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Publications
Tiova Scope - Issue - 4
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Acute Exacerbations of COPD |
Introduction |
The clinical course of COPD is intermittently interrupted by acute exacerbations. Patients with symptomatic COPD have been reported to experience one to four exacerbations per year The frequency of these exacerbations, increases with the severity of their pulmonary disease. Acute exacerbation is a determinant of disease progression in COPD. Its occurrence has been related to lower survival rates. Acute exacerbations of COPD (AECOPD) is also an important cause of health expenditure due to hospitalization, outpatient care and drug consumption.
During exacerbations, the intensification of treatment is required; there is an increase in the need for physician visits, visits to the emergency department and hospitalization. |
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Exacerbations that require admission to the hospital may only affect a small proportion of the COPD population, but they make a disproportionate demand on the expenditure on this condition.
Exacerbations have both short and long-term consequences for the health of the individual concerned. There may be permanent impairment of lung function, functional ability and health status.
Seemingal et al have shown that 35 days after an exacerbation only 75% of patients had regained their original PEFR and 7.1% had not returned to baseline lung function at 3 months. In the same study approximately 30% of patients had still not regained their previous mobility at3 months after discharge and 65% were unable to do house work that they could previously manage. Patients with frequent exacerbations (3 or more per year) have a worse quality of life when assessed by the St. George Respiratory Questionnaire (SGRQ) than those with less frequent exacerbations.
- After an exacerbation readmission is common with an estimated figure of 34% at 3 months, 44% at 6 months, 70% at 1 year
- Estimates of in-hospital mortality from a single episode of exacerbation ranges from 4% to 11%.
Better management of COPD with a goal of reducing hospitalizations for exacerbations can reduce the burden of COPD on several fronts.
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Definition |
The definition of an exacerbation of COPD is variable. The BTS guideline defines it as a worsening of the previous stable situation which may include increased breathlessness, sputum volume, sputum purulence, wheeze, chest tightness, or fluid retention. A similar broad definition has been used in a recent consensus statement which defined an exacerbation as:
‘A sustained worsening of the patient's condition, from the stable state and beyond normal day to day variations that is acute in onset and necessitates a change in regular medication in a patient with underlying COPD.'
In 1987, Anthonisen and colleagues classified exacerbations and a grading system for the severity had been developed. This clinical grading system considers three cardinal signs of exacerbations and is the most widely accepted.
| Anthonisen's Typing of Exacerbations |
| Cardinal Signs |
| Worsening dyspnea, increase in sputum volume and purulence |
| Other Signs |
| Upper respiratory tract infection in past 5 days, fever without other apparent cause, wheezing, increase cough and increase respiratory rate or heart rate by 20% above baseline |
| All 3 cardinal symptoms |
Type I (SEVERE) |
| 2 of 3 cardinal symptoms |
Type 2 (MODERATE) |
| 1 of 3 cardinal symptoms |
Type 3 (MILD) |
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The etiology of COPD exacerbations is not fully understood. Clearly, infectious and non-infectious agents have been shown to be causes. Yet nearly 30% of exacerbations are as a result of unknown factors.
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Assessing and Managing Exacerbations |
The assessment of the severity of an acute exace rbation will usually be based on certain elements:
1. Signs and Symptoms
2. Laboratory Tests
1. Signs and Symptoms
- The baseline condition of the patient is essential to assess severity. Cough, sputum volume and colour, dyspnea, and especially limitation of daily activities have to be evaluated. Dyspnea, when present at rest or when impairing the ability of the patient to complete one sentence, is an indicator of severe exacerbation. The most important signs of severity are the presence of confusion or a change in alertness; when these signals are present, patients require immediate medical attention and evaluation in the hospital. If fever is present, pneumonia should be suspected. Other signs that may indicate a severe, acute exacerbation are paradoxical chest wall movements, worsening of central cyanosis, signs of right congestive heart failure, and hemodynamic in stability. Coma and cardiac arrhythmia are life - threatening and require admission into the intensive care unit.
2. Laboratory Tests
Spirometric tests might be useful to assess an acute exacerbation of COPD and can be repeated to monitor progress. However, it is not uncommon in patients with severe COPD to detect only minimal spirometric changes despite significant symptom aggravation. Treatment decision should never be based only on the result of a spirometric test in an exacerbation of COPD. Measurement of peak expiratory flow (PEF) has been adopted by some health professionals, but it can grossly underestimate the disease severity and is very patient dependent.
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Assessment of arterial oxygen saturation (SaO2) could also be used. An SaO2 level less than 90%, when breathing ambient air, usually indicates respiratory failure in patients when they have had a previously normal Sa0 2 level. However, patients with COPD might have chronic respiratory failure with reduced SaO 2 , and some of them might already be on long-term home oxygen. When available, prior tests of lung function and arterial blood gases can be very helpful for comparison with those made during acute episodes.
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Chest radiographs are useful if pneumonia, congestive heart failure, pneumothorax, or pleural effusion is suspected.
- Sputum culture is not usually recommended as a routine test for acute exacerbation unless there is pneumonia or the patient is unresponsive to the selected antibiotic.
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Hospital Management |
The risk of dying from an exacerbation of COPD is closely related to
1. The development of respiratory acidosis
2. The presence of significant comorbidities, and
3. The need for ventilatory support.
Patients lacking these features are not at high risk of dying, but those with severe underlying COPD often require hospitalisation in any case.
| Indications for Hospital Assessment or Admission for Exacerbations of COPD |
Marked increase in intensity of symptoms, such as sudden development of resting dyspnea
Severe background COPD
Onset of new physical signs
(e.g. cyanosis, peripheral edema)
Failure of exacerbation to
respond to initial medical management
Significant comorbidities
Newly occurring arrhythmias
Diagnostic uncertainty
Older age
Insufficient home support |
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Drug Therapy |

