COPD 50-50 club

[Jabbed]

Is there any significance to this moniker aside from the shock factor of PaO2 50 mmHg and PaCO2 50 mmHg? Is the acute management of an exacerbation still the same with a target SpO2 of 88-92% and PaO2 of 60-70 mm Hg?

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[jdh71]

Is there any significance to this moniker aside from the shock factor of PaO2 50 mmHg and PaCO2 50 mmHg? Is the acute management of an exacerbation still the same with a target SpO2 of 88-92% and PaO2 of 60-70 mm Hg?

Those numbers aren't that shocking.

But I'm not sure what the question is though.

 

[235009]

I think the teaching point is simply that patients with COPD can have a higher than "normal" baseline PCO2 at rest so you should aim to get them back to that rather than "normalize" it.

 

[Mad Jack]

Is there any significance to this moniker aside from the shock factor of PaO2 50 mmHg and PaCO2 50 mmHg? Is the acute management of an exacerbation still the same with a target SpO2 of 88-92% and PaO2 of 60-70 mm Hg?

If their baseline SpO2 is in the 88-92% range, their baseline PaCO2 is usually going to be higher than 50. You're usually looking at high 50s to mid 60s with some of the end stagers, but their bicarb is high enough that it's kind of meh. Just don't overventilate them if they're tubed (that's a good way to get them stuck on the vent forever, once they realize how much easier it is to not do all that breathing work and they've lost their bicarb buffer, lot of the time they just don't want to wean) and don't hyperoxygenate them. I've never seen the mythical "they just stopped breathing because they got too much O2 and it knocked out their hypoxic drive" patient, but you can knock their drive out enough that they start to decomp due to hypoventilation, which you don't want.

So if you get someone in on an exacerbation, look up their prior labs (usually these people have a history of admits a mile long). See what their CO2 and O2 were like as close to their last discharge as possible to get an idea of what you're working with. If there's no gas close to their last discharge, check their SpO2s and their electrolyte panel (the bicarb on that is actually more accurate than what you get off of an ABG anyway, as ABGs use a formula calculated bicarb and not an actual lab-measured value) before they were let go to give you an idea of what their personal normal is. If they're on home O2, just assume you're shooting for 88-92% oxygen-wise, as you've got to have a resting O2 of 88% for insurance to cover it.

 

[lymphocyte]

I've never seen the mythical "they just stopped breathing because they got too much O2 and it knocked out their hypoxic drive" patient, but you can knock their drive out enough that they start to decomp due to hypoventilation, which you don't want.

For whatever weird reason, this is my biggest pet peeve myth in all of medicine. It's almost certainly not the case that by giving oxygen you're "knocking out" ventilatory drive causing pure alveolar hypoventilation. Not only is there no good evidence, there's evidence to the contrary.

A much better explanation is that permissive O2 reverses hypoxic vasoconstriction and promotes oxygenation of dead space. More dead space, more CO2 retention.

In COPD exacerbation, you want to bolus O2 to improve stats (never withhold oxygen, as I've seen some nurses and JMOs suggest), but don't crank it up and walk away either. Set a reasonable O2 target (flat portion of the dissociation curve if possible) and follow with ABGs. If you're not careful, you'll undo all of the lungs' hardwork by completely reversing hypoxic vasoconstriction and ventilating dead space, causing CO2 narcosis.

Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.

 

[Mad Jack]

For whatever weird reason, this is my biggest pet peeve myth in all of medicine. It's almost certainly not the case that by giving oxygen you're "knocking out" ventilatory drive causing pure alveolar hypoventilation. Not only is there no good evidence, there's evidence to the contrary.

A much better explanation is that permissive O2 reverses hypoxic vasoconstriction and promotes oxygenation of dead space. More dead space, less ventilation, more CO2 retention.

Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.

Thanks for the article- the cases I've seen over the years make sooooo much more sense now. It's unfortunate that so many people are still teaching it the old way- even in the lecture material I had for the boards, it was still described as a drive abnormality rather than a worsening V/Q defect, and I hadn't even considered the Haldane Effect on things. This is literally one of those mind blowing moments in my life.

