Pro Tips & Practical Insights from Dr. Jim O’Brien
Are acute COPD exacerbations taking the wind out of YOUR sails? Join us as we navigate the stormy waters that can be AECOPD with our guest expert, Dr. Jim O’Brien from National Jewish Health Center.
Intro, disclaimer, guest bio
What is a COPD
Case from Kashlak – Natalie Harrison
Knee jerk reaction: Determining level of illness & disposition
Initial work-up considerations
What’s in your differential?
The second-order assessment – shuffling the differential, honing in on the patient
AECOPD: Triggers & Pathophysiology
Treatment Pearls I: Steroids
Treatment Pearls II: Antibiotics
Treatment Pearls III: Bronchodilators
Treatment Pearls IV: Oxygen Therapy
Preparing for discharge
Take home points
Lightning Round! Getting to know Dr. O’Brien & Picks of the Week*
An ounce of prevention is worth a pound of cure! Preventing AECOPD is the first step to managing acute exacerbations! Talk to your patients about smoking cessation, appropriate use of inhalers and make sure you have a good idea as to their disease trajectory.
Don’t forget vaccines, specifically for COVID, influenza and pneumonia
When approaching a patient with a possible AECOPD, don’t forget about the presence of PE as being a complicating/triggering factor!
Consider broad spectrum antibiotics – informed by prior culture data when available – when first admitting a COPD patient. Keep in mind covering for those at risk for or with a history of P. aeruginosa and MRSA
Steroids are recommended in AECOPD – how much, we don’t really know! GOLD recommends 40mg daily for 5 days, while Dr. O’Brien recommends consideration for a higher dose perhaps in sicker patients
Oxygen therapy comes in many flavors – heated, humidified high-flow nasal cannula, CPAP and bi-level non-invasive ventilation can all be good options in the right patient. They all can decrease work-of-breathing!
Non-invasive ventilation, for home use, has been shown to reduce recurrent exacerbations and decrease mortality in patients with COPD and persistent hypercapnia
Discharge planning is critical! Ensure close follow up and intermediate follow up, review medications, consider adjuncts (azithromycin, roflumilast) and pulmonary rehabilitation
AECOPD – Notes
Basics of AECOPD & the Initial Assessment
What is a COPD exacerbation?
Dr. O’Brien tells patients they are having an AECOPD if they have a change in the three “cardinal symptoms” of COPD: Cough, dyspnea, or volume/character of sputum (specifically increased purulence).
Often driven pathophysiologically by airway edema at the small-airway level
Need for hospitalization = more severe exacerbation
What precipitates exacerbations?
More than half of patients admitted with AECOPD are found to have an underlying suspected infectious (viral or bacterial) cause
POCUS: Evidence of RV dysfunction/dilation? Evidence of LV dysfunction/failure? Pericardial effusion? Pneumothorax? B-lines (evidence of pulmonary edema)?
BMP (to assess anion gap, bicarbonate – compared to prior if possible)
CBC (anemia?, leukocytosis?)
Blood gas (ABG or VBG – primarily to assess carbon dioxide levels)
Chest X-ray (to assess for presence of pneumonia, effusions, etc.)
BMI matters! The phenotypes colloquially referred to as the “Pink Puffer” and “Blue Bloater” can help frame the illness.
The “Pink Puffer” is characterized as having a maintained brain-stem response to hypoxemia & hypercapnia, thus resulting in their body working to maintain normal levels of oxygen and carbon dioxide which, over the long term, results in cachexia. Hypoxemia and hypercapnia in these patients may be related to an acute decompensation that must be addressed promptly.
The “Blue Bloater” usually is overweight or obese, with concomitant sleep apnea, and as a result, has a blunted response to hypoxemia and hypercapnia. When these patients are seen in the ED, their elevated carbon dioxide and hypoxemia are often acute-on-chronic processes indicative of greater physiologic reserve.
Consider other diagnoses / complicating factors
Endocarditis / valvular disease
Pulmonary Embolism (in some studies 25-30% of AECOPD patients were found to have PE!)
