---is a term coined by the authors of a report in the Archives of Internal Medicine of two cases of hyperammonemia with encephalopathy after re-feeding with protein supplements (such as Mighty Shakes) in patients without liver disease. The report is confounded by the fact that one patient was on divalproex sodium, which also has a known association with hyperammonemic encephalopathy in patients without liver disease. That patient, however, had been on the drug long term with good tolerance, and after withdrawal of protein supplement had resolution of encephalopathy despite resumption of the drug.
The authors cite several mechanisms. Cachexia is associated with down regulation of urea cycle enzymes. Muscle is a site of ammonia removal, and decreased muscle mass may play a role. Finally, heterozygous defects in urea cycle enzymes which may be asymptomatic during health and normal nutrition, could play a role.
This is a report of only two cases although the authors believe many cases are unrecognized. It could be considered a form of refeeding syndrome.
HT to Clinical Cases and Images.
Monday, February 28, 2011
More evidence that preoperative statin therapy is beneficial
In patients undergoing infrarenal aortic surgery:
Methods: In this observational study involving 1,674 patients undergoing aortic reconstruction, we prospectively assessed chronic statin therapy compared with no statin therapy, with regard to serious outcomes, by propensity score and multivariable methods...
...statins were associated with an almost threefold reduction in the risk of death in patients undergoing major vascular surgery (odds ratio: 0.40; 95% CI: 0.28–0.59) and an almost twofold reduction in the risk of postoperative myocardial infarction (odds ratio: 0.52; 95% CI: 0.38–0.71). Likewise, the use of chronic statin therapy was associated with a reduced risk of postoperative stroke and renal failure.
Friday, February 25, 2011
Fake-notes-real-docs: was it civil disobedience
---as some have suggested? NO, says Dr. Rich:
Read and listen to the entire post.
These young doctors had no thought of risking their personal freedom, or anything else they hold dear, for a higher cause. They went forth to show their solidarity with The Cause, with every assurance that their actions were entirely consistent with the New Ethics of their profession. That for many Progressives they have become heroes confirms this conviction.
But the moment it occurred to them that not everybody agreed with what they were doing, or understood why they were doing it, or expressed that perhaps there should be repercussions, they had second thoughts. And they did not remain at their stations, bravely flaunting the law, Gandhi-like, until the authorities showed up to drag them away, but rather, once they understood that they might get into trouble, they hightailed it the hell out of there.
Read and listen to the entire post.
Use of proton pump inhibitors with thienopyridines
---especially clopidogrel (Plavix).
I first blogged about the clopidogrel-PPI interaction here and updated the topic here. At that time there was considerable controversy although it was believed that some PPIs interacted less than others and that pantoprazole was probably safe. Recently an ACCF/ACG/AHA consensus statement has been published along with an evidence synthesis and recommendations. If you're expecting a definitive answer you won't find it there. Unfortunately the evidence doesn't come through in the way we'd like.
In outcome based studies you'd think pantoprazole would have proven safer. Not necessarily so. You'd expect prasugrel (Effient) to perform better than clopidogrel. Not necessarily so. The degree of clinical risk from the interactions among all these drugs is far from clear. The authors make eleven summary recommendations based on precautionary principles which include a reminder that among all the PPIs omeprazole is associated with the strongest interaction but again the clinical significance is not clear.
I first blogged about the clopidogrel-PPI interaction here and updated the topic here. At that time there was considerable controversy although it was believed that some PPIs interacted less than others and that pantoprazole was probably safe. Recently an ACCF/ACG/AHA consensus statement has been published along with an evidence synthesis and recommendations. If you're expecting a definitive answer you won't find it there. Unfortunately the evidence doesn't come through in the way we'd like.
In outcome based studies you'd think pantoprazole would have proven safer. Not necessarily so. You'd expect prasugrel (Effient) to perform better than clopidogrel. Not necessarily so. The degree of clinical risk from the interactions among all these drugs is far from clear. The authors make eleven summary recommendations based on precautionary principles which include a reminder that among all the PPIs omeprazole is associated with the strongest interaction but again the clinical significance is not clear.
Electrocardiographic differentiation of narrow complex tachycardias
Sure it's SVT. But is it AVRT, AVNRT, FAT or something else? Here's a nice update. Free full text.
Related content here.
Cost effective, low tech bedside electrophysiology.
Related content here.
Cost effective, low tech bedside electrophysiology.
Vancomycin MIC and outcomes in MRSA pneumonia
From a recent article in Chest:
Methods: Adult patients in ICUs with a diagnosis of MRSA HAP, VAP, or HCAP were entered in the study....
We've seen several papers to this effect before, which I blogged here.
Methods: Adult patients in ICUs with a diagnosis of MRSA HAP, VAP, or HCAP were entered in the study....
Results: The study sample consisted of 158 patients. All-cause mortality at day 28 was 32.3%. The majority of MRSA isolates had a vancomycin MIC greater than or equal to 1.5 mg/mL (115/158, 72.8%). Propensity score analysis demonstrated an increase in 28-day mortality as vancomycin MIC increased from 0.75 to 3 mg/mL (P less than or equal to .001)....
Conclusions: Mortality in patients with MRSA HAP, VAP, and HCAP increases as a function of the vancomycin MIC, even for strains with MIC values within the susceptible range. Evaluation of vancomycin MICs should be contemplated at the institutional level and for individual cases of MRSA pneumonia. The use of vancomycin therapy in patients with MRSA pneumonia caused by isolates with MICs between 1 and 2 mg/mL should be undertaken with caution, and alternative therapies should be considered.
We've seen several papers to this effect before, which I blogged here.
Duration of anticoagulation after VTE
Here is a synthesis of evidence and expert opinion.
Key points and observations:
Evidence is gradually driving a shift in thinking towards longer duration of treatment.
Though the precise duration of treatment for various situations may be uncertain, management and follow up are long term.
Although the risk of recurrence after spontaneous VTE is greater, the distinction between spontaneous and provoked VTE should not be absolute in making treatment decisions.
“Hypercoagulability work ups” are controversial and should be considered on an individual basis.
There is an emerging conflict between population based and individualized approaches. The former, which represents the current consensus (provoked=limited treatment, spontaneous=long term) works well in clinically obvious situations but is simplistic. The latter approach may be better in gray areas. The authors suggest a hybrid approach and provide an algorithm.
Key points and observations:
Evidence is gradually driving a shift in thinking towards longer duration of treatment.
Though the precise duration of treatment for various situations may be uncertain, management and follow up are long term.
Although the risk of recurrence after spontaneous VTE is greater, the distinction between spontaneous and provoked VTE should not be absolute in making treatment decisions.
“Hypercoagulability work ups” are controversial and should be considered on an individual basis.
There is an emerging conflict between population based and individualized approaches. The former, which represents the current consensus (provoked=limited treatment, spontaneous=long term) works well in clinically obvious situations but is simplistic. The latter approach may be better in gray areas. The authors suggest a hybrid approach and provide an algorithm.
Thursday, February 24, 2011
Would you tolerate those occasional computer glitches in a commercial aircraft?
It's a reasonable question to ask as we go full speed ahead with EMR/CPOE, given all the patient safety comparisons with the airline industry. Scot Silverstein talks about it, along with a nice Windows 7 horror story (which is why I'm glad I have Linux at home).
In just over two and a half years we'll all be required to use ICD-10
---as required by CMS. Great. Job security for the coders and clin-doc specialists, and Medicare terminology will only be 21 years out of date (ICD-10 was finalized in 1992).
Docs' attitudes about EMRs
A casual look at this recently reported survey suggests that doctors' attitudes about EMRs are, on the whole, positive. When looked at in light of past surveys, however, that optimism is decreasing as docs become more skeptical according the the WSJ Health Blog.
