History and exam

Key diagnostic factors

A sustained increase from the baseline level of dyspnea beyond day-to-day variation is usually observed in patients with an acute exacerbation.[10]

A change in the character and frequency of cough is often identified.[10] This change should be beyond day-to-day variations of the patient's typical cough.[1]

All patients with COPD have expiratory flow limitation, and this may lead to wheezing. Patients experiencing an acute exacerbation may be found to have greater severity of wheezing and prolongation of the expiratory phase of breathing on exam. However, wheezing is not identified in many patients.

Changes in either volume or character (thickness, color) or both are frequently observed. The presence of purulent sputum appears to be sensitive and specific for high bacterial loads and may help identify subsets of patients who may most benefit from therapy with antibiotics.[176][177]

Tachypnea is frequently seen and may be severe. It is important to observe the patient for signs of respiratory failure.

Possible sign of impending respiratory failure.

Other diagnostic factors

A past medical history of COPD should be sought, as well as of other conditions that may impact the likelihood of another acute problem considered in the differential diagnosis. People with a history of two or more exacerbations in the preceding year or those with history of hospitalization due to exacerbation in the previous year are considered at high risk of subsequent exacerbations.[1]

It is important to determine if patients have a history of significant exposure to tobacco smoke and whether they are currently smoking.

It is important to determine if patients have a history of heartburn, bitter taste in the mouth, coughing or choking after eating, hiatal hernia, and/or gastroesophageal reflux or difficulty swallowing.[64][65] However, gastroesophageal reflux should be considered as a potential cause of recurrent exacerbations even if the patient lacks the above-noted typical symptoms and signs of gastroesophageal reflux.

No available studies guide whether the treatment of reflux improves exacerbations of COPD.

These symptoms and other nonspecific symptoms such as insomnia, decreased activity level and loss of appetite are commonly identified in people with an acute exacerbation of COPD.[172][175]

While these symptoms have great impact on the quality of life of the patient, they are generally not used to determine whether an exacerbation is present.

This may result from worsened airflow limitation and chest hyperinflation.[13] However, the possibility of a myocardial infarction or pneumothorax should be considered if marked chest tightness or other chest discomfort is present.

This may develop as a result of increased hypoxic vasoconstriction due to exacerbation-induced hypoxemia. The resulting increase in pulmonary vascular resistance and/or pulmonary artery pressure can lead to acute right heart failure. Elevated jugular venous pressure, hepatojugular reflux, peripheral edema, and relative hypotension may be present.

It should be determined whether the patients has a history of significant exposure to black smoke such as wood smoke, dust, and/or other pollutants.

Including drowsiness, confusion, and/or personality change.

Signs of a bacterial infection (based on increased sputum purulence and/or volume) may be considered an indication for antimicrobial therapy.[1] In general, <50% of people with acute exacerbations experience fever.[23][30][34]

The presence of a high and/or persistent fever should lead to consideration of the presence of bacterial pneumonia or influenza virus infection.

Sign of impending respiratory failure.

Sign of impending respiratory failure.

Risk factors

Bacterial pathogens are thought to be responsible for the majority of acute exacerbations of COPD. Evidence suggests that the presence of purulent sputum is frequently associated with a bacterial lower respiratory tract infection.[23] Because the lower respiratory tract in people with COPD is not sterile, the interpretation of culture results of both upper and lower respiratory tract specimens must be made with caution. There is mixed evidence as to whether greater bacterial colony counts over baseline levels are present in patients with an acute exacerbation of COPD.[58][59]

The most frequently identified bacterial pathogens include Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis.[30][50] The role of other gram-positive pathogens such as Staphylococcus aureus and gram-negative pathogens such as Pseudomonas aeruginosa in the pathogenesis of acute exacerbations of COPD is less certain, but patients with more severe COPD and greater frequency and/or severity of exacerbations, or those who have been hospitalized recently or had recent (within 2 weeks) daily use of systemic corticosteroids (i.e., >10 mg/day of prednisone) are more likely colonized with these pathogens.[30][60]

Of note, it has been shown that acquisition of a new strain of bacteria by people with COPD is a risk for an acute exacerbation.[61] Alterations in the innate and/or adaptive immune response may result in cyclical perpetuation of inflammation and infection.[41]

Concurrent infection with both bacterial and viral respiratory tract pathogens has been associated with more severe episodes.[49] Treatment of moderate to severe exacerbations with antibiotics has been associated with improved outcomes.[62][63] Influenza vaccination may have protective effect in reducing risk of Pseudomonas aeruginosa infection.[30]

Gastroesophageal reflux and swallowing dysfunction with associated aspiration are common triggers for exacerbations of COPD.[64][65] No available studies guide whether the treatment of reflux improves exacerbations of COPD.

It has been estimated that respiratory viruses are responsible for 22% to 50% of acute exacerbations.[32]

The rhinovirus has been isolated from patients with acute exacerbations of COPD more often than other viruses.[66]

Influenza, respiratory syncytial virus, parainfluenza, coronavirus, adenovirus, and human metapneumovirus have also been associated with episodes.[30][33][34][67]

Exacerbations associated with respiratory viruses have been shown to be more severe and take longer to resolve compared with those attributed to other triggers.[66][68] Co-infection with viruses and bacterial pathogens is not uncommon.

It has been hypothesized that the chronic presence of respiratory viruses in the lower respiratory tract may play a role in the pathogenesis of COPD.[69]

Increasing levels of pollutants, specifically nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and black smoke particulates including wood smoke, have been associated with a greater rate of acute exacerbations and hospital admissions for people with COPD.[73][74][75] Peaks of air pollution can also increase hospitalizations and mortality.[76]

Exposure to many of these pollutants has been found to induce an inflammatory response in the respiratory tract.[27]

Atypical organisms (Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species) have been associated with acute exacerbations though with conflicting results.[70][71][72] There is insufficient evidence to suggest that antimicrobial coverage of atypical bacterial pathogens improves outcomes.

Changes in temperature and humidity are associated with increased risk for acute exacerbations of COPD.[27][77] However, it remains unclear whether changes in ambient temperature and/or humidity or changes in risk for infection due to respiratory viruses and/or other pathogens account for this association.

Exacerbation rates and all-cause mortality tend to be higher during winter months.[18]

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