Recommendations
Key Recommendations
Many definitions for acute exacerbation of COPD have been proposed and include several of the same components. Episodes may be diagnosed in people with a history of COPD who experience any of the following: worsening respiratory symptoms and physiologic status; or worsening of degree of cough, level of dyspnea (particularly during exertion), and/or the volume and character of sputum, particularly if these changes are acute in onset, sustained over time, beyond the normal day-to-day variation, or lead to a change in the patient's baseline medication regimens.[1][10][80][115][116][117]
Exacerbations are defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as mild, moderate, or severe after the event has occurred.[1] Severe exacerbations may have associated acute respiratory failure and should be dealt with in hospital. Mild and moderate exacerbations may be dealt with in primary care or as an outpatient.
Clinical evaluation
Most patients presenting with a potential acute exacerbation are stable enough that they may be evaluated and managed in the outpatient setting. Clinical evaluation should include determination of the following:
vital signs (including oxygen saturation via pulse oximetry or ABG)
mental status
severity of the level of dyspnea and airflow obstruction
history of symptoms associated with the patient's chief complaints
the ability to continue to provide self-care at home.
The patient’s medical record should be reviewed to check for recent spirometry results confirming a diagnosis of COPD. If there is no recorded spirometry result, and the patient is admitted to hospital for an exacerbation, spirometry should subsequently be arranged to confirm the diagnosis of COPD. It is now recognized that bronchodilator response has little value in differentiating asthma from COPD and that obstruction found only on postbronchodilator measurements is uncommon. GOLD states that prebronchodilator spirometry can be used as an initial test to investigate whether patients have airflow obstruction.[1] Consideration should also be given as to whether there are other findings (e.g., history of chronic bronchitis symptoms, and/or emphysema or chronic inflammatory airways disease evident on CT imaging) to suggest a diagnosis of COPD.
The risk of exacerbations should also be assessed: people with severe or very severe airflow obstruction, those 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]
Patients should be questioned regarding:
changes in their baseline level of dyspnea, cough, wheeze, and sputum production
character of the sputum
presence of fever
any other focal complaints (e.g., chest pain, signs/symptoms of an upper respiratory tract infection, palpitations, lightheadedness, or leg swelling)
their understanding and adherence with their current medical regimen for COPD, including the use of supplemental oxygen and any change in their requirement for rescue inhaler use.
On examination, auscultation may reveal wheeze, and it is important to observe patients for signs of respiratory failure (e.g., tachypnea, accessory muscle use, chest retractions, paradoxical movements of the abdomen, silent chest, confusion, drowsiness, and/or cyanosis), and/or signs of cor pulmonale, hemodynamic instability, or worsened mental status.
Auscultation sounds: Expiratory wheeze
Auscultation sounds: Polyphonic wheeze
Prognostic scores, such as the DECAF score (Dyspnea, Eosinopenia, Consolidation, Acidemia, and atrial Fibrillation), can be used to assess the severity of the exacerbation. The DECAF score is a predictor of inpatient mortality among hospitalized patients with COPD, and potentially a means of determining which patients may be safely treated for their acute exacerbations in the home setting.[118][119]
Laboratory evaluation and imaging
Diagnostic tests are typically reserved for those with moderate to severe exacerbations. Features of a more severe exacerbation include, but are not limited to, unstable vital signs, severe symptoms, low oxygen saturation on pulse oximetry, evidence of ventilatory failure, or mental status change (e.g., confusion, lethargy, coma). Diagnostic testing should also be considered if the diagnosis of an episode is uncertain.
Diagnostic tests for people with moderate to severe exacerbations may include:
Pulse oximetry: at rest, with exertion, and/or during sleep
Chest x-ray: may show hyperinflation, flattened diaphragms, increased retrosternal airspace, bullae, and a small, vertical heart; CT scan may be considered to characterize the features of COPD and to exclude other conditions, such as pulmonary embolism or tracheobronchomalacia
ECG
ABG
CBC with differential
CRP
Basic metabolic panel for electrolytes, BUN levels, creatinine
Sputum analysis.
C-reactive protein (CRP) is also a potential biomarker to guide the use of antibiotics during exacerbations of COPD. A decision to withhold antibiotics, based on low CRP levels at the point of care, has been associated with reduced antibiotic prescriptions without worse clinical outcomes.[120][121][122]
The eosinophil count may also be a useful indicator of likelihood of benefit from inhaled corticosteroids.[1] Evidence suggests that on average blood eosinophil counts are higher in COPD patients. In patients with frequent exacerbations and elevated blood eosinophil levels addition of inhaled corticosteroids to the double bronchodilator regimen should be considered.[1]
Sputum cultures or endotracheal aspirates (in patients who are intubated) are recommended for the assessment of bacterial infection in patients with severe lung function impairment, those with a history of frequent exacerbations, and/or in patients hospitalized with COPD exacerbations or who require mechanical ventilation, as gram-negative bacteria (such as Pseudomonas species) or resistant pathogens may be present.[1][40] Consideration may also be given to obtaining a sputum culture in patients who have bronchiectasis and suspected infectious exacerbations as a feature of their COPD.
Where feasible, tests for respiratory viruses should be conducted in hospitalized patients, to prevent healthcare-associated transmission of the pathogen (e.g., influenza, respiratory syncytial virus, and parainfluenza virus). Patients with COPD presenting with new or worsening respiratory symptoms, fever, and/or other symptoms consistent with COVID-19 should be tested for SARS-CoV-2, particularly at times of high COVID-19 prevalence in the community, alongside adoption of protective strategies (e.g., physical distancing, handwashing, and use of face coverings).[1]
Other laboratory investigations to consider include cardiac troponin and B-type natriuretic peptide (BNP). Elevations in cardiac troponin can occur due to unrecognized myocardial injury resulting from a COPD exacerbation. Elevations in serum BNP levels can help determine if a congestive heart failure exacerbation is present.
How to record an ECG. Demonstrates placement of chest and limb electrodes.
How to obtain an arterial blood sample from the radial artery.
Emerging investigations
Procalcitonin is emerging as a promising biomarker for the diagnosis of bacterial infections as it tends to be higher in severe bacterial infections and low in viral infections. The Food and Drug Administration has approved procalcitonin as a test for guiding antibiotic therapy in patients with acute respiratory tract infections. However, evidence for the efficacy of procalcitonin-guided protocols is conflicting and further research is required to establish its use in clinical practice for COPD.[1][123][124][125] Importantly, procalcitonin-guided antibiotic use is not recommended for COPD exacerbations in the intensive care unit setting, as this has been associated with increased mortality.[124]
Assessment of vitamin D and immunoglobulin levels should be considered in patients with a history of COPD exacerbations as low levels are associated with an increased risk of COPD exacerbation.[126][127][128] See Secondary prevention.
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