Eleanor Roosevelt's miliary tuberculosis---the most fabled diagnostic error in the history of medicine, or not?
For over 20 years following the death of Eleanor Roosevelt various stories of her final illness circulated around. The gist was that she had miliary Tb which for months was misdiagnosed as an idiopathic disease (aplastic anemia by most accounts) and erroneously treated with prednisone. Now that her medical record has been unsealed for over 20 years you might think we'd have pat answers about what really happened, but we don't.
I recently blogged it here and linked to a story published in Medscape. That article by Albert Lowenfels, MD, based on his review of the medical record, was pretty straightforward and seemed to confirm some of the accounts we'd heard: that Roosevelt's original hematologic disorder was actually tuberculosis involving the bone marrow. Did that constitute a medical error? Maybe not. Although in retrospect she was misdiagnosed and inappropriately treated for months, misdiagnosis does not equal error.
I have since found another version of Roosevelt's diagnosis and treatment and now things get a little muddy. That account, written by Dr. Barron Lerner, implies that the original diagnosis of aplastic anemia was correct. Later, some weeks before it grew out of her final bone marrow aspirate, Tb was considered and two antituberculous drugs (INH and streptomycin, the only ones they had then) were started because by then her illness had evolved from pancytopenia with febrile reactions to transfusions to FUO.
To make it even more interesting, both authors indicate Roosevelt had a resistant organism, but differ on the type of resistance, one saying the infection was resistant to streptomycin and the other saying it was resistant to both drugs.
So if this was a diagnostic error it was likely without consequence given the resistant organism. It's not at all clear, though, that the misdiagnosis was due to error unless, as implied in this CCJM article, it was a case of VIP syndrome in which the ordinary principles or care were compromised because Eleanor Roosevelt was a VIP:
But that doesn't make a lot of sense either because a bone marrow aspiration hurts a heck of a lot more than the biopsy.
I recently blogged it here and linked to a story published in Medscape. That article by Albert Lowenfels, MD, based on his review of the medical record, was pretty straightforward and seemed to confirm some of the accounts we'd heard: that Roosevelt's original hematologic disorder was actually tuberculosis involving the bone marrow. Did that constitute a medical error? Maybe not. Although in retrospect she was misdiagnosed and inappropriately treated for months, misdiagnosis does not equal error.
I have since found another version of Roosevelt's diagnosis and treatment and now things get a little muddy. That account, written by Dr. Barron Lerner, implies that the original diagnosis of aplastic anemia was correct. Later, some weeks before it grew out of her final bone marrow aspirate, Tb was considered and two antituberculous drugs (INH and streptomycin, the only ones they had then) were started because by then her illness had evolved from pancytopenia with febrile reactions to transfusions to FUO.
To make it even more interesting, both authors indicate Roosevelt had a resistant organism, but differ on the type of resistance, one saying the infection was resistant to streptomycin and the other saying it was resistant to both drugs.
So if this was a diagnostic error it was likely without consequence given the resistant organism. It's not at all clear, though, that the misdiagnosis was due to error unless, as implied in this CCJM article, it was a case of VIP syndrome in which the ordinary principles or care were compromised because Eleanor Roosevelt was a VIP:
A striking example of the potential effects of VIP syndrome is the death of Eleanor Roosevelt from miliary tuberculosis acutissima: she was misdiagnosed with aplastic anemia on the basis of only the results of a bone marrow aspirate study, and she was treated with steroids. The desire to spare this VIP patient the discomfort of a bone marrow biopsy, on which tuberculous granulomata were more likely to have been seen, caused the true diagnosis to be missed and resulted in the administration of a hazardous medication.11 The hard lesson here is that we must resist the pressure to simplify or change customary medical care to avoid causing a VIP patient discomfort or putting the patient through a complex procedure.
But that doesn't make a lot of sense either because a bone marrow aspiration hurts a heck of a lot more than the biopsy.
Wednesday, February 23, 2011
Fake notes by real docs: it's about our professional culture, not individual docs
I blogged yesterday that the fake notes real docs scandal in Wisconsin was more about a cultural shift in the profession than about the docs handing out notes. A recent Pajamas Media article examines the Wisconsin situation in light of the cultural shift towards a “new professionalism.”
Although I say “new” it's an agenda that's been playing out for several years. It's one that has been advanced by some of our professional organizations. The article cites two documents, one issued by the ACP and the other by the AMA. The ACP paper, titled Medical Professionalism in the New Millennium: A Physician Charter strongly implies but comes just short of saying explicitly that this new professionalism demands doctors advocate in their communities for a progressive agenda. The AMA paper is of the same ilk but deals more with medical education. That paper advocates a de-emphasis on the sciences in favor of community organization, systems thinking and social justice. At first glance the recommendations seem soft because they are vague. But it's the vagueness that makes the slope toward UW Family Medicine style ethics more slippery. (For a nice fisking of the AMA paper read this).
I'd be remiss if I didn't mention the AMSA. Though not directly involved in what's happening in Wisconsin this is just their kind of project, which makes their absence seem conspicuous. AMSA, the largest and best organized medical student group, has been profoundly influential in student education and professional development. AMSA's extensive web site is almost complertely devoted to activism and advocacy. (In fact, the only clinical content to be found is promotional and non-critical material about complementary and alternative medicine).
The influence of this culture is well illustrated by this post and embedded video from Ann Althouse in which one of the street docs said he thought this was an “OK thing to do” in the cause of social activism.
So if it's about a pervasive culture more than individuals what about the doctors handing out the notes? Should they get a slap on the wrist or go to the wood shed? What should the university and the medical society do? I'm glad I'm not in the position of deciding, but I would be more lenient than some, especially toward the poor residents. After all they were just doing what trainees are expected to do, emulating the faculty mentors (and even their program director!) who were out there doing the same thing. Maybe a special accountability rests with the department chair for allowing this mindset to flourish.
I'm not interested in careers being damaged. I do think, though, that this almost ranks with quackademic medicine in the category of things worthy to be held up for ridicule. Maybe the blogosphere will change medical culture, maybe not. If nothing else the Wisconsin event has great entertainment value.
Although I say “new” it's an agenda that's been playing out for several years. It's one that has been advanced by some of our professional organizations. The article cites two documents, one issued by the ACP and the other by the AMA. The ACP paper, titled Medical Professionalism in the New Millennium: A Physician Charter strongly implies but comes just short of saying explicitly that this new professionalism demands doctors advocate in their communities for a progressive agenda. The AMA paper is of the same ilk but deals more with medical education. That paper advocates a de-emphasis on the sciences in favor of community organization, systems thinking and social justice. At first glance the recommendations seem soft because they are vague. But it's the vagueness that makes the slope toward UW Family Medicine style ethics more slippery. (For a nice fisking of the AMA paper read this).
I'd be remiss if I didn't mention the AMSA. Though not directly involved in what's happening in Wisconsin this is just their kind of project, which makes their absence seem conspicuous. AMSA, the largest and best organized medical student group, has been profoundly influential in student education and professional development. AMSA's extensive web site is almost complertely devoted to activism and advocacy. (In fact, the only clinical content to be found is promotional and non-critical material about complementary and alternative medicine).
The influence of this culture is well illustrated by this post and embedded video from Ann Althouse in which one of the street docs said he thought this was an “OK thing to do” in the cause of social activism.
So if it's about a pervasive culture more than individuals what about the doctors handing out the notes? Should they get a slap on the wrist or go to the wood shed? What should the university and the medical society do? I'm glad I'm not in the position of deciding, but I would be more lenient than some, especially toward the poor residents. After all they were just doing what trainees are expected to do, emulating the faculty mentors (and even their program director!) who were out there doing the same thing. Maybe a special accountability rests with the department chair for allowing this mindset to flourish.
I'm not interested in careers being damaged. I do think, though, that this almost ranks with quackademic medicine in the category of things worthy to be held up for ridicule. Maybe the blogosphere will change medical culture, maybe not. If nothing else the Wisconsin event has great entertainment value.
Donald Berwick's incoherence
Although few people, including Berwick's detractors, seem to have noticed, I have blogged for some time about the fact that Dr. Berwick, the recess-appointed head of CMS, talks out of both sides of his mouth (see posts here, here and here). It makes it very difficult to know where he stands. (Central planners take note: when your head of CMS goes on record be prepared to toss it down the memory hole because the tune is likely to change in six months).
Well, the incoherence apparently surfaced again when Berwick testified on February 10 before the House Ways and Means Committee. According to this piece by David Catron when Berwick was questioned about his love affair with the NHS, his opposition to free market principles and his support of rationing he weaseled out.
Dr. Berwick, you're a fascinating guy. We'd love to know where you stand. Why not take a couple of months off, do some mindful meditating, decide what you really think about health care policy, then come on back.
Well, the incoherence apparently surfaced again when Berwick testified on February 10 before the House Ways and Means Committee. According to this piece by David Catron when Berwick was questioned about his love affair with the NHS, his opposition to free market principles and his support of rationing he weaseled out.
Dr. Berwick, you're a fascinating guy. We'd love to know where you stand. Why not take a couple of months off, do some mindful meditating, decide what you really think about health care policy, then come on back.
Tuesday, February 22, 2011
Introducing the University of Wisconsin department of Family Medicine, division of social activism
When Health Care BS tried to post this the other day it looked as though someone had cleaned out the department, as most of the links to the bios and pictures went to empty place holders. (I know they were up and live when I looked early Sunday, so someone has taken them down). Fortunately Left Coast Rebel captured the images and posted them directly, along with contact information and links to videos showing the exceptional clinical skills of the individual docs in action.
And you thought medicine was about the doctor-patient relationship? “How 20th century!”
Please read this post from Health Care BS on the real docs-fake notes story. Here's the message: We're dealing with something more significant than individual docs behaving badly. Yes, there's that, but if you think that's all it is you're missing the main point. Go to the web sites of state medical boards and you'll find notices about dozens of doctors every month committing far worse breaches and they're not considered particularly newsworthy.
No, what's going on here is something more pervasive. It's about an emerging new definition of professionalism which, as discussed in the post, is being advanced by our professional organizations (well, some of the more prominent ones, anyway). Pause here for a disclaimer. I'm not implying that the official boosters of this new professionalism advocate fraud. I am suggesting that this new emphasis on social activism and community concern over individual patient care has consequences, and we are seeing those consequences in action.
No, what's going on here is something more pervasive. It's about an emerging new definition of professionalism which, as discussed in the post, is being advanced by our professional organizations (well, some of the more prominent ones, anyway). Pause here for a disclaimer. I'm not implying that the official boosters of this new professionalism advocate fraud. I am suggesting that this new emphasis on social activism and community concern over individual patient care has consequences, and we are seeing those consequences in action.
Ethicist “stunned, absolutely stunned” about the behavior of Wisconsin street docs
Dr. Arthur Derse, an ethicist at the Medical College of Wisconsin, is thus quoted in yesterday's Atlantic article. From that piece we learn that the UW is investigating, the Wisconsin Medical Society is aware, the state medical board is aware, and the author of the Atlantic piece, Ford Vox, has requested interviews with the involved FP faculty docs.
Vox opines:
Well, not now.
DB weighs in here.
Vox opines:
It's sad, but what puzzles me most is how in the world three of the four physicians I can identify from these videos and other media reports are faculty members of UW's Family Medicine department, and one is a senior resident in that same department. It's a good training program, committed to providing sorely-needed primary care doctors to the state of Wisconsin. It teaches professionalism, and its faculty are supposed to model integrity.
Well, not now.
DB weighs in here.
The definition of an internist
I'm always on the lookout for a good definition of Internal Medicine. Here's one from the C. Thorpe Ray Internal Medicine Society at Tulane. Not perfect but one of the better definitions I've seen, and I particularly like this (my emphasis):
The internist is the specialist who is often called in the hospital and/or clinic to aid in diagnosing complex adult patient presentations involving multiple organ systems.
Paul Levy's resignation
I know I'm late with this. Levy resigned as CEO of Beth Israel Deaconess Medical Center on January 7. I became aware the other day when I surfed over to his blog now named Not Running a Hospital. After a brief post acknowledging the resignation on January 7 he continued the blog, under its new name, seamlessly.
Here's one of many media stories about the resignation, quoting Levy's very carefully crafted apology:
Here's one of many media stories about the resignation, quoting Levy's very carefully crafted apology:
"Over the last nine years, I have certainly made mistakes of degree, emphasis, and judgment,'' Levy said in his e-mail. "I have apologized to you directly for some of those, but I do so again, in the hope that such errors will not overshadow the many accomplishments and contributions of our hospital to the community and the health care industry. On the personal level, if I have slighted any one of you in any way or given you any cause for concern about my warm regard and respect for you, I doubly apologize.''
Monday, February 21, 2011
University of Wisconsin announces investigation of its doctors accused of handing out fake excuses to serve a political agenda
Earlier today they released this memo. A couple of observations. The statement opens with:
It was clearly Internet, especially the bloggers, that resulted in the swiftness of this action. A little further on it says:
Maybe so, but don't forget these folks were faculty members and among them was the director of the FP residency program.
Via Gateway Pundit.
There are reports on both social media and news websites that a number of UW Health physicians were signing "medical excuse" notes for protesters at the Capitol on Feb. 19.
It was clearly Internet, especially the bloggers, that resulted in the swiftness of this action. A little further on it says:
These UW Health physicians were acting on their own and without the knowledge or approval of UW Health.
Maybe so, but don't forget these folks were faculty members and among them was the director of the FP residency program.
Via Gateway Pundit.
Scrupulous EBM, superb clinical skills and exemplary ethics---medicine at its finest on the street in Wisconsin
The doc mentioned here was apparently not one of the faculty members at UW. He practices Family Medicine in nearby Oregon Wisconsin.
Via Gateway Pundit.
Fake notes by fake docs or fake notes by real docs?
PJ Tatler, initially cautious as I was, now seems to believe the latter as the story progresses, and is naming names.
Hard as it is to believe the right wing could pull off such an elaborate hoax it's also hard to believe faculty mentors of a residency program would do something like this.
PJ Tatler has contacted the chair of Family Medicine and awaits a response. I'll be watching for that.
Health Care Renewal weighs in here with an interesting take: It's the face of post modern medicine.
Hard as it is to believe the right wing could pull off such an elaborate hoax it's also hard to believe faculty mentors of a residency program would do something like this.
PJ Tatler has contacted the chair of Family Medicine and awaits a response. I'll be watching for that.
Health Care Renewal weighs in here with an interesting take: It's the face of post modern medicine.
Is the fake doctor note story fake?
I have to admit, although the case is growing that these were real docs on faculty at the University of Wisconsin, I'm still finding it hard to believe. Not that there aren't bad apple docs out there that would help patients lie, but that the faculty of a residency program would do such a thing. Well, according to a couple of leftist blogs the story is bogus. If so why aren't the accused faculty in the University of Wisconsin family practice program denying it publicly? I know I would be.
Either way the white coats handing out excuses in those videos bear striking resemblance to some of the faculty pictures on the UW web site.
Either way the white coats handing out excuses in those videos bear striking resemblance to some of the faculty pictures on the UW web site.