Iron deficiency anemia vs anemia of chronic disease
Hyponatremia (often seen in chronic heart failure and/or SIADH related to lung disease)
Treatment and Management Pearls
Benefits: reduce time to next exacerbation, contribute to more swift recovery and limit treatment failures
Otherwise, Dr. O’Brien explains the literature is very limited regarding approach to steroid use/dose
One large study in 2010 demonstrated PO is equivalent to high-dose IV but that study had some limitations based upon data collection
Dr. O’Brien will often use methylprednisolone (IV), dosing 60 mg two or three times daily
The COPD GOLD guidelines cite 40mg prednisone, oral, for five days but do not elaborate further nor does the guidelines differentiate between different exacerbating patients
Do you taper? Dr. O’Brien cites the literature which, generally does not “support” tapering, or longer courses of steroids but also reminds us of the challenges of such studies and the importance of tailoring therapy based upon the patient in front of you
Dr. O’Brien generally agrees with GOLD, which suggests a benefit for antibiotics in those with worsening of all three “cardinal symptoms” of COPD, worsening of two of these symptoms if one is worsening/more purulent sputum, or those requiring any mechanical respiratory support
Dr. O’Brien considers the presence of other forms of lung disease, such as bronchiectasis, when it comes to determining the utility of antibiotics
He also strongly recommends reviewing prior culture results to help inform the choice of antibiotic, as well as prior history of antibiotic exposure (specific concerns are for potential P. aeruginosa or MRSA infection)
Dr. O’Brien’s risk factors regarding P. aeruginosa: bronchiectasis, history of broad-spectrum antibiotic use, recent hospitalization, chronic steroid use, history of very severe COPD
Dr. O’Brien’s risk factors regarding MRSA: history of nasal colonization, recent systemic antibiotic exposure, recent hospitalization, chronic steroid use
What to use? If you are treating empirically, Dr. O’Brien recommends consideration of a 3rd generation cephalosporin, or a respiratory fluoroquinolone such as levofloxacin or moxifloxacin, often with azithromycin – likely due to its immunomodulatory effect
Don’t hang your hat on a negative sputum culture! Dr. O’Brien suggests that ~50% of cases of pneumonia won’t generate a positive sputum culture, although some studies suggest the yield may be even worse [Musher 2004, Shariatzadeh 2009, Naidus 2018]!
Dr. O’Brien recommends tailoring therapy to be broad enough to cover likely pathogens based on patient risk factors, but not unnecessarily broad if such risk factors (known prior resistant respiratory pathogens, repeated hospitalizations, antibiotic exposures, significant structural lung disease, etc.) do not exist
Be on the look out for influenza as these patients may be co-infected with MRSA and could benefit from the use of oseltamivir if they present within five days of initial symptoms
No great, high-quality data for short-acting bronchodilators in AECOPD, however, they are used by convention
Home inhalers: Dr. O’Brien states that continuing long acting medications is often reasonable as it can keep patients in a rhythm with their medication regimen
Be on the lookout of excessive antimuscarinic activity that can contribute to issues such as urinary retention
You do, indeed, need oxygen to live!
Nasal cannula, oxymask and non-rebreather provide supplemental oxygen without physiologic assistance – can be used when work-of-breathing is of less concern
Consider targeting 88-94% to provide adequate oxygenation while mitigating the Haldane Effect (The greater the oxygen tension in the the blood, the greater hemoglobin’s affinity is for oxygen, and the lower it’s affinity is for carbon dioxide, contributing to carbon dioxide retention)
High-flow nasal cannula and non-invasive positive pressure ventilation provide both supplemental oxygen & physiologic support
Hello Thank you very much for your excellent work of keeping us informed in several topics. Although I generally liked this one, I feel obliged to say two-three comments mostly regarding antibiotic stewardship. 1. First, I want to alert the fact that most AECOPD due infections are due to viral and not bacterial infections. It's true that it's not easy to differentiate a viral from a bacterial AECOPD in the most severe causes, but I'd say that in a AECOPD with no clear pneumonia, the burden of proof is on the side of having to prove that an acute tracheobronchitis is a bacterial and not a viral one (bacterial much rarer, in about 1/3 of cases as far as I know). 2. Second, I don't agree with the empiric choice of a cephalosporin. If we've already stepped further and really think we're talking about a bacterial infection, amoxicilin/clavulanate is a perfectly reasonable choice in patients with no clear risk factors for Pseudomonas and MRSA (and even in those cases, a 3rd gen ceph wouldn't be the right choice). We could also argue about amoxicilin plus macrolid, amoxicilin/clavulanate plus macrolid and amoxicilin/clavulanate alone, but that's a more complex one and a different topic. Misuse of 3rd generation cephalosporins are one of the most concerning stewardship problems worldwide, and I think we must use them judiciously. 3. Finally, I understand that in the end the local sensitivity pattern is the most important thing. But I'd only suggest a cephalosporin if the resistance pattern of H. influenza, M. catarralis and S. pneumoniae to amoxicilin/clavulanate would be really concerning, which I think it's not in most practices, but correct me if I'm wrong. Thank you again for the episode and keep up the great work! Bernardo