 

[Psai]

Thanks for the article- the cases I've seen over the years make sooooo much more sense now. It's unfortunate that so many people are still teaching it the old way- even in the lecture material I had for the boards, it was still described as a drive abnormality rather than a worsening V/Q defect, and I hadn't even considered the Haldane Effect on things. This is literally one of those mind blowing moments in my life.
View attachment 205897

Ya bro haldane effect so your blood cells suck at picking up co2 to get rid of it and shunting because higher oxygen concentration in alveoli opens up blood vessels in places with crappy ventilation so you blow off less co2. Leads to more co2 retention which is the main problem in copd exacerbation, not hypoxia. I get so pissed when the nurse is like yeah I did vitals and they are perfect. We're aiming for 92% o2 sat for the patient, not 100% for your chart to look pretty. Stop messing with the oxygen level!

 

[jdh71]

For whatever weird reason, this is my biggest pet peeve myth in all of medicine. It's almost certainly not the case that by giving oxygen you're "knocking out" ventilatory drive causing pure alveolar hypoventilation. Not only is there no good evidence, there's evidence to the contrary.

A much better explanation is that permissive O2 reverses hypoxic vasoconstriction and promotes oxygenation of dead space. More dead space, more CO2 retention.

In COPD exacerbation, you want to bolus O2 to improve stats (never withhold oxygen, as I've seen some nurses and JMOs suggest), but don't crank it up and walk away either. Set a reasonable O2 target (flat portion of the dissociation curve if possible) and follow with ABGs. If you're not careful, you'll undo all of the lungs' hardwork by completely reversing hypoxic vasoconstriction and ventilating dead space, causing CO2 narcosis.

Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.

Yup

Though I don't recommend a bunch of ABGs. If you believe your SpO2 there is no reason for more ABGs. A single VBG assuring yourself of positive trend or confirming further failure should be all you really need.

 

[lymphocyte]

Yup

Though I don't recommend a bunch of ABGs. If you believe your SpO2 there is no reason for more ABGs. A VBG assuring yourself of positive trend or confirming failure should be all you really need.

VBG vs ABG is a debate I've had with an attending and never want to have again. I think the evidence and logic supports VBG, but opinions seem to strongly vary...

 

[Mad Jack]

Yup

Though I don't recommend a bunch of ABGs. If you believe your SpO2 there is no reason for more ABGs. A VBG assuring yourself of positive trend or confirming failure should be all you really need.

VBG+chem panel gets you your CO2 and bicarb with so much less pain and hassle for the patient

 

[Mad Jack]

VBG vs ABG is a debate I've had with an attending and never want to have again. I think the evidence and logic supports VBG, but opinions seem to strongly vary...

I feel like teaching hospitals are much more aggressive about ABGs- a lot of the attendings at the big teaching hospital I used to work at were very ABG happy. There's no need for it, but it seems like the attitude of "we've got practically unlimited resources, so why not" prevails.

 

[jdh71]

Chronic lungers are not in practice what you are taught in pathophys. It's not emphysema OR chronic bronchitis. It both. And often depends on which more than the other. Often in the context(s) of bad heart, secondary pulmonary hypertension, and sleep or obesity disordered breathing. These patients are fooking wrecks.

I treat exacerbating lungs as aggressive as **** and then back off and allow the patient to recalibrate on their own following this for a few days in the hospital where I can watch them closer.

I use a lot steroids. Quick tapers are not very helpful in my opinion. I treat most of these guys with 40mg of prednisone per day for 14 days then stop. No taper. No taper. See them back in clinic in about a month.

 

[jdh71]

VBG vs ABG is a debate I've had with an attending and never want to have again. I think the evidence and logic supports VBG, but opinions seem to strongly vary...

If you have reason to disbelieve you sat? Fine get some ABGs. But if you believe it. You're just sticking an artery for no good reason. Of course if you have an arterial line in the patient and it's no big deal why not? The patient won't be going home where an blood gas can be obtained. So figuring out what works with their oxygen tank and home spo2 sensor makes a lot of sense to me.

 

[lymphocyte]

Chronic lungers are not in practice what you are taught in pathophys. It's no emphysema or chronic bronchitis. It both. And often depends on which more than the other. Often the context of bad heart, secondary pulmonary hypertension, and sleep or obesity disordered breathing. These patients are fooking wrecks.

I treat exacerbating lungs as aggressive as **** and then back off and allow the patient to recalibrate on their own following this for a few days in the hospital where I can watch them closer.

I use a lot steroids. Quick tapers are not very helpful in my opinion. I treat most of these guys with 40mg of prednisone per day for 14 days then stop. No taper. No taper. See them back in clinic in about a month.

