A. Patient with Signs Symptoms of COPD Exacerbation
- Acute exacerbation is defined as a recent deterioration of the person's
clinical and functional state that is due to worsening of their COPD. Typical
symptoms and signs of COPD exacerbation are given below (adapted from the
European Respiratory Society Consensus Statement, Siafakas 1995).
1. Is There Evidence of Severe Exacerbation?
| Intervention | References | Grade of Evidence | Strength of Recommendation |
| Loss of alertness or two or more of: dyspnea at rest, respiratory rate > 25/min, pulse > 110/min, increased cyanosis, and use of accessory muscles. | ERS, Siafakas 1995 | C | 2a |
B. Patient with a Diagnosis of COPD - Chronic obstructive pulmonary disease (COPD) is defined by the American Thoracic Society (ATS) in Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease (1995). Further detail on lung function testing is found in another ATS publication (1991).
b. Chronic bronchitis is defined as the presence of chronic productive cough for 3 months of each of two successive years in a patient in whom other causes of chronic cough have been excluded.
c. Emphysema is defined as abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.
d. Asthma is by definition associated with reversible airflow
obstruction. Patients with asthma whose airflow obstruction is completely
reversible are not considered to have COPD. The obstruction in many patients
with COPD may include a significant reversible component. Some patients
with asthma may develop irreversible airflow obstruction indistinguishable
from COPD.
(2) Environmental (chronological) - May disclose important risk factors
(3) Cough (chronic, productive) - Frequency and duration, whether or not productive (especially on awakening)
(4) Wheezing
(5) Acute chest illnesses - Frequency, productive cough, wheezing, dyspnea, fever
(6) Dyspnea
d. Laboratory
(2) Spirometry (pre- and postbronchodilation) - Essential to confirm presence and reversibility of airflow obstruction and to quantify maximum level of ventilatory function (ATS 1995)
(3) Lung volumes - Measurement of more than forced vital capacity is not necessary except in special circumstances (e.g., presence of giant bullae)
(4) Carbon monoxide diffusing capacity - Unnecessary except in special instances (e.g., dyspnea out of proportion to severity of airflow limitation)
(5) Arterial blood gases are not needed in staged mild disease, but remain the standard for determining the need for oxygen therapy
(6) Alpha1-antitrypsin (AAT) - AAT deficiency accounts for
less than 1 percent of COPD. Obtain a serum AAT level to screen for AAT
deficiency in the following situations:
(8) If on therapy, reevaluate or begin trial of therapy with inhaled
anticholinergic (IAC). A trial of IAC therapy is recommended in apparently
asymptomatic patients with an FEV1 of less than 50 percent of
predicted, since this degree of obstruction is usually associated with
dyspnea. This is based on the well-known phenomenon of patients "adapting
to their disability." Such a lack of symptoms may result from the patient's
avoiding activities or simply thinking along the lines of "Doesn't everyone
get short of breath doing this activity at my age?"
Ipratropium and short-acting inhaled beta2-agonist in typical doses
(2 to 4 inhalations) on a scheduled rather than prn use are generally equally
effective as bronchodilators, although some studies suggest that ipratropium
has a greater peak and a longer duration of action. The side effects of
each are similar, except for increases in heart rate and tremor, (neither
of which is typical at these doses) occur almost exclusively with beta2-agonist.
Dyspnea may be improved to a greater extent with inhaled beta2-agonist.
Some patients will have a response to one but not the other, so in any
trial of therapy, both should be tried if improvement is not optimal with
the first choice. There is evidence that ipratropium improves baseline
pulmonary function (after withholding ipratropium for 6 to 12 hours) whereas
beta2-agonist do not.
| Intervention | References | Grade of Evidence | Strength of Recommendation |
| Baseline FEV1 and FVC increased with 90 days after ipratropium initiation. | Rennard 1996 | B | 2a |
| Ipratropium 40 g qid or metaproterenol 1.5 mg qid by inhalation were equally efficacious and safe over a 90-day period. | Tashkin 1986 | A | 1 |
| No difference between 200 g albuterol and 40 g ipratropium in magnitude, but duration was 1 hour longer with ipratropium on day 85. | Combivent 1994 | A | 1 |
| Ipratropium produced more and longer bronchodilation than did albuterol. | Braun 1989 | B | 2a |
| The distance walked was greater with 7 days of albuterol (180 g) or ipratropium (36 g ) qid; also dyspnea was less with albuterol. | Blosser 1995 | B | 2a |
| Of 80 responsive patients in a group of 100, 16 responded only to albuterol; 17 responded only to ipratropium; and 47 responded to both. | Nisar 1992 | C | 1 |
2. Patients should know how to recognize an exacerbation, features of a severe exacerbation, and steps to take in initial home self-management. These may include maximal bronchodilator therapy, and antibiotics for purulent bronchitis. Additional corticosteroid therapy should be considered in consultation with the primary care provider for those who are steroid responsive.
3. This plan should be provided in the form of written or verbal instructions with guidance for contacting the primary care provider if in doubt about the course of action or if there is deterioration in the patient's condition.
| Intervention | References | Grade of Evidence | Strength of Recommendation |
| Encourage sputum clearance by coughing.
Encourage fluid intake. Avoid sedatives and hypnotics. Initiate, increase dose and frequency of beta2-agonists and/or ipratropium inhalations as instructed. Consider antibiotics for increase/purulent sputum. Consider prescribed corticosteroids regimen in patient with steroid responsiveness. Instructions on when to contact primary provider or go to ED. |
Rennard 1996 | B | 2a |
b. Decrease respiratory rate
c. Decrease heart rate
d. Increase in function and endurance
| Intervention | References | Grade of Evidence | Strength of Recommendation |
| Precautions when using pharmacotherapy. | ATS 1995 | C | 1 |
7. Recommendation - MDI with, if necessary, a spacer is preferred unless not recommended by manufacturer; a hand-held nebulizer should be used only if client unable to use an MDI.
| Intervention | References | Grade of Evidence | Strength of Recommendation |
| 52 percent used MDI once daily or less rather than the required three times daily. | Rand 1995 | C | 1 |
| Adherence with intermittent positive pressure breathing (IPPB) or nebulizers was 50.6 percent. | Turner 1995 | C | 1 |
| Maximum bronchodilation similar between nebulizer and MDI beta2-agonist. Nebulizer dose twice MDI dose to produce same effect. | Mestitz 1989 | B | 1 |
| Dose of nebulized albuterol produced the same bronchodilation in any of peak expiratory flow rate, FEV1, or forced vital capacity was about 10 times higher than with MDI. | Jenkins 1987 | B | 1 |
| No difference in outcome between nebulizer and MDI. Nebulized metaproterenol dose was about seven times higher than with the MDI. | Turner 1988 | B | 1 |
| It took about 12.5 times as much nebulized albuterol to achieve the same increase in FEV1 as with MDI. | Harrison 1983 | B | 1 |
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