Fluoroquinolone usage and tuberculosis
Fluoroquinolones have partial activity against tubercle bacilli. The clinical impact among patients treated for pneumonia has been controversial. Here are some concerning findings from a new meta-analysis:
Results
Nine eligible studies (four for delays and five for resistance issues) were included in the meta-analysis from the 770 articles originally identified in the database search. The mean duration of delayed diagnosis and treatment of pulmonary TB in the fluoroquinolone prescription group was 19.03 days, significantly longer than that in the non-fluoroquinolone group (95% confidence interval (CI) 10.87 to 27.18, p less than 0.001). The pooled odds ratio of developing a fluoroquinolone-resistant M. tuberculosis strain was 2.70 (95% CI 1.30 to 5.60, p=0.008). No significant heterogeneity was found among studies in the meta-analysis.
Conclusions
Empirical fluoroquinolone prescriptions for pneumonia are associated with longer delays in diagnosis and treatment of pulmonary TB and a higher risk of developing fluoroquinolone-resistant M. tuberculosis.
Sunday, February 20, 2011
Happy hospitalist weighs in on the fake doctor note scandal and calls out UW Family Practice residency program director
Local media coverage of Wisconsin docs demonstrating the new professionalism by writing fake excuses
From NBC15:
Well, it looks like the media reports are taking it for granted that these are real docs, as hard as that is to believe. At least some of these docs are on faculty. The University, while disavowing the whole thing, says they'll look into it.
The doctors' actions are not without consequences. According to the same report the absence of large numbers of teachers from work is forcing schools to close. The teachers are getting notes from the street docs so they'll get paid. Community medicine at its finest!
The report also illustrates the brilliant clinical reasoning at play:
HT to Pundit Press.
Doctors from numerous hospitals set up a station near the Capitol on Saturday to provide notes to explain public employees' absences from work. One of those doctors was Lou Sanner, who practices family medicine at the University of Wisconsin School of Medicine and Public Health.
Well, it looks like the media reports are taking it for granted that these are real docs, as hard as that is to believe. At least some of these docs are on faculty. The University, while disavowing the whole thing, says they'll look into it.
The doctors' actions are not without consequences. According to the same report the absence of large numbers of teachers from work is forcing schools to close. The teachers are getting notes from the street docs so they'll get paid. Community medicine at its finest!
The report also illustrates the brilliant clinical reasoning at play:
"We see a lot of sore throats from speaking out, sore feet from walking, a lot of people kind of chilly, under stress we say the best thing you can do is be with a large support group," said one physician.
HT to Pundit Press.
So it's real docs handing out fake excuses
---at least according to USA Today:
Sounds like this guy's got it all figured out. Sanner's on the faculty of Family Practice at the University of Wisconsin. If it's the real Dr. Sanner (and I'm still finding it hard believe real docs would do this) I bet he could teach those residents how to crank out RVUs at lightning speed.
HT Pundit Press.
Doctors from numerous hospitals set up a station near the Capitol to provide notes to explain public employees' absences from work. Family physician Lou Sanner, 59, of Madison, said he had given out hundreds of notes. Many of the people he spoke with seemed to be suffering from stress, he said.
"What employers have a right to know is if the patient was assessed by a duly licensed physician about time off of work," Sanner said. "Employers don't have a right to know the nature of that conversation or the nature of that illness. So it's as valid as every other work note that I've written for the last 30 years."
Sounds like this guy's got it all figured out. Sanner's on the faculty of Family Practice at the University of Wisconsin. If it's the real Dr. Sanner (and I'm still finding it hard believe real docs would do this) I bet he could teach those residents how to crank out RVUs at lightning speed.
HT Pundit Press.
Sick of the Wisconsin governor---what's the ICD-9 code for that?
Via Pundit Press:
Being sick of the Wisconsin Governor is not billable code as far as Medicare is concerned and daring an interviewer to get in the middle of a private consultation between a patient and caregiver in the middle of thousands of people is not what is meant by bedside manner. What a joke. All this professionalism is making me sick!
Instapundit on the fake doctor notes in Wisconsin
Posted here along with lots of links:
Exactly.
If the doctor involved is actually signing these, he should be brought before the medical licensing board. I would imagine that criminal prosecution is possible, too. And if his name is being forged, then somebody else is a criminal. Either way, if teachers turn in excuses signed by Dr. Shropshire, further inquiry is merited . . .
Exactly.
Another Wisconsin “patient” gets a fake doctor note
The “patient” wasn't a real protester, he was a plant. As for the guy providing the note, hard as it is to believe, could he be a real doc? Why else would he provide contact info for his clinic and tell the “patient” his employer is welcome to call for verification? We'll probably find out soon enough. In the comment thread at the YouTube site the fake patient claims to have the doc's credentials.
Is this the new professionalism? Well, it's about social justice and community health!
Via Gateway Pundit.
Is this the new professionalism? Well, it's about social justice and community health!
Via Gateway Pundit.
Doctors show their professionalism in Wisconsin protests---NOT!
Apparently they're handing out “sick notes” so the protesters can skip work. According to one these folks truly are sick---of their governor. Another, confronted by a reporter, gets morally superior and invokes HIPAA!
At the time this piece was posted it was not clear these were real docs. Let's hope they weren't.
HT Gateway Pundit.
Friday, February 18, 2011
Long term mortality after PE
From a new study:
The 3-month, 6-month, 1-year, 3-year, and 5-year cumulative mortality rates were 8.3%, 11.1%, 16.3%, 26.7%, and 31.6% respectively. Annual mortality did not improve over the 7-year period. The postdischarge mortality of 8.5%/patient-year was 2.5-fold that of an age- and sex-matched general population...
Conclusions— In a contemporary adult population, PE is associated with a substantially increased long-term mortality, of which nearly half is cardiovascular. Our study highlights the urgent need to develop long-term surveillance strategies in this population.
The electrocardiogram and the severity of COPD
From the Annals of Noninvasive Electrocardiography:
Methods: ECGs were interpreted blindly in 63 patients with severe COPD (group 1) versus 83 patients with mild or moderate COPD (group 2).
Conclusions: RAE, RVH, RBBB, marked clockwise rotation of heart, a QS pattern in leads III and aVF, LAD, PACs, and SVTs were significantly more prevalent in patients with severe COPD than in patients with mild or moderate COPD.
Thrombectomy devices for ischemic stroke---what's the evidence?
Although two FDA approved devices are promising the level of evidence is low according to this review. Related editorial here.
Thursday, February 17, 2011
Systemic lupus erythematosus and accelerated atherosclerosis
New topic review:
This review summarizes the evidence that autoantibodies in SLE might contribute to the pathogenesis of atherosclerosis by causing injury to the endothelium and altering the metabolism of lipoproteins involved in atherogenesis.
Hospitals that spent more had lower mortality
---for six common medical conditions in this study:
Results: For each of 6 diagnoses at admission—acute myocardial infarction, congestive heart failure, acute stroke, gastrointestinal hemorrhage, hip fracture, and pneumonia—patient admission to higher-spending hospitals was associated with lower risk-adjusted inpatient mortality. During 1999 to 2003, for example, patients admitted with acute myocardial infarction to California hospitals in the highest quintile of hospital spending had lower inpatient mortality than did those admitted to hospitals in the lowest quintile (odds ratio, 0.862 [95% CI, 0.742 to 0.983]). Predicted inpatient deaths would increase by 1831 if all patients admitted with acute myocardial infarction were cared for in hospitals in the lowest quintile of spending rather than the highest. The association between hospital spending and inpatient mortality did not vary by region or hospital size.
Electrocardiography and echocardiography in the diagnosis of cardiac amyloidosis
Electrocardiography and echocardiography are emerging as powerful noninvasive diagnostic techniques in the diagnosis of cardiac amyloidosis. A new paper in the Annals of Noninvasive Electrocardiography reports:
By primary CA I believe the authors, although this is not explicit, mean AL amyloidosis with cardiac involvement as opposed to either senile or hereditary transthyretin related amyloidosis.