So much yes in this post. Especially about the clear-cut distinction between COPD and emphysema. And now there's even interesting literature on asthma-COPD overlap syndromes. And a taper for 40mg/14 days is indeed unnecessary. Even GC > 5mg can cause harm and slow taper really hasn't been shown to reduce HPA-dysfunction in multiple patient sub-groups.

Liu D, Ahmet A, Ward L, et al. A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy Asthma Clin Immunol. 2013;9(1):30.

Postma DS, Rabe KF. The Asthma-COPD Overlap Syndrome. N Engl J Med. 2015;373(13):1241-9.

 

[Psai]

So much yes in this post. Especially about the clear-cut distinction between COPD and emphysema. And now there's even interesting literature on asthma-COPD overlap syndromes.

And a taper for 40mg/14 days is indeed unnecessary. Even GC > 5mg can cause harm and slow taper really hasn't been shown to reduce HPA-dysfunction in multiple patient sub-groups.


Liu D, Ahmet A, Ward L, et al. A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy Asthma Clin Immunol. 2013;9(1):30.

Postma DS, Rabe KF. The Asthma-COPD Overlap Syndrome. N Engl J Med. 2015;373(13):1241-9.

That New England paper is really good at explaining it. No one brought up the whole asthma/copd thing until I took a pulm elective and I was like hey this makes a lot of sense.

 

[jdh71]

And yes. The five day course. That was sold to me as gospel until I trained under one of the authors involved in the study. And he lawled. This made me scratch my head. Deciding on 5 or 14 is really a gestalt of baseline severity. Moderate/mild folks with a good reason (viral Illness or allergies) for exacerbation get five days. Old buzzards with FEV1s less than a liter on oxygen with baseline pCO2s of 56 get 14 days. It just works better for worse lungs over the long term. You can get a bad chronic lunger out of a hospital in less than five days. But you end up doing catch up on the flip side in the outpatient setting.

I think of an exacerbation like a house fire. If it's not good and out. It catches again. Flares up. Maybe not as bad as before. But still.

 

[lymphocyte]

Ya bro haldane effect so your blood cells suck at picking up co2 to get rid of it and shunting because higher oxygen concentration in alveoli opens up blood vessels in places with crappy ventilation so you blow off less co2. Leads to more co2 retention which is the main problem in copd exacerbation, not hypoxia.

Just be careful how you use shunting and ventilation. Commonly confused (not saying you are, just for the preclinicals reading this). Shunt-type problems and dead-space problems are *almost* mirror opposites in terms of V/Q mismatch. In COPD with permissive oxygenation, there's almost always a predominant dead-space problem; that's why you have more hypercapnia than hypoxemia (which itself is different from hypoxia).

And can I just say that John B(amf) West anticipated this whole discussion with an amazingly well-written paper from the 70s?

http://www.nejm.org/doi/full/10.1056/NEJM197106032842202

 

[Psai]

When I said shunting I mean that adding extra o2 above what's required to keep the o2 sat at around 88-92% causes pulmonary capillary vasodilation and this brings increased amounts blood to alveoli that aren't being ventilated. So there is greater inefficiency in gas exchange leading to worsening hypercapnia. I probably am using it wrong though, my medicine is a little rusty atm.

 

[lymphocyte]

If you have reason to disbelieve you sat? Fine get some ABGs. But if you believe it. You're just sticking an artery for no good reason. Of course if you have an arterial line in the patient and it's no big deal why not? The patient won't be going home where an blood gas can be obtained. So figuring out what works with their oxygen tank and home spo2 sensor makes a lot of sense to me.

This is how the debate went: "Yeah, but why"? "Because trends matter more, VBG is good enough, bicarb gives you chronicity." "Yeah, but why not"? "Because you keep sticking the patient, it hurts, could cause vasospasm, iatrogenic injury." "Yeah, but still." Etc. Appeal to authority often wins the argument in medicine...

I'm sure I'll feel differently when I'm an attending... "You snotty med students think you know so much"!

 

[StrongIslandDoc]

If their baseline SpO2 is in the 88-92% range, their baseline PaCO2 is usually going to be higher than 50. You're usually looking at high 50s to mid 60s with some of the end stagers, but their bicarb is high enough that it's kind of meh. Just don't overventilate them if they're tubed (that's a good way to get them stuck on the vent forever, once they realize how much easier it is to not do all that breathing work and they've lost their bicarb buffer, lot of the time they just don't want to wean) and don't hyperoxygenate them. I've never seen the mythical "they just stopped breathing because they got too much O2 and it knocked out their hypoxic drive" patient, but you can knock their drive out enough that they start to decomp due to hypoventilation, which you don't want.

