This book includes a plain text version that is designed for high accessibility. To use this version please follow this link.
stockley.qxp 7/8/09 3:52 pm Page 33
Treatment of Acute Exacerbations of Chronic Obstructive Pulmonary Disease
therapy.
21
Recent data have suggested that early improvement in the Table 1: Factors to Consider When Deciding
general feeling of wellbeing (within two to four days) prevents the
Where to Treat a Patient
patient seeking treatment even though other symptoms persist.
21
Finally,
exacerbations are often classified according to healthcare utilisation.
Factor Treat at Home Treat in Hospital
‘Mild’ reflects just an increase in bronchodilator use, ‘moderate’ the
Able to cope at home Yes No
Breathlessness Mild Severe
introduction of antibiotics and/or steroids and ‘severe’ the need for
General condition Good Poor/deteriorating
hospitalisation. These definitions are often used in clinical trials but may
Level of activity Good Poor/confined to bed
not reflect the degree of pathophysiological changes. This definition was
Cyanosis No Yes
established by Seemungal et al.,
22
who also acknowledged that <50% of
Worsening peripheral oedema No Yes
symptom-based exacerbations were unreported and often not treated.
Level of consciousness Normal Impaired
Already receiving LTOT No Yes
Pathogenesis Social circumstances Good Living alone/
During an exacerbation, significant changes are seen in the lung
not coping
physiology. An increase in airway resistance secondary to
Acute confusion No Yes
bronchospasm, oedema and increased sputum viscosity leads
Rapid rate of onset No Yes
to increased expiratory flow limitation. As a consequence there is air
Significant co-morbidity No Yes
(particularly cardiac disease
trapping with increased end-expiratory lung volume,
23
resulting in
and insulin-dependent diabetes)
dynamic hyperinflation. This dynamic hyperinflation has several
Changes on chest radiograph No Present
detrimental effects on COPD patients during an exacerbation, namely:
Arterial pH level ≥7.35 <7.35
Arterial PaCO
2
≥7kPa <7kPa
• worsening of respiratory mechanics (compliance, increased elastic
LTOT = long-term oxygen therapy; PaCO2 = partial pressure of carbon dioxide in arterial blood.
loading, muscle fatigue); Source: Thorax, 2004.
17
© 2004 BMJ Publishing Group Ltd. Reproduced with permission.
• impaired gas exchange (due to worsening ventilation/perfusion
[VQ] mismatch); Differential Diagnosis
• increase in pulmonary artery pressure (secondary to hypoxic Several other problems can present with the same symptoms as an
vasoconstriction), which may lead to right heart failure; and exacerbation. These include pneumonia, congestive cardiac failure,
• neuromechanical uncoupling as a consequence of a difference in pulmonary embolism, pleural effusion, pneumothorax and cardiac
the central drive and the response of the tired respiratory muscles,
23
dysrrhythmias, all of which are more prevalent in COPD.
leading to respiratory failure.
Management
These effects all contribute to the increased sensation of dyspnoea Where to Treat the Patient
during exacerbations.
22
Assessment of a patient with an acute exacerbation of COPD should
consider not only the severity of the exacerbation but also the resources
Causes needed and their availability. Treatment can be undertaken at home with
Bacterial associations with exacerbations have been detected in up to appropriate intervention, a short stay in hospital with supervised early
60% of episodes.
13,24
The most common bacterial organisms include discharge or, for severe episodes, prolonged hospital admission. Table 1
Haemophilus influenzae, Moraxella catarrhalis and Streptococcus illustrates the factors that influence this decision.
pneumoniae.
25–28
The acquisition of a new strain of the same organism is
associated with an increase in the likelihood of an exacerbation
18
and the It has been demonstrated that patients treated at home with
ability to generate more inflammation.
18,29
These observations are likely appropriate facilities have similar mortality and readmission rates to
to explain the increase in bacterial numbers that occurs in episodes hospitalised patients.
34
They also have a better quality of life, better
associated with an increase in inflammatory cytokines
30
and neutrophil knowledge of their disease and improved self-management, and overall
recruitment manifesting as sputum purulence.
31
Viruses have been are more satisfied with their treatment compared with those admitted to
detected in 23–60% of exacerbations,
13,24
although their role remains hospital. Importantly costs are reduced by 38%.
34
It is believed that 25%
contentious. No cause has been found in 25% of cases,
24
although of patients admitted with an acute exacerbation of COPD would be
pollution is associated with increased incidence of exacerbations.
32
suitable for a hospital-at-home service.
35
Bacterial and viral co-isolation have been shown to be associated with
greater lung impairment and a longer hospital stay in patients with an Investigations
acute exacerbation.
24
Predisposing factors include current smoking, When a patient is admitted, several investigations should be performed:
severe disease and bacterial colonisation when stable.
• chest X-ray to rule out pneumonia or pneumothorax;
Clinical Features • pulse oximetry to determine oxygen saturation: if <90%, arterial
Features of an acute exacerbation of COPD vary between patients. blood gases (ABGs) should be taken to identify chronic type II
The common symptoms include cough, wheeze, dyspnoea, increased respiratory failure, which requires controlled oxygen therapy and
sputum volume and purulence. Signs of an exacerbation include those who may be candidates for non-invasive/invasive ventilation
increased respiratory rate, tachycardia, pyrexia, central cyanosis, (acute or acute on chronic type II respiratory failure);
signs of hypercapnia, use of accessory muscles and signs of right • routine blood tests including full blood count (to identify
heart failure. The severity of symptoms during an exacerbation is polycythaemia or bleeding) and renal function (electrolyte
related to the patient’s stable physiology, which also affects the abnormalities can be associated with exacerbations, e.g.
duration of their symptoms.
10,33
hyponatraemia or hypokalaemia);
19
EUROPEAN RESPIRATORY DISEASE 33
Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68
Produced with Yudu - www.yudu.com