Related post here.
Results: The voltage of SV1+ RV6 less than 1.2 mV has a sensitivity of 91% and specificity of 89% for the identification of primary CA, yields the positive and negative predictive values of 91% and 89%, respectively. Among ECHO parameters, there were no significant differences between the 2 groups, except for left ventricular ejection fraction (47 ± 12% in primary CA vs 67 ± 11% in the control, P less than 0.001). However, the combined indexes of ECG and ECHO parameters, including the ratio of RI/LVPW as well as RV5/LVPW and RV6/LVPW, were significantly lower in the patients with primary CA than the control. The ratio of RI/LVPW less than 0.4 has the sensitivity of 91% and specificity of 100%, yields the positive and negative predictive values of 100% and 91%, respectively. The ratios of RV5(6)/LVPW less than 0.7 have the sensitivity of 91% and specificity of 89%, yield the positive and negative predictive values of 91% and 89%, respectively.
Conclusion: Patients with clinically suspected primary CA, combined indexes of ECGs and ECHOs could be used as the noninvasive diagnostic tools.
By primary CA I believe the authors, although this is not explicit, mean AL amyloidosis with cardiac involvement as opposed to either senile or hereditary transthyretin related amyloidosis.
Related post here.
Bedside clinical skills
Here is another essay lamenting the decline in basic clinical skills. More and more we hear about how the marvelous advances in technology can supplant old fashioned physical examination. Sometimes it's true. Thoracentesis, for example, is better done by ultrasound guidance than by percussion. But the fact remains that without the underpinnings of basic clinical skills high technology is at times rendered useless, even dangerous. Nine clinical anecdotes in the article illustrate the case well.
Wednesday, February 16, 2011
The Cooley and DeBakey feud
Here's a history of the feud between the two men, and it's final resolution, from Dr. Cooley's perspective.
Idolizing the democratization of knowledge
---leads to more and more tabloid medicine, and we're not necessarily better off for it.
The EMR facilitates higher coding. What does it really mean?
Some concerning questions asked in this post from Health Care Renewal.
AHRQ to become Obamacare's propaganda machine???
I don't know if all this is true. If it is it's very concerning:
Yikes. Maybe I'll get a chance to parse this in a few days when I get some down time from work.
House Republicans plan to cut $360 million in Obamacare funding in this year's budget. That's a good start, enough to slow implementation of the health care law but not stop it. But not good enough to stop the administration from spending $100 million to run an ad campaign and hire a sales team to push Obamacare to thousands of doctors. That's right. Obamacare will use a sales force (with cars and expense accounts) to convince doctors that government health guidelines are the way to go.
The home of this marketing machine is Agency for Healthcare Research and Quality (AHRQ). Its budget of nearly $1 billion a year (starting in 2014 it will be more) is scheduled to be cut by only $25 million this fiscal year. Perhaps Republicans don't know that AHRQ is the operating system for Obamacare as well as its campaign manager.
Yikes. Maybe I'll get a chance to parse this in a few days when I get some down time from work.
Tuesday, February 15, 2011
Stan the Man receives the Medal of Freedom
From the St. Louis Post Dispatch:
WASHINGTON - Stan Musial joined leading politicians, cultural heroes and human rights leaders today in receiving the Presidential Medal of Freedom, the nation's highest civilian honor.
I grew up watching Stan the Man. I started going to Cardinal games at the age of eight. My father was acquainted with Leo Ward, traveling secretary for the Cards, and we had the opportunity to watch some games from his box seats on the first base line at Busch Stadium I, AKA Sportsman's Park, where we saw Stan “up close and personal” when he played first base.
Stan was loyal to the St. Louis fans and never wanted to play for any other team. He once offered to take a cut in pay during a slump. One time my dad was dining at Stan's restaurant. There was Stan sweeping the floor.
It's great to see him honored in this way. He's been one of the game's under rated players.
Palliative care and advance care planning in COPD
When COPD becomes advanced it carries a worse prognosis than many forms of cancer. Here are a few key points and observations of my own concerning a recent review article on palliative care and advance care planning in COPD.
If you define palliative care as excellence in comprehensive care and patient education for complex chronic illness, then all treatment modalities for COPD are palliative. If on the other hand palliative care is defined as treatment modalities that do not aim to prolong life then chronic oxygen therapy and antibiotics for acute exacerbation would be excluded because of evidence that they prolong life, as well as possibly non-invasive and invasive mechanical ventilation.
Because education is an important part of palliative care, it also encompasses advance care planning. Unfortunately advance care planning and the education that it requires are not keeping up with the growing burden of COPD. This may be driven by low awareness and poor efforts at early diagnosis, as illustrated by a recent paper showing that hospitalization for exacerbation is often the first occasion for diagnosing the disease, which by then is often late stage. (You can't do advance care planning if you haven't even made the diagnosis!).
Another reason why patients with COPD receive less palliative care and advance care planning than comparable diagnoses such as lung cancer and heart failure may be an under appreciation of the prognostic implications and symptom burden of COPD. Here's a sad and frightening statistic cited in the review:
There are many barriers to advance care planning, both patient centered and physician centered. One of these is the lack of time, or perceived lack of time available in the ambulatory clinic, the setting where such discussions are most likely to be effective, as opposed to the hospital. Another barrier is the unique and often deceptive clinical trajectory of COPD. From the review:
Because the clinical trajectory is so unpredictable, palliative care and advance care planning should start early in the disease process. A major barrier to doing that is the mistaken notion that palliative care equates to end of life care. Refinements in the definition of palliative care may help to remedy that problem.
The ambulatory clinic, during periods of disease stability, is the most effective setting for these conversations. Ironically it is the time when such discussions are least likely to occur. In the hospital during an acute exacerbation there may be too many distractions, twists and turns for the patient and the family members to think clearly.
If you define palliative care as excellence in comprehensive care and patient education for complex chronic illness, then all treatment modalities for COPD are palliative. If on the other hand palliative care is defined as treatment modalities that do not aim to prolong life then chronic oxygen therapy and antibiotics for acute exacerbation would be excluded because of evidence that they prolong life, as well as possibly non-invasive and invasive mechanical ventilation.
Because education is an important part of palliative care, it also encompasses advance care planning. Unfortunately advance care planning and the education that it requires are not keeping up with the growing burden of COPD. This may be driven by low awareness and poor efforts at early diagnosis, as illustrated by a recent paper showing that hospitalization for exacerbation is often the first occasion for diagnosing the disease, which by then is often late stage. (You can't do advance care planning if you haven't even made the diagnosis!).
Another reason why patients with COPD receive less palliative care and advance care planning than comparable diagnoses such as lung cancer and heart failure may be an under appreciation of the prognostic implications and symptom burden of COPD. Here's a sad and frightening statistic cited in the review:
Only 63% of patients dying with COPD despite being housebound with extensive symptoms and recent admissions knew that they were going to die [19].
There are many barriers to advance care planning, both patient centered and physician centered. One of these is the lack of time, or perceived lack of time available in the ambulatory clinic, the setting where such discussions are most likely to be effective, as opposed to the hospital. Another barrier is the unique and often deceptive clinical trajectory of COPD. From the review:
The disease trajectory of COPD represents an additional barrier. Patients experience a gradual decline in physical capacities over many years punctuated by episodic acute exacerbations followed by functional improvements that usually do not reach previous baseline levels (Fig. 1) [10••,28]. This trajectory contrasts with advanced cancers, which usually provide more obvious transitions toward EOL and signals for ACP. The episodic deteriorations and partial recoveries with COPD lull physicians into thinking ACP can wait until a future date and clouds the definition of what constitutes ‘end of life’ because points of transition are so poorly recognizable [13••].