So if you get someone in on an exacerbation, look up their prior labs (usually these people have a history of admits a mile long). See what their CO2 and O2 were like as close to their last discharge as possible to get an idea of what you're working with. If there's no gas close to their last discharge, check their SpO2s and their electrolyte panel (the bicarb on that is actually more accurate than what you get off of an ABG anyway, as ABGs use a formula calculated bicarb and not an actual lab-measured value) before they were let go to give you an idea of what their personal normal is. If they're on home O2, just assume you're shooting for 88-92% oxygen-wise, as you've got to have a resting O2 of 88% for insurance to cover it.

It is my sincerest hope that this is a play on words of the physiology, and not intended to mean behavior learned by the patient, lol.

 

[ACSurgeon]

For whatever weird reason, this is my biggest pet peeve myth in all of medicine. It's almost certainly not the case that by giving oxygen you're "knocking out" ventilatory drive causing pure alveolar hypoventilation. Not only is there no good evidence, there's evidence to the contrary.

A much better explanation is that permissive O2 reverses hypoxic vasoconstriction and promotes oxygenation of dead space. More dead space, more CO2 retention.

In COPD exacerbation, you want to bolus O2 to improve stats (never withhold oxygen, as I've seen some nurses and JMOs suggest), but don't crank it up and walk away either. Set a reasonable O2 target (flat portion of the dissociation curve if possible) and follow with ABGs. If you're not careful, you'll undo all of the lungs' hardwork by completely reversing hypoxic vasoconstriction and ventilating dead space, causing CO2 narcosis.

Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012;16(5):323.

As others describe, it's not about giving so much oxygen that you suppress their respiratory drive, it's about jacking up the effectiveness of their ventilation.

I have seen patients with a minute ventilation 2-4x normal with respiratory acidosis who normalize after turning down the FiO2. It was truly one of the cooler physiology lessons in critical care.

 

[lymphocyte]

As others describe, it's not about giving so much oxygen that you suppress their respiratory drive, it's about jacking up the effectiveness of their ventilation.

I have seen patients with a minute ventilation 2-4x normal with respiratory acidosis who normalize after turning down the FiO2. It was truly one of the cooler physiology lessons in critical care.

+1. Seeing this exact same thing happen as a MS2 (and then being asked by the consultant, "Why"?) was what sent me down the respirology rabbit hole in the first place...

 

[BigRedBeta]

Good stuff here. Thank you for the citations as well.

I personally have seen hypoxia induced apnea twice - it does exist, I promise you. But both kids had recurrent medulloblastoma, had gotten lots of radiation to their posterior fossa and had centrally mediated hypopnea that led to their chronic respiratory failure and PCO2's in the 65-70 range with bicarbs of 35-40. One had undergone a stem cell transplant and had bad GVHD of his lungs on top of that. On more than one occasion some new H/O nurse on nights would watch him desat, crank up his O2 and then minutes later call a code when he went apneic and then transfer back to the PICU for 24 hours.

Again, different disease processes, and that's the important lesson here. Final common pathways don't tell the whole story.

 

[VA Hopeful Dr]

And yes. The five day course. That was sold to me as gospel until I trained under one of the authors involved in the study. And he lawled. This made me scratch my head. Deciding on 5 or 14 is really a gestalt of baseline severity. Moderate/mild folks with a good reason (viral Illness or allergies) for exacerbation get five days. Old buzzards with FEV1s less than a liter on oxygen with baseline pCO2s of 56 get 14 days. It just works better for worse lungs over the long term. You can get a bad chronic lunger out of a hospital in less than five days. But you end up doing catch up on the flip side in the outpatient setting.

I think of an exacerbation like a house fire. If it's not good and out. It catches again. Flares up. Maybe not as bad as before. But still.

Same thing happened to me in residency, everyone decided that 5 days was plenty. All of a sudden we started getting more bouncebacks. I started doing occasional 14d then 7 day taper (overkill, but meh) and none of my patients came back within 30 days.

 

[lymphocyte]

Good stuff here. Thank you for the citations as well.

