Residence in/travel to a country/area or territory with local transmission, or close contact with a confirmed or probable case of COVID-19, in the 14 days prior to symptom onset.
Signs and symptoms are similar so it may be difficult to differentiate between the conditions clinically. Maintain a high index of suspicion for COVID-19 in patients with COPD who present with symptoms of an exacerbation, especially if accompanied by fever, impaired taste or smell, or gastrointestinal complaints.
The situation is evolving rapidly; see our COVID-19 topic for further information.
Real-time reverse transcription polymerase chain reaction: positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA.
An increase in cough may be the first symptom of an asthma exacerbation. Ask about the presence of chest tightness.
Progressive worsening of wheeze and shortness of breath may occur. Assess for accessory muscle use, tachypnoea, and tachycardia.
Key risk factors include: viral infection, exposure to cigarette smoke, exposure to allergens, atopic eczema, environmental irritants, poor indoor air quality, gastro-oesophageal reflux disease, history of asthma, use of oral corticosteroids, non-compliance to asthma medication.
Extent of asthma exacerbation can be determined by measuring peak flow as a percentage of normal value: mild >80%; moderate 60% to 80%; severe <60%.
Oxygen saturation values measured by pulse oximetry vary with degree of exacerbation: mild >95%; moderate 91% to 95%; severe <90%.
Treatment with a short-acting bronchodilator can also be used as a diagnostic trial. Lack of response is extremely unusual and suggests that the condition is not caused by asthma.
Patients with systolic left-sided or biventricular congestive heart failure will often have a history of heart failure. Underlying diastolic heart failure is often under-recognised.
Physical examination may note signs consistent with heart failure, such as an elevated jugular venous pressure, extra heart sounds, coarse breath sounds with crackles above the lung bases, wheezing, and dependent pitting oedema. It may be difficult to distinguish heart failure, particularly left-sided heart failure, from an acute exacerbation of COPD.
Many aspects of acute exacerbations including dyspnoea, cough, and sputum production may be found in patients with pneumonia and it is often not possible to differentiate without chest imaging.
About 10% to 15% of patients presenting with an apparent acute exacerbation are found to have pneumonia, or other abnormalities, defined by chest imaging. Patients with pneumonia have in general been found to experience higher fevers, more acute onset of illness, and somewhat greater severity of acute illness when compared with COPD patients without pneumonia. The presence of pneumonia as a cause of respiratory decompensation in a patient with COPD does not necessarily imply the presence of a COPD exacerbation per se (i.e., the presence of worsened airflow limitation related to airways inflammation and/or bronchoconstriction), and as such careful consideration should be given as to whether systemic corticosteroids are warranted in such patients.
Chest imaging in patients with pneumonia should identify changes consistent with an infiltrative process in the lung parenchyma.
Pleural effusions may exacerbate dyspnoea in patients with COPD. Physical examination may demonstrate decreased or absent breath sounds with dullness to percussion related to a pleural effusion.
Chest imaging is recommended.
Patients with COPD found to have pneumothoraces may or may not have additional signs or symptoms suggestive of a respiratory tract infection, but their presentation may closely mirror that of an acute exacerbation. Decreased breath sounds may be identified on the affected side and tracheal deviation away from the affected side and/or hypotension may be present in patients with a tension pneumothorax.
Chest imaging is recommended to exclude a possible pneumothorax in patients with more than mild episodes.
Clinically, pulmonary embolism may present with signs and symptoms similar to an acute exacerbation of COPD, and the two are difficult to distinguish. Pulmonary embolism should be considered as a cause of the acute symptoms if no other identifiable trigger for the exacerbation is evident. People with prior thrombo-embolic disease or underlying malignancy may be at particular risk.
A low systolic blood pressure and/or the inability to increase the PaO2 >60 mmHg with oxygen may indicate the presence of a pulmonary embolism.
Pulmonary embolus may be diagnosed using D-dimer assay, spiral computed tomography angiogram, or pulmonary angiography in patients with COPD. Test selection should be based on local expertise. Dopplers of the lower extremities may be considered to evaluate for deep vein thrombosis.
Clinically, may be difficult to distinguish. Chest pain may be more apparent, with radiation down left side. Nausea, jaw pain, and/or diaphoresis may be present.
An electrocardiogram should be performed, especially for patients who may require hospitalisation for care of an acute exacerbation of COPD, to identify possible cardiac ischaemia and arrhythmias.
Differentiating features may include palpitations, light-headedness, loss of consciousness, and/or collapse.
An electrocardiogram should be performed, especially for patients who may require hospitalisation for care of an acute exacerbation of COPD or who are experiencing palpitations or dizziness, to identify possible cardiac ischaemia and arrhythmias.
Large airway obstruction typically presents with dyspnoea and wheeze (particularly during exertion and with forced exhalation manoeuvre), and it is commonly mistaken for refractory exacerbations of COPD; variable intrathoracic upper airway obstruction is often caused by tracheobronchomalacia, an aspirated object, or central airway tumour; variable extrathoracic upper airway obstruction is commonly caused by vocal cord paralysis, as well as by inflammation and swelling of the perilaryngeal soft tissues and intermittent vocal cord spasm associated with GORD, undiagnosed or untreated obstructive sleep apnoea, and chronic post nasal drip; fixed upper airway obstruction may be caused by tracheal stenosis (e.g., due to prior intubation for mechanical ventilation), extrinsic compression of central airways (e.g., lymphadenopathy or mass), or large airway tumour; auscultation over the larynx, trachea, and main bronchi during both quiet breathing and forced exhalation or hyperpnoea manoeuvre should be done to evaluate for the presence of upper airway obstruction; complete resolution of wheezing during resting quiet breathing that is present during exertion or a forced exhalation manoeuvre argues against the presence of bronchoconstriction related to COPD exacerbation.
Spirometry with flow volume loop can identify the presence of upper airway obstruction; when tracheobronchomalacia is suspected, CT scanning with inspiration and expiration views or direct bronchoscopic airway inspection can be diagnostic.
While oxygen therapy is clearly indicated for many patients with COPD and acute exacerbations, excessive oxygen leads to further degradation of the patient's respiratory physiology. Exposure to oxygen leads to decrease of hypoxic vasoconstriction of arteries supplying poorly ventilated spaces, increasing the degree of V/Q mismatch and/or intrapulmonary shunt. An excess of oxygen may also decrease the capacity of erythrocytes to carry CO2 (Haldane effect). These changes may then result in worsening of the patient's hypercarbia and respiratory acidosis. Selected patients with impaired respiratory drive may also develop worsening hypercarbia.
An ABG should be performed for patients who are hypoxaemic or are receiving oxygen therapy who present with an apparent acute exacerbation of COPD.
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