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The BronkoTest COPD Monitoring Pack has been produced for patients at the request of healthcare professionals and facilitates communication and understanding of such episodes and reasons for different treatments between the healthcare professional and the patient. Exacerbations of COPD are a major cause of morbidity and mortality. Frequent episodes are associated with worse health status (Ref. 1) and a greater deterioration in lung function (Refs. 2,3). The
reasons for the deterioration in lung function are not certain but
probably relate to inflammation. Exacerbations can be associated
with inflammation and an accumulation of neutrophils in the sputum,
although not in every case (Ref. 4).
It is important to note that neutrophils contain proteolytic enzymes
that have the ability to produce all the pathological features of
COPD including emphysema (Ref. 5),
mucous gland hyperplasia (Ref. 6),
mucus hypersecretion (Ref. 7) and damage
to the mucociliary escalator which is a critical feature of the
lungs host defence (Ref. 8). Thus,
it would seem logical that exacerbations that are associated with
neutrophil influx would be the episodes most likely to result in
progressive deterioration in COPD.
The
neutrophil is the key component of the secondary defence system
of the lung. During bacterial exacerbations new, or an increased
number, of bacteria are found in secretions (Ref.
9). The increased bacterial concentration is associated with
production of a key neutrophil chemoattractant (LTB4) necessary
to drive neutrophil influx (Ref. 10, 11).
The release of LTB4 is very dependent upon the bacterial load (Ref.
12). A steady state occurs in many patients with COPD who are
"colonised" by bacteria but feel relatively well in their
baseline state. When bacterial numbers rise (>106 colony forming
units/ml) due either to new infection or loss of control of colonising
bacteria, the neutrophils numbers in the lung also rise and release
the damaging enzyme, neutrophil elastase (Fig. 1). Prompt and appropriate
treatment for these episodes is required but management that includes
antibiotic therapy depends on recognising the bacterial cause of
the episodes.
There is a general consensus that antibiotic therapy is effective in exacerbations of COPD. However, emerging microbial resistance urges caution and expedient use of such therapy. In the best controlled study of antibiotic therapy (considered the gold standard) Anthonisen and his colleagues graded the episodes based on symptoms (Ref. 13). An exacerbation of COPD is "a sustained episode in which the patient's symptoms exceed the normal daily variability and requires a new intervention" (Ref. 14). The key symptoms are:
The
Anthonisen study overall confirmed that antibiotics were beneficial
but the clearest effect was seen if all 3 of these symptoms were
present. Of these 3, the key is sputum purulence.
Purulent sputum reflects the neutrophils influx into the secretions. This is because the neutrophils contains myeloperoxidase (a green protein unique to this cell). Thus purulence of sputum can be used as a guide. It not only reflects the likelihood of identifying bacteria (Fig. 2) but also the bacterial load (Ref. 15), the inflammation (Ref. 16) and damaging potential of the secretions (its proteolytic enzyme content). Using sputum purulence as a marker it was possible to withhold antibiotic therapy in patients with exacerbations of COPD if the sputum was mucoid and remained so throughout the episode as it resolved (Ref. 4). On the other hand, those with purulent sputum showed resolution of the sputum colour and their other symptoms with antibiotic therapy over 5-7 days. Thus, simple observation of sputum colour can help determine the need for antibiotic therapy in acute exacerbations of COPD if pneumonia is not suspected. Sputum colour is also useful for monitoring the response to therapy.
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The healthcare professionals' starter pack