I personally have seen hypoxia induced apnea twice - it does exist, I promise you. But both kids had recurrent medulloblastoma, had gotten lots of radiation to their posterior fossa and had centrally mediated hypopnea that led to their chronic respiratory failure and PCO2's in the 65-70 range with bicarbs of 35-40. One had undergone a stem cell transplant and had bad GVHD of his lungs on top of that. On more than one occasion some new H/O nurse on nights would watch him desat, crank up his O2 and then minutes later call a code when he went apneic and then transfer back to the PICU for 24 hours.

Again, different disease processes, and that's the important lesson here. Final common pathways don't tell the whole story.

Very interesting. Something to read up on. I can't think through the pathophysiology at all. I thought medullary chemoreceptors were only sensitive to CSF pH? And I guess it would be a pure alveolar hypoventilation since it's centrally-mediated apnea, as opposed to a worsening V/Q mismatch in the COPD case.

We had a consultant who used to say: "Kids aren't just little people. They're weird people."

 

[BigRedBeta]

And I guess it would be a pure alveolar hypoventilation since it's centrally-mediated apnea, as opposed to a worsening V/Q mismatch in the COPD case.

We had a consultant who used to say: "Kids aren't just little people. They're weird people."

Hahaha, yeah the kiddos can be different.

I had interpreted the central hypopnea as collateral damage from the radiation therapy, particularly in these kids who have gotten multiple rounds of radiation. I should probably look into it more given that my hospital serves as the neuro-onc center within our larger pediatric health system...

 

[PlutoBoy]

Same thing happened to me in residency, everyone decided that 5 days was plenty. All of a sudden we started getting more bouncebacks. I started doing occasional 14d then 7 day taper (overkill, but meh) and none of my patients came back within 30 days.

Meh. I agree that clinical judgment plays a role in how much steroids one should give but most of the time I'd rather stick to the guidelines.

This has been studied already (REDUCE trial) and higher steroid dosages/longer therapy did not lead to a lower readmission rate as your posts and @jdh71 suggest. There was even a trend towards longer hospital stay in the high dose group.

I genuinely frown upon anyone that gives Solumedrol 125 mg q6h to a COPD Exacerbation.

http://jama.jamanetwork.com/mobile/article.aspx?articleid=1688035

Conclusions and Relevance

"In patients presenting to the emergency department with acute exacerbations of COPD, 5-day treatment with systemic glucocorticoids was noninferior to 14-day treatment with regard to reexacerbation within 6 months of follow-up but significantly reduced glucocorticoid exposure. These findings support the use of a 5-day glucocorticoid treatment in acute exacerbations of COPD."

As you may know, the GOLD guidelines now recommend lower dosages for less time largely based on the aforementioned evidence.

COPD Guidelines - Pocket Version - Go to page 22.

http://www.goldcopd.it/materiale/2015/GOLD_Pocket_2015.pdf

I'm not saying I have never used a longer tapering or that I never will in the future but the evidence suggests that you should not do this routinely.

 

[jdh71]

Meh. I agree that clinical judgment plays a role in how much steroids one should give but most of the time I'd rather stick to the guidelines.

This has been studied already (REDUCE trial) and higher steroid dosages/longer therapy did not lead to a lower readmission rate as your posts and @jdh71 suggest. There was even a trend towards longer hospital stay in the high dose group.

I genuinely frown upon anyone that gives Solumedrol 125 mg q6h to a COPD Exacerbation.

http://jama.jamanetwork.com/mobile/article.aspx?articleid=1688035

Conclusions and Relevance

"In patients presenting to the emergency department with acute exacerbations of COPD, 5-day treatment with systemic glucocorticoids was noninferior to 14-day treatment with regard to reexacerbation within 6 months of follow-up but significantly reduced glucocorticoid exposure. These findings support the use of a 5-day glucocorticoid treatment in acute exacerbations of COPD."

As you may know, the GOLD guidelines now recommend lower dosages for less time largely based on the aforementioned evidence.

COPD Guidelines - Pocket Version - Go to page 22.

http://www.goldcopd.it/materiale/2015/GOLD_Pocket_2015.pdf

I'm not saying I have never used a longer tapering or that I never will in the future but the evidence suggests that you should not do this routinely.

Except there are no real guidelines for length of treatment in COPD. So if you're sticking to them you aren't really on an moral high ground. Plus any doctor that can be replaced with a treatment algorithm should be.