Because the clinical trajectory is so unpredictable, palliative care and advance care planning should start early in the disease process. A major barrier to doing that is the mistaken notion that palliative care equates to end of life care. Refinements in the definition of palliative care may help to remedy that problem.
The ambulatory clinic, during periods of disease stability, is the most effective setting for these conversations. Ironically it is the time when such discussions are least likely to occur. In the hospital during an acute exacerbation there may be too many distractions, twists and turns for the patient and the family members to think clearly.
Statins don't change the small dense LDL phenotype
This is just the latest of many studies with similar findings:
So you've treated your CAD patient “to goal” with statin therapy. If the patient had small dense LDL (AKA LDL pattern B) to begin with, he or she still will if all you did was use a statin. What this and many other studies have shown is that statin therapy alone will not change your patient from pattern B to the much less risky pattern A. Most of the pattern B folks have the metabolic syndrome but a significant number do not. Once you've titrated the statin to goal many patients will carry residual risk, which is why relative risk reduction for events attributable to statin therapy is on the order of 30%, not 100%.
Our study suggests that statin therapy—whether or not recipients have coronary artery disease—does not decrease the proportion of small, dense LDL among total LDL particles, but in fact increases it, while predictably reducing total LDL cholesterol, absolute amounts of small, dense LDL, and absolute amounts of large, buoyant LDL. If and when our observation proves to be reproducible in subsequent large-scale studies, it should provide new insights into small, dense LDL and its actual role in atherogenesis or the progression of atherosclerosis.
So you've treated your CAD patient “to goal” with statin therapy. If the patient had small dense LDL (AKA LDL pattern B) to begin with, he or she still will if all you did was use a statin. What this and many other studies have shown is that statin therapy alone will not change your patient from pattern B to the much less risky pattern A. Most of the pattern B folks have the metabolic syndrome but a significant number do not. Once you've titrated the statin to goal many patients will carry residual risk, which is why relative risk reduction for events attributable to statin therapy is on the order of 30%, not 100%.
Unintentionally funny medical writing
Here is a brief compilation. From the article:
Read the rest.
Twenty-seven years ago, one of us (HLF) helped create a series of “Dizzy Awards”—awards honoring baseball immortal and legendary syntax-mangler Dizzy Dean. The Dizzys are given for excellence in unintentionally comical, bewildering, or downright terrible medical writing.1–5 These awards also recognize poor editing.6–8 The “winners” are excerpts from articles in prominent medical publications.
Last year, we wrote the 9th report in this series.9 Since that time, we have harvested a new crop of winners...
Read the rest.
Monday, February 14, 2011
Surgical risk in patients with liver disease
In evaluating patients with cardiac disease for non-cardiac surgery we've gotten away from “clearing” patients. There just aren't that many contraindications to elective surgery, and when present they're pretty obvious: critical aortic stenosis, recent unstable coronary syndromes, uncontrolled arrhythmias and decompensated heart failure.
In the case of liver disease it gets a little more tricky, because there are several contraindications you might not be used to thinking about. Transactions of the American Clinical and Climatological Association, one of the best kept secrets among medical journals by the way, has recently published an excellent review on the topic. It's available as open access full text, so go read it in the original, but here are some spoilers. There's a list of well known contraindications. Know them. Absent such a specific contraindication, if the patient has stable cirrhosis, do a Child or a MELD.
In the case of liver disease it gets a little more tricky, because there are several contraindications you might not be used to thinking about. Transactions of the American Clinical and Climatological Association, one of the best kept secrets among medical journals by the way, has recently published an excellent review on the topic. It's available as open access full text, so go read it in the original, but here are some spoilers. There's a list of well known contraindications. Know them. Absent such a specific contraindication, if the patient has stable cirrhosis, do a Child or a MELD.
Update on chronic tachycardia-induced cardiomyopathy
Chronic tachycardia-induced cardiomyopathy was one of the first topics I blogged about in 2005. In that post I linked to an important review in the American Journal of Medicine. Since then more experience has accumulated, which is nicely summarized in this new review. Free full text.
Acute exacerbation of interstitial lung disease (AEILD)
Back in the old days this was known as Hamman-Rich syndrome. It can occur de novo or as an exacerbation of previously known stable ILD. It can present as ARDS that's not run-of-the-mill ARDS (see here and here).
Recently a new review was published in Current Opinion in Pulmonary Medicine. Worth having in the full text.
Recently a new review was published in Current Opinion in Pulmonary Medicine. Worth having in the full text.
Invasive pulmonary aspergillosis in critically ill COPD patients
You may be used to thinking of Aspergillus as a neutrophil opportunist. However, it can cause invasive disease in COPD patients whose immune deficits consist of impaired local defenses, corticosteroid use (high cumulative doses) and the use of multiple antibiotics. If you encounter new or progressive infiltrates in a COPD patient recently treated with broad spectrum antibiotics and high cumulative doses of corticosteroids, think of it.
Saturday, February 12, 2011
Digging out from what we hope will be the last blast of winter
It was a record setting event here and folks were ill prepared.
Friday, February 11, 2011
Flecainide 22 years after CAST: safe at last? (For atrial fib, that is)
In 1989 CAST reported increased non-fatal cardiac arrest, arrhythmic mortality, and all cause mortality attributable to the use of flecainide for suppression of ventricular ectopic beats following myocardial infarction. Although that was in the pre-Internet era we had real time cable news coverage available to hype the results. I remember well when the announcement came. It was the middle of a busy afternoon at my clinic and the switchboards lit up like a Christmas tree. We had to pull a couple of employees away from their usual duties to handle the patient calls.
Although the CAST investigators recommended that flecainide be removed from clinical use as a treatment for ventricular arrhythmias post MI they acknowledged that the results did not necessarily apply to other uses of the drug:
But it didn't matter. Flecainide was suddenly cyanide and the trial lawyers got busy. There was no reason, though, to think it wouldn't be safe for other indications.
A little background. Even though the pilot to CAST, CAPS, showed no adverse safety signal, ventricular proarrhythmic effects of flecainide were already known, and it was no secret. This came from EP lab data, back when EP catheter guided antiarrhythmic drug therapy was the order of the day. But these studies suggested that the proarrhythmic effect was confined largely to patients in whom the drug was being used to suppress bad (symptomatic) ventricular arrhythmias, and who had bad structural heart disease. There was no reason to think it was bad for people with healthier hearts taking it to stay out of a fib.
In the ensuing years, accumulated experience suggested that indeed it is safe for this indication in patients with good LV function and no significant CAD. That was the topic of the new paper that prompted this post, but first a digression.
In the aftermath of CAST sotolol became a popular alternative to help keep patients out of a fib. While sotolol was in development, long before it was launched, it held the promise of being a “non-toxic amiodarone.” That promise didn't hold up because sotolol proved to have proarrhythmic effects of its own. But, unlike the case with flecainide, the adverse experience with sotolol did not come in the form of a breaking news type clinical trial for the media to grab hold of. Also unlike flecainide sotolol's proarrhythmia, torsades de pointes, was less predictable. It was not restricted to patients with diseased hearts and occurred in treatment of supraventricular as well as ventricular arrhythmias. In addition to idiosyncratic patient susceptibility, risk factors included dosage, renal function, electrolyte disturbances and interacting drugs. These factors made safe use of the drug pretty tricky. Proper patient selection and safety monitoring were elaborate. So much so that when it came time to consider approval of sotolol, already in use for life threatening ventricular arrhythmias, for the more benign condition of atrial fibrillation, the FDA would only approve a special branded version (Betapace-AF). Betapace-AF came with its own patient information materials and special product labeling for professionals. You can view the black box warning against substituting any other form of sotolol for Betapace-AF here. It was the elaborate and complex nature of the product labeling, which if meticulously followed would minimize proarrhythmia, that justified separate branding.