1. Bronchodilators
Bronchodilator therapy refers to the use of ft-agonists, anticholinergic agents and methylxanthines (theophylline, aminophylline).
b 2 -agonists and anticholinergics have been shown to improve airflow during AECOPD. The GOLD report recommends short-acting b 2 -agonists as the preferred bronchodilators for AECOPD. If no response is seen, the addition of an anticholinergic is recommended.
Aminophylline is recommended only if needed in severe AECOPD after treatment with b 2- agonists or anticholinergics. Theophylline is not recommended for a patient in the midst of an exacerbation.


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2. Corticosteroids
Systemic corticosteroids (CS) are increasingly being used in AECOPD and are recommended in the GOLD report and the ACP-ASIM/ACCP guidelines. Data has shown that CS reduced the number of treatment failures and length of hospitalizations. Oral CS in the out-patient treatment of AECOPD improved gas exchange, spirometry and symptoms.
The GOLD report recommends the use of a 10-day regimen and recommends against long-term treatment with systemic CS. Long-term CS can cause steroid myopathy which contributes to muscle weakness and respiratory failure. It appears that a short course of systemic CS is warranted in patients with moderate-severe AECOPD.
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Corticosteroids used for the treatment of acute exacerbation
of chronic obstructive pulmonary disease |
Drug |
Formulation |
Dose |
Methylprednisolone |
Intravenous |
125 mg every 6 h |
Hydrocortisone |
Intravenous |
100 mg every 24 h |
Prednisone |
Oral |
60 mg every 24 h |
| a . All f or maximum 2-week course |
3. Antibacterials
Bacterial colonization or infections have been implicated in causing AECOPD in a majority of the patients. Therefore, it seems intuitive to treat these patients with antibacterials, however the data in the literature is controversial. The GOLD report recommends antibacterials for patients with AECOPD who have increased sputum or purulence in addition to dyspnea.
The choice of the antibacterial agent has also been controversial. The main microbes associated with AECOPD are S. pneumoniae, H. influenzae and M catarrhalis. The choice of agents should reflect local patterns of antibiotic sensitivity among S. pneumoniae, H. influenzae and M catarrhalis. The optimum duration of therapy has not been determined conclusively and can range from 3-14 days.
4. Oxygen Therapy
Oxygen therapy is the cornerstone of hospital treatment of COPD exacerbations. Adequate levels of oxygenation (PaO2 > 8.0 kPa 60 mmHg or SaO2> 90%) are easy to achieve in uncomplicated exacerbations, but CO2 retention can occur insidiously with little change in symptoms. Once O2 is started, arterial blood gases should be checked 30 minutes later to ensure satisfactory oxygenation without CO2 retention or acidosis.
Venturi masks are more accurate sources of controlled O2 than are nasal prongs but are more likely to be removed by the patient.
5. Ventilatory Support
The benefit of non-invasive positive pressure ventilation (NPPV) in AECOPD is also well documented. It has been seen that NPPV given to patients with AECOPD reduced the need for endotracheal intubation, the length of the hospital stay and in-hospital mortality. More recently, the benefits of NPPV in terms of respiratory rates, patient levels, reduction in intubation, reduction in mortality and improved costs have been observed. Patients with decreased pH levels and hypercarbia are the best candidates for NPPV.

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Prevention of Future Exacerbations |
Helping patients to understand their disease and teaching them about factors that contribute to exacerbations is essential; smoking cessation should be promoted as it is central to modifying the natural history of the disease. Other measures have been suggested, such as vaccination and regular drug treatment. Regular maintenance treatment with Tiotropium bromide once daily has demonstrated significant reduction in exacerbations when compared to Ipratropium over a period of 1 year. Treatment with Tiotropium:
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Reduced the number of exacerbations by 24%
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Delayed the time to first exacerbation
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Delayed time to first hospitalization
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Reduced number of hospitalizations/patient/year (38%)
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Reduced number of hospitalization days/patient/year (33%)
But, most importantly, to effectively reach as many patients as possible, implementation of these measures should be done at the primary level. A supported discharge plan by the Doctor to the patient can also help in preventing future exacerbations.

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Learning points |
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Exacerbations of COPD are the most common cause of emergency respiratory admissions.
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It is likely that they accelerate decline or pulmonary function and health status.
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The majority of patients admitted to hospital for an exacerbation are readmitted within a year.
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Evidence suggests that we can tailor our treatment of an exacerbation using clinical and arterial blood gas criteria rather than the blanket prescribing which is the widespread practice at present.
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Frequency of future exacerbations can be reduced by pharmacological and physical means and should be pursued in a more systematic manner.
Further Reading :
- Borbeau J et al. In Comprehensive Management of Chronic Obstructive Pulmonary Disease, BC Dekker Publication 2002.
- Thorax 2002; 57 (Suppl 11): ii15-ii23.
- Drugs 2003; 63 (14): 1481-1488.
- GOLD Guidelines 2003.
- Pearson et al. In COPD: Critical Debates, Blackwell Science Publishing 2003. 6. Swiss Med Wkly 2003; 133: 247-257. 7. Eur Respir J 2002; 19: 209-216
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Supported Discharge Plan For Patients |
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