Patients are nuanced. Five days works . . . until it doesn't. 14 days is a good way to make sure. Which I argue is not only better for physicians it's better for patients.

 

[PlutoBoy]

Except there are no real guidelines for length of treatment in COPD. So if you're sticking to them you aren't really on an moral high ground. Plus any doctor that can be replaced with a treatment algorithm should be.

Patients are nuanced. Five days works . . . until it doesn't. 14 days is a good way to make sure. Which I argue is not only better for physicians it's better for patients.

Except the evidence available shows otherwise. A longer course does not prevent future exacerbations or readmissions. Did you even read the article?

I never said there is no room for clinical judgement but I'd rather use guidelines as a guide than your "experience". Thanks.

 

[lymphocyte]

Meh. I agree that clinical judgment plays a role in how much steroids one should give but most of the time I'd rather stick to the guidelines.

Patients are nuanced..

Except the evidence available shows otherwise.

Actually the evidence doesn't show that. The guidelines suggest they do. But they don't.

@jdh71 nailed it. This is exactly the problem with EBM that gets promulgated into guidelines.

REDUCE was 314 patients with no significant difference in GC-related side-effects for 5 or 14-course therapy. And the latest Cochrane review is based on a grand total of 582 patients (including those from the SCOPE trial). Not exactly high-powered stuff here (so to speak). All of this is non-inferiority with no difference in side-effects. There's simply no good evidence to generalise across disease severity.

Sicker patients need more glucocorticoids. That's the logic behind slamming metpred in acute or impending respiratory failure. Why doesn't that same logic apply to less acute patients? When the evidence is equivocal, you have to rely on first principles.

Walters JA, Wang W, Morley C, Soltani A, Wood-baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2011;(10):CD006897.

 

[PlutoBoy]

Bingo. @jdh71 nailed it. This is exactly the problem with EBM that gets promulgated into guidelines.

REDUCE was 314 patients with no significant difference in GC-related side-effects for 5 or 14-course therapy. And the latest Cochrane review is based on a grand total of 582 patients (including those from the SCOPE trial). Not exactly high-powered stuff here (so to speak).

Sicker patients need more glucocorticoids. That's the logic behind slamming metpred in acute or impending respiratory failure. Why doesn't that same logic apply to less acute patients? When the evidence is equivocal, you have to rely on first principles.

Walters JA, Wang W, Morley C, Soltani A, Wood-baker R. Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2011;(10):CD006897.

1) Your review predates REDUCE

2) This is the conclusion of the review:

The finding in this review that there is no significant increase in treatment failure with shorter systemic corticosteroid treatment for seven days or less for acute exacerbations of COPD...

You want to do 21 day tapers, do it. But shorter courses are at the very least not inferior. If it makes you feel good to blast your patients with solumedrol 125 mg IV q6h for three days and then discharge them on a 21 day prednisone taper do it. But you are not doing it based on rational evidence.

 

[lymphocyte]

1) Your review predates REDUCE

2) This is the conclusion of the review:

The finding in this review that there is no significant increase in treatment failure with shorter systemic corticosteroid treatment for seven days or less for acute exacerbations of COPD...

You want to do 21 day tapers, do it. But shorter courses are at the very least not inferior. If it makes you feel good to blast your patients with solumedrol 125 mg IV q6h for three days and then discharge them on a 21 day prednisone taper do it. But you are not doing it based on rational evidence.

Pardon, but who said anything about 21 day tapers? I said no tapers. The (actual) evidence supports this. And you keep quoting the conclusions; read the damn study. How can you generalise the findings across the spectrum of disease severity?

And if you want to cite REDUCE, fine. But once again, non-inferior with no difference in treatment-related adverse effects.

 

[PlutoBoy]

Pardon, but who said anything about 21 day tapers? I said no tapers. The (actual) evidence supports this. And you keep quoting the conclusions; read the damn study. How can you generalise the findings across the spectrum of disease severity?

And if you want to cite REDUCE, fine. But once again, non-inferior with no difference in treatment-related adverse effects.

So if a shorter course was non inferior, why expose the patient to harm?

 

[lymphocyte]

So if a shorter course was non inferior, why expose the patient to harm?

COPD is not a binary thing (and it doesn't hew to GOLD classification either). It's a spectrum of disease. The literature thus far has been underpowered to uncover benefit or harms across the entire spectrum of disease.

