Thursday, April 30, 2009
ER-hospitalist tensions
Having trouble getting along with your ER colleagues? Talk to each other! That and other tips from Today’s Hospitalist.
Wednesday, April 29, 2009
Experts can be good for patients
---and now that’s evidence based. From JAMA:
Via Dr. Wes.
Conclusions In this registry, nonelectrophysiologists implanted 29% of ICDs. Overall, implantations by a nonelectrophysiologist were associated with a higher risk of procedural complications and lower likelihood of receiving a CRT-D device when indicated compared with patients whose ICD was implanted by an electrophysiologist.
Via Dr. Wes.
Tuesday, April 28, 2009
Urine sediment exam in acute renal failure
I love it when low technology offers powerful diagnostic tools. Thomas E. Brittingham, M.D., one of Vanderbilt’s great teachers, would tell third year medical students:
Recently the performance of urine microscopy in the diagnosis of ATN was systematically evaluated:
Examination of the peripheral blood film and of the urinary sediment are powerful diagnostic tools, much as is physical examination of the heart. The power of these tests is unappreciated by many physicians….
Recently the performance of urine microscopy in the diagnosis of ATN was systematically evaluated:
Results: The urinary sediment scoring system was highly predictive of the final diagnosis of ATN. In patients with a high pretest probability of ATN (initial diagnosis of ATN), any casts or RTEC (score 2) resulted in very high positive predictive value and low negative predictive value for a final diagnosis of ATN. In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary
sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.
Conclusions: Urine sediment examination is a valuable diagnostic tool for confirming the diagnosis of ATN. A score of 2 on an ATN urinary sediment scoring system is an extremely strong predictor of ATN.
Pneumococcