CRP and Antibiotic use in Acute COPD Exacerbations
By Dr. Nihal Varkey
Edited by Kevin Cao
Does CRP Help Reduce Antibiotic Prescriptions in Acute COPD Exacerbations?
As we all know, many of the exacerbations we see in the ED are precipitated by either infection, cold weather, pulmonary embolus, pneumothorax, CHF or trauma. We have an algorithm for treating exacerbations that uses a combination of the GOLD criteria, which stratifies exacerbations based on severity, and the Anthonisen criteria which is a subjective means of using our clinical gestalt to see who needs antibiotics.
With there being a strong push for limiting the use of antibiotics and preventing resistance, I wanted to take a look at this study which questions whether testing C-Reactive Protein (CRP) changes our management and limits our antibiotic use for COPD exacerbations.
The authors of this trial wanted to test point of care CRP in patients with acute COPD exacerbations. They hypothesized that the results of Point-of-care (POC) CRP may help inform prescribing decisions for acute COPD exacerbations. It was a multicenter, open-label, randomized controlled trial where patients were recruited from 86 general medical practices in the UK.
Patients with a diagnosis of COPD seen by a physician for an acute COPD exacerbation were randomized into two groups: usual care guided by CRP POC testing (CRP-guided group) and usual care alone (the control group).
Clinicians were then advised that antibiotics are unlikely to be beneficial when the CRP level is lower than 20 mg per liter, likely to be beneficial when the CRP level is higher than 40 mg per liter, and might be beneficial when the CRP level falls between these extremes and purulent sputum is present.
Clinicians were asked to base prescribing decisions on “a comprehensive assessment of likely risks and benefits” and not solely on the CRP level.
The percentage of patients who reported using antibiotics within 4 weeks after randomization was significantly lower in the CRP-guided group than in the control group (57% vs. 77%), yet clinical outcomes were similar in the two groups.
What’s the bomb?
What were the strengths?
What were the limitations?