You can't just lump patients together like that and then try to individuate the conclusions. That's a huge limitation of EBM. And it's where clinical judgement and experience and first-principles play a role. It's also why I keep telling medical students that they should have absolutely zero concerns from NPs wielding Guideline-Driven Medicine (only the patients should be concerned...).

 

[jdh71]

Except the evidence available shows otherwise. A longer course does not prevent future exacerbations or readmissions. Did you even read the article?

I never said there is no room for clinical judgement but I'd rather use guidelines as a guide than your "experience". Thanks.

Yeah. But you're not even an expert in pulmonary medicine (whereas ostensibly my board certification says I am) and a guy who couldn't hack it in hospital medicine right? You don't like the gray areas. You like it spelled out so you don't have to think. I think my experience with pulmonary patients is a rather important one given the nuanced nature of patients and valid enough. You can't create a study that will likely solve this question. And non-inferiority isn't saying what you're suggesting here. Nor is 5 days in any kind of guideline. It's often a great starting place. And many patients even the fairly severe can get away with a short course. Some can't. This is why you see the noninferiority. Some patients simply need more. Plus there is more than just reexacerbation to consider. Especially since many patients I see hospital follow up aren't acutely exacerbating but aren't anywhere back to baseline with regards to cough, ambulatory symptoms and rescue inhaler use.

In primary care you guys probably should use the five days.

 

[jdh71]

So if a shorter course was non inferior, why expose the patient to harm?

No evidence for harm in the paper youre hawking though.

 

[Psai]

So if a shorter course was non inferior, why expose the patient to harm?

Absence of evidence is not evidence of absence. Where is the evidence of harm? We all know the side effects of steroids but you're not gonna give a patient a buffalo hump and cataracts from an extra 9 days of steroids.

 

[PlutoBoy]

COPD is not a binary thing (and it doesn't hew to GOLD classification either). It's a spectrum of disease. The literature thus far has been underpowered to uncover benefit or harms across the entire spectrum of disease.

You can't just lump patients together like that and then try to individuate the conclusions. That's a huge limitation of EBM. And it's where clinical judgement and experience and first-principles play a role. It's also why I keep telling medical students that they should have absolutely zero concerns from NPs wielding Guideline-Driven Medicine (only the patients should be concerned...).

Sure. Clinical judgement has a role. It definitely does. But you can't justify practicing medicine with disregard for the best available evidence 99% of the time.

I've said jtmyself, I'm not saying I wouldn't do it occasionally but this should not be routine. There should be other factors at play to make you disregard the guidelines and the best (not perfect) evidence.

In short, most COPDers aren't readmitted due to a lack of steroids or so the best available evidence suggests.

EBM has its limits but it is better than nothing.

 

[PlutoBoy]

Yeah. But you're not even an expert in pulmonary medicine (whereas ostensibly my board certification says I am) and a guy who couldn't hack it in hospital medicine right? You don't like the gray areas. You like it spelled out so you don't have to think. I think my experience with pulmonary patients is a rather important one given the nuanced nature of patients and valid enough. You can't create a study that will likely solve this question. And non-inferiority isn't saying what you're suggesting here. Nor is 5 days in any kind of guideline. It's often a great starting place. And many patients even the fairly severe can get away with a short course. Some can't. This is why you see the noninferiority. Some patients simply need more. Plus there is more than just reexacerbation to consider. Especially since many patients I see hospital follow up aren't acutely exacerbating but aren't anywhere back to baseline with regards to cough, ambulatory symptoms and rescue inhaler use.

In primary care you guys probably should use the five days.

Ad hominem attacks as an argument? I'm over it. Moving on.

 

[PlutoBoy]

Absence of evidence is not evidence of absence. Where is the evidence of harm? We all know the side effects of steroids but you're not gonna give a patient a buffalo hump and cataracts from an extra 9 days of steroids.

Agree. However, the kind of patients that would ostensibly benefit from a longer course of steroids are the ones that are readmitted rather often and thus being exposed to the same "beneficial therapy".

Longer course of steroids do not prolong the time before next exacerbation or decrease the readmission rate. This is the best evidence that we have.

 

[jdh71]

Ad hominem attacks as an argument? I'm over it. Moving on.

There wasn't a single ad hominem argument. I don't think you are comfortable in gray areas. You aren't any an "expert" and I apparently am based on training and board certification - it's also why I see the weird stuff. I have a much more nuanced opinion and I tend to agree that in general if you're treating from a non expert opinion stand point start at 5 days.

