Chronic inflammation is the underlying mechanism that causes structural changes and the resulting symptoms of COPD. Variations in the airways and lung parenchyma cause physiologic changes that result in the clinical symptoms of chronic bronchitis and COPD. These are mucous hypersecretion, airway edema, and ciliary dysfunction, which cause cough and expectoration; airflow obstruction and hyperinflation lead to progressive dyspnea and fatigue, wheezing and chest tightness. Patients with chronic bronchitis are prone to mucous plugging of the airways, which creates ventilation and perfusion abnormalities resulting in hypoxemia and hypercapnia. This can cause pulmonary vasculature changes, pulmonary hypertension, and cor pulmonale with signs of cyanosis and lower-extremity edema.1,2
The BODE index assigns 0-10 total points to the increasing severity of four variables: BMI, airflow Obstruction measured by FEV1, Dyspnea measured by the Modified Medical Research Council, and Exercise tolerance measured by the distance walked in six minutes. The higher the score, the more severe is the disease. The BODE index may be used to guide management, especially referral to pulmonary rehabilitation, use of home oxygen, and possibly to hospice stay. The index is a better predictor of mortality than FEV1 alone, even when corrected for comorbidity, and is recommended in evaluating all patients with COPD.4
Clinical assessment of an AECB/COPD should include evaluating the severity of airflow obstruction, presence and number of comorbid conditions, number of prior exacerbations and need for hospitalization, hemodynamic instability and oxygenation, prior antibiotic use, and the ability to care for self at home. Although there is no agreed classification for staging the severity of an AECB/COPD, the American Thoracic Society and the European Respiratory Society have issued joint guidelines for the assessment and diagnostic evaluation of COPD.2 Severity of the condition increases from level I to level III. These levels will guide management and help unify the world pulmonary consensus on severity.
Not all patients with a cough and dyspnea or declining respiratory function have COPD or an exacerbation of COPD. It should be determined whether the decline in respiratory status is due to a trigger causing an exacerbation or due to a coexisting separate disease process. The differential diagnosis includes asthma, congestive heart failure, bronchiectasis, TB, atypical pneumonitis, interstitial lung disease (ILD), lung cancer, and bronchiolitis. Initial spirometry will aid in determining whether airflow limitation is present and if so, if is it reversible.2 Chest radiography can evaluate infiltrates, pulmonary vascular congestion, and cardiac size. Complete pulmonary function tests with lung volumes and/or CT may be needed if ILD is suspected. Arterial blood gases are important in patients with severe symptoms, severe airflow limitation, or clinical signs of hypoxemia. Diagnostic utility of sputum culture in patients with chronic bronchitis is controversial due to chronic colonization of the airways with bacterial pathogens. However, a change in baseline sputum characteristics indicates AECB and this may be associated with a different strain of an existing pathogen or a new bacterial agent.1