In real world practice, and this is only a subjective observation, generic sotolol (after all, it's the same medication) is often substituted off label for the branded Betapace-AF, increasing the risk of unsafe use. I suspect this practice is widespread, driven in part by the thinking that Betapace-AF is little more than a pharmaceutical industry gimmick. I've often wondered how many adverse events, including deaths, are attributable to such thinking and how sotolol's safety record in a fib compares with flecainide. Although there's been no single large trial to catch the attention of the news media and trial lawyers I imagine the info's out there somewhere. (Note to self: good question for a future literature search).
That brings me back to flecainide and this paper which reviews its use in a fib and concludes that when used in patients without significant structural heart disease it's quite safe. The paper also provides a nice general review of atrial fibrillation management and general aspects of the pharmacology of flecainide.
Although the CAST investigators recommended that flecainide be removed from clinical use as a treatment for ventricular arrhythmias post MI they acknowledged that the results did not necessarily apply to other uses of the drug:
We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.
But it didn't matter. Flecainide was suddenly cyanide and the trial lawyers got busy. There was no reason, though, to think it wouldn't be safe for other indications.
A little background. Even though the pilot to CAST, CAPS, showed no adverse safety signal, ventricular proarrhythmic effects of flecainide were already known, and it was no secret. This came from EP lab data, back when EP catheter guided antiarrhythmic drug therapy was the order of the day. But these studies suggested that the proarrhythmic effect was confined largely to patients in whom the drug was being used to suppress bad (symptomatic) ventricular arrhythmias, and who had bad structural heart disease. There was no reason to think it was bad for people with healthier hearts taking it to stay out of a fib.
In the ensuing years, accumulated experience suggested that indeed it is safe for this indication in patients with good LV function and no significant CAD. That was the topic of the new paper that prompted this post, but first a digression.
In the aftermath of CAST sotolol became a popular alternative to help keep patients out of a fib. While sotolol was in development, long before it was launched, it held the promise of being a “non-toxic amiodarone.” That promise didn't hold up because sotolol proved to have proarrhythmic effects of its own. But, unlike the case with flecainide, the adverse experience with sotolol did not come in the form of a breaking news type clinical trial for the media to grab hold of. Also unlike flecainide sotolol's proarrhythmia, torsades de pointes, was less predictable. It was not restricted to patients with diseased hearts and occurred in treatment of supraventricular as well as ventricular arrhythmias. In addition to idiosyncratic patient susceptibility, risk factors included dosage, renal function, electrolyte disturbances and interacting drugs. These factors made safe use of the drug pretty tricky. Proper patient selection and safety monitoring were elaborate. So much so that when it came time to consider approval of sotolol, already in use for life threatening ventricular arrhythmias, for the more benign condition of atrial fibrillation, the FDA would only approve a special branded version (Betapace-AF). Betapace-AF came with its own patient information materials and special product labeling for professionals. You can view the black box warning against substituting any other form of sotolol for Betapace-AF here. It was the elaborate and complex nature of the product labeling, which if meticulously followed would minimize proarrhythmia, that justified separate branding.
In real world practice, and this is only a subjective observation, generic sotolol (after all, it's the same medication) is often substituted off label for the branded Betapace-AF, increasing the risk of unsafe use. I suspect this practice is widespread, driven in part by the thinking that Betapace-AF is little more than a pharmaceutical industry gimmick. I've often wondered how many adverse events, including deaths, are attributable to such thinking and how sotolol's safety record in a fib compares with flecainide. Although there's been no single large trial to catch the attention of the news media and trial lawyers I imagine the info's out there somewhere. (Note to self: good question for a future literature search).
That brings me back to flecainide and this paper which reviews its use in a fib and concludes that when used in patients without significant structural heart disease it's quite safe. The paper also provides a nice general review of atrial fibrillation management and general aspects of the pharmacology of flecainide.
Social media as a CME tool
Although the idea is not at all new social media are still not being utilized to their potential. Thomas Sullivan, who blogs at Policy and Medicine, guest posted at Kevin MD on this topic. He wrote:
These are some of the things I try to accomplish through blogging.
Although I agree largely with what Sullivan said this comment, citing an article by Brian S. McGowan, PhD, concerns me:
I know a lot of people will disagree with me here, but, sorry, IMHO you just can't Tweet a conference. You'll miss too many nuances and not do the content justice. (You can Tweet an article so long as you link to the primary source. You can't do that for a conference presentation).
The question of how social media fit into CME overlaps but goes considerably beyond the notion of Web 2. Web 2 traditionally comprised wikis and blogs. But the notion of social media casts a wider net. Now you have to include Twitter, Facebook and Myspace, and that's where the conversation gets more complicated. Should there be a hierarchy, like the EBM pyramid? How high on the pyramid should an outlet be to be considered worthy?
Many barriers remain to be resolved before social media find their proper place in prime time in the world of CME. One of these is an inconsistency of attitudes towards social media by health care organizations. While some organizations, particularly academic medical centers, embrace certain media for educational purposes, others have restrictive policies. After all, no one wants their employees Facebooking on the job.
First, using social media will support CME activities, initiatives, and healthcare professional learning. Such support would include using social media to direct HCPs to accredited CME events, peer reviewed journals, and clinical studies. This would give HCPs a reliable source of information to depend on, which is especially important considering “a Manhattan Research report from April 2010 suggests that up to 50 percent of healthcare providers have used the online, user-compiled encyclopedia Wikipedia in practice.” Accordingly, the CME community should begin using social media to prevent HCPs from relying on less credible and less regulated sources of medical information, especially since the broader medical community is already doing so....
Through the use of social media technologies, CME professionals can disseminate outcomes and assessment data through numerous channels, and discuss stories of the benefits and value of CME.
These are some of the things I try to accomplish through blogging.
Although I agree largely with what Sullivan said this comment, citing an article by Brian S. McGowan, PhD, concerns me:
As evidence to the lack of use of social media in the CME community, McGowan pointed out that of “the more than 1,500 attendees at the 2010 Annual Meeting of the Alliance for Continuing Medical Education, only six people were tweeting via Twitter—and only a couple were contributing more than “come see my booth”-type messages.”
I know a lot of people will disagree with me here, but, sorry, IMHO you just can't Tweet a conference. You'll miss too many nuances and not do the content justice. (You can Tweet an article so long as you link to the primary source. You can't do that for a conference presentation).
The question of how social media fit into CME overlaps but goes considerably beyond the notion of Web 2. Web 2 traditionally comprised wikis and blogs. But the notion of social media casts a wider net. Now you have to include Twitter, Facebook and Myspace, and that's where the conversation gets more complicated. Should there be a hierarchy, like the EBM pyramid? How high on the pyramid should an outlet be to be considered worthy?
Many barriers remain to be resolved before social media find their proper place in prime time in the world of CME. One of these is an inconsistency of attitudes towards social media by health care organizations. While some organizations, particularly academic medical centers, embrace certain media for educational purposes, others have restrictive policies. After all, no one wants their employees Facebooking on the job.
VA health care
They've got a model electronic medical record. They look great on all the “metrics.” They're a central planner's dream. But what's the experience really like on the ground? Here are some of Happy's observations.
Thursday, February 10, 2011
How biased is commercially supported CME?