It's a free country and you can move on.

But the bottom line is that the study you are trying to beat us over the head here with doesn't really say what you want it to say. It's being used as s place to hide. There are very good reasons for 14 days of steroids quite often and even the study you are thumping doesn't support "bad outcomes". Some people afraid of steroids and I get that. Probably best used in the hands of people more familiar.

 

[lymphocyte]

Sure. Clinical judgement has a role. It definitely does. But you can't justify practicing medicine with disregard for the best available evidence 99% of the time.

In short, most COPDers aren't readmitted due to a lack of steroids or so the best available evidence suggests.

EBM has its limits but it is better than nothing.

Actually, sometimes EBM is worse than nothing. Because it often encourages you to treat individual patients like "most patients." Unless you're very careful about the inclusion criteria, sub-group analysis, study power, etc.--that's a very wrong conclusion to draw and could cause harm.

And you keep using the word "evidence." Evidence is more than just research studies. Evidence includes reasoning from first principles, clinical judgment, clinical experience, debate with your colleagues, etc. The problem with EBM is that it equivocates statistics (the aggregation of data) with evidence. It's a very important distinction to make, because you can't always individuate statistics. That's when you have to look to other evidence.

 

[PlutoBoy]

Actually, sometimes EBM is worse than nothing. Because it often encourages you to treat individual patients like "most patients." Unless you're very careful about the inclusion criteria, sub-patient analysis, study power, etc.--that's a very wrong conclusion to draw and could cause harm.

And you keep using the word "evidence." Evidence is more than just research studies. Evidence includes reasoning from first principles, clinical judgment, clinical experience, debate with your colleagues, etc. The problem with EBM is that it equivocates statistics (the aggregation of data) with evidence. It's a very important distinction to make, because you can't always individuate statistics. That's where you have to look at other evidence.

Sometimes, yes. But not most of the time.

Reasoning from first principles should also tell you that even if there is no evidence of harm in treating someone with high doses and prolonged courses of steroids, it has to do more harm than a short low dose course. But then someone may say that it doesn't and start citing the evidence when it suits their narrative.

Patients should be individualized, yes. But the criteria should not a physician's hunch.

For example, it is rather clueless to say that five days work until it doesn't to justify a longer course of therapy.

What about 14 days? Should I believe that it always works or does it work until it doesn't?

If the latter, then why not do 21 days? Surely more steroids should be good by that rationale and so on and so forth.

This is why we need to rely on quantifiable measures. Of course, I acknowledge that there is room for clinical judgment but you have to justify your rationale on something else than a hunch.

Regardless, there is probably nothing more that you and I can add to this rather interesting topic until we have more (gasp) evidence

Thanks for the chat.

 

[PlutoBoy]

There wasn't a single ad hominem argument. I don't think you are comfortable in gray areas. You aren't any an "expert" and I apparently am based on training and board certification - it's also why I see the weird stuff. I have a much more nuanced opinion and I tend to agree that in general if you're treating from a non expert opinion stand point start at 5 days.

It's a free country and you can move on.

But the bottom line is that the study you are trying to beat us over the head here with doesn't really say what you want it to say. It's being used as s place to hide. There are very good reasons for 14 days of steroids quite often and even the study you are thumping doesn't support "bad outcomes". Some people afraid of steroids and I get that. Probably best used in the hands of people more familiar.

Appeal to authority and ad hominem attacks. Come back when you have something meaningful to say.

 

[lymphocyte]

But then someone may say that it doesn't and start citing the evidence when it suits their narrative.

We actually cited all of the relevant data. You "cited" conclusions and derivative guidelines. Who's trying to sell a narrative?

 

[jdh71]

Appeal to authority and ad hominem attacks. Come back when you have something meaningful to say.

I said plenty that was meaningful. Your feelings are just hurt now.

You were not attacked. And you are also not an expert.

In medicine if expert opinion was valued or helpful then you'd never consult anyone. But I bet you do. All the time. You like experts and their opinions fine until apparently you don't.

 

[Psai]

It's not an appeal to authority fallacy when the person in question is actually an authority in the subject. It's very frustrating when people try to use that argument as if it leads to equality between differing opinions.

If 5 days is good enough, why not 4? Or 3, 2, or even 1? Any evidence against that?

I am a big proponent of clinical judgment and would take it over the mindless implementation of "evidence based medicine" any day. Of course it depends on who the clinician is.