on steroids, the
Sputum colour number
most common being hyperglycaemia (risk ratio [RR] 5.88),
40
which in its
own right may have a detrimental effect on resolution.
42
• electrocardiogram (ECG) to identify underlying dysrhythmias or
suspected infarct; and Antibiotics
• blood cultures as appropriate. The role of antibiotics has remained contentious. A slight but
significant benefit was shown in the meta-analysis reported by Saint.
43
Often the peak flow is monitored, but this has not been shown to be More recently, a meta-analysis of five studies comparing antibiotics
helpful in the management of COPD.
32
versus placebo was undertaken,
40
which confirmed that antibiotics
reduced treatment failure (defined as requiring additional antibiotics
Treatment within the first seven days or unchanged/deterioration within 21 days)
Oxygen by 46% in patients with an exacerbation of COPD. In three of the trials
Oxygen is an important part of management in acute exacerbations of the in-hospital mortality was reduced by 78%. Antibiotics appeared to
COPD. If a patient has oxygen saturations <90% or partial pressure of be less beneficial for ambulatory patients, and it is recommended that
oxygen in the arterial blood (PaO
2
) <8kPa, he or she should be started all patients who are ventilated be treated with antibiotics.
19
on oxygen therapy. If there are no blood gases available, it is wise to start
24% oxygen via Venturi mask until checked. Although controlled oxygen A paper by Stockley et al.
44
showed a clear relationship between
is better provided by Venturi mask, nasal cannulae tend to be preferred sputum purulence, bacterial isolation and increased bacterial load.
by patients and a starting flow of 1 litre/minute is equivalent to 24% Figure 1 illustrates the percentage of patients with clinically stable
oxygen. Once oxygen is started, ABGs need be checked every 30–60 COPD who had bacterial yield versus sputum colour (as per
minutes until stable, aiming for saturations >90%/PaO
2
>8kPa without a Bronkotest
©
).
44
Sputum colour number 1 correlates to mucoid sputum,
significant rise in PaCO
2
or reduction in pH. ABGs should be repeated if increasing to sputum colour number 5 for the most purulent. The need
the oxygen delivery is changed at any time, unless the patient is for antibiotics in this study was defined as increased sputum
confirmed to be stable and not at risk of type II failure, in which case purulence and the presence of at least one of the following: dyspnoea
saturation monitoring may suffice. or increased sputum volume. Purulent sputum was found to have a
sensitivity of 94.4% and specificity of 77% for the yield of a high
Bronchodilators bacterial load, and was also accompanied by an increased C-reactive
The two main bronchodilators given during exacerbations of COPD are protein (CRP) and significant airway inflammation with increased
β
2
-agonists and antimuscarinics. Bronchodilators relax airway smooth cytokine concentrations. Those with mucoid sputum improved without
muscle, facilitating expiration and reducing dynamic hyperinflation. antibiotics and had a minimal change in CRP and no change in
There is no evidence of any differential or additive benefit of these two bacterial load
44
or cytokine concentrations.
30
The data suggest sputum
classes of bronchodilator.
36–38
They are given at an increased dose and/or purulence alone is an indicator for antibiotic therapy.
frequency compared with routine therapy and usually via nebulisers,
even though the mode of administration (metered-dose inhaler [MDI] The choice of antibiotic should depend on allergic history and local
and spacer or nebulisers) has no effect on bronchodilation.
39
However, guidelines that take into account local resistance data. Quinolones
patients tend to prefer nebulisers, especially when they are unwell, as it have been shown to delay time to next exacerbation,
45
which may be
is easier to deliver larger doses of bronchodilator with this mode; in an advantage in some patients.
contrast, co-ordinating delivery with inspirations becomes problematic
with an MDI and spacer. It is important to specify the nebuliser driving Theophylline
gas as air or oxygen; the former is safer in patients with type II Theophylline is now a second-line agent in the management of acute
respiratory failure. COPD exacerbations. It is a phosphodiesterase inhibitor that causes
bronchodilation by increasing cyclic adenosine monophosphate (AMP)
Steroids and guanosine 5’-monophosphate (GMP). Several studies have
A recent systematic review and meta-analysis was undertaken of 10 compared oral and intravenous (IV) theophylline in patients with non-
studies involving 959 patients, comparing steroids with placebo in acidotic exacerbations of COPD,
46,47
and failed to demonstrate a benefit
34 EUROPEAN RESPIRATORY DISEASE
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