All CME is biased to an extent. Everyone who's knowledgeable on a subject has a point of view, which will invariably sneak into presentations and writings whether or not there is commercial support. The real question in the raging family fight (as blogger Billy Rubin puts it) over CME funding is whether the bias in industry supported CME is worse than that of non-supported offerings in a meaningful way. It's a debate that has real consequences because those who argue in the affirmative seek policy change which would eventually end CME funding by industry. Though probably in the minority and backed with little more than a collection of anecdotes and popular belief (which, as Thomas Stossel recently pointed out, often takes on the intensity of religious fervor) they seem to be winning in terms of policy change (policy change, mind you, not evidence or logic).
Until recently there was no research quality evidence (yes, there was a lot of soft science on the psychology of influence and performance indicators attributable to drug rep promotion but nothing about outcomes from CME) to guide the discussion. (For convenience here I'll loosely use the terms pharmascold and pharmapologist to describe the proponents and opponents, respectively, of restrictive policy change). Absent such research quality evidence the debate usually followed a pattern. The pharmascolds made their appeal to popular belief (industry money is dirty, so if it supports CME it has to be degrading) and numerous anecdotes. (For a nice collection of anecdotes read Daniel Carlat's blog; he's got a bunch of them). Aside from the fact that collections of anecdotes do not equal data, there are anecdotes to support either side. I could cite plenty of examples of non-supported CME offerings that reflect presenters' biases. The government sponsored NCCAM CME offerings, for example, reflect a pervasive bias about what scientific standard ought to be applied to health claims. Even the highly respected UptoDate, from which I often obtain CME credit, is biased, containing many articles which conclude with authors' recommendations based on what they prefer at their institutions. On the other side the pharmapologists argued about unintended consequences and said “show me the evidence to justify policy change and its negative consequences.”
Which leads me to a post from yesterday by Thomas Sullivan (for the sake of discussion we'll call him a pharmapologist) at Policy and Medicine concerning his point-counterpoint with Dr. Howard Brody who takes the pharmascold position (his main post in question being here.) Much of the discussion was over recent research data, a huge new database which, in the form of three published studies, looked to see if there was a difference in perceived bias between industry and non-industry funded activities. (There wasn't. You can find links to the studies in the Thomas Sullivan post). He provided a detailed point by point summary of the exchange, so I'll just make a couple of observations. I read with interest this paragraph from his post:
In addition, with waning industry support offerings are becoming more expensive. Increasing distance to meeting sites inflates travel expenses. If you get an educational stipend those expenses can eat it up pretty fast. In my own case the last 15 CME hours for 2010 were out of pocket at around $100 an hour. (For that particular meeting, which may be on its last legs, the course directors have had to fork up some of their own money just for its sponsoring institution to break even.)
Do I think I'm entitled to industry support? Not at all. But the fact remains that as support diminishes my options for CME are more and more restricted. Like the health care system that provides my stipend, I'm on a budget. I have competing financial demands. When money's not an object choices increase. When it becomes an object they diminish. I live with that fact with humor, not rancor or self pity. As a matter of fact I really, really get a laugh out of one tired pharmascold argument: that by giving up industry support doctors somehow “take control” of CME. I'm not sure how that's supposed to work, because as industry support slips away I'm less and less in control of my options.
And about those three studies? Dr. Brody dismisses them with a bit of circular reasoning:
The reasoning is circular because its conclusion is assumed in its premise. It goes something like: “commercial CME is excessively biased compared to non-industry CME. These docs didn't report that. Ergo all these docs (well over a million in the studies, by the way) are either too lazy to give appropriate responses or lacked the ability to detect bias.” It's as if the idea of inappropriate bias attributable to commercial support in comparison to non-supported CME is so self evident as to be axiomatic. External evidence be danged.
Dr. Brody then offers up the straw man and shifts the burden of proof with this:
No one's claiming that no bias exists in CME programs. As to the burden of proof, shouldn't that be on the shoulders of those who want major policy change with all its potential unintended consequences?
Until recently there was no research quality evidence (yes, there was a lot of soft science on the psychology of influence and performance indicators attributable to drug rep promotion but nothing about outcomes from CME) to guide the discussion. (For convenience here I'll loosely use the terms pharmascold and pharmapologist to describe the proponents and opponents, respectively, of restrictive policy change). Absent such research quality evidence the debate usually followed a pattern. The pharmascolds made their appeal to popular belief (industry money is dirty, so if it supports CME it has to be degrading) and numerous anecdotes. (For a nice collection of anecdotes read Daniel Carlat's blog; he's got a bunch of them). Aside from the fact that collections of anecdotes do not equal data, there are anecdotes to support either side. I could cite plenty of examples of non-supported CME offerings that reflect presenters' biases. The government sponsored NCCAM CME offerings, for example, reflect a pervasive bias about what scientific standard ought to be applied to health claims. Even the highly respected UptoDate, from which I often obtain CME credit, is biased, containing many articles which conclude with authors' recommendations based on what they prefer at their institutions. On the other side the pharmapologists argued about unintended consequences and said “show me the evidence to justify policy change and its negative consequences.”
Which leads me to a post from yesterday by Thomas Sullivan (for the sake of discussion we'll call him a pharmapologist) at Policy and Medicine concerning his point-counterpoint with Dr. Howard Brody who takes the pharmascold position (his main post in question being here.) Much of the discussion was over recent research data, a huge new database which, in the form of three published studies, looked to see if there was a difference in perceived bias between industry and non-industry funded activities. (There wasn't. You can find links to the studies in the Thomas Sullivan post). He provided a detailed point by point summary of the exchange, so I'll just make a couple of observations. I read with interest this paragraph from his post:
CME providers are concerned about the decreasing support for CME programs because it means fewer programs for health care practitioners, less innovative and collaborative programs, greater inconvenience for doctors in both timing and geography, larger and less interactive programs, and broader programs that do not address the specific needs of target audiences.
In addition, with waning industry support offerings are becoming more expensive. Increasing distance to meeting sites inflates travel expenses. If you get an educational stipend those expenses can eat it up pretty fast. In my own case the last 15 CME hours for 2010 were out of pocket at around $100 an hour. (For that particular meeting, which may be on its last legs, the course directors have had to fork up some of their own money just for its sponsoring institution to break even.)
Do I think I'm entitled to industry support? Not at all. But the fact remains that as support diminishes my options for CME are more and more restricted. Like the health care system that provides my stipend, I'm on a budget. I have competing financial demands. When money's not an object choices increase. When it becomes an object they diminish. I live with that fact with humor, not rancor or self pity. As a matter of fact I really, really get a laugh out of one tired pharmascold argument: that by giving up industry support doctors somehow “take control” of CME. I'm not sure how that's supposed to work, because as industry support slips away I'm less and less in control of my options.
And about those three studies? Dr. Brody dismisses them with a bit of circular reasoning:
What did the studies show? When physicians attend CME programs, they have to check off boxes on an evaluation sheet, stating whether they do or don't think that the presentation they just listened to showed inappropriate or excessive commercial bias. What all three studies showed is that the vast majority of docs, most all the time, check the NO box. To me that suggests that either the docs are lazy about what boxes they check, or else that they may be unable to detect bias when it might actually exist.
The reasoning is circular because its conclusion is assumed in its premise. It goes something like: “commercial CME is excessively biased compared to non-industry CME. These docs didn't report that. Ergo all these docs (well over a million in the studies, by the way) are either too lazy to give appropriate responses or lacked the ability to detect bias.” It's as if the idea of inappropriate bias attributable to commercial support in comparison to non-supported CME is so self evident as to be axiomatic. External evidence be danged.
Dr. Brody then offers up the straw man and shifts the burden of proof with this:
To suggest that a study that consists of these data show positively that no bias exists in CME programs seems a far stretch. (There might in fact be no commercial bias in CME programs, but you'd need far better methods than in these three studies to know that.)
No one's claiming that no bias exists in CME programs. As to the burden of proof, shouldn't that be on the shoulders of those who want major policy change with all its potential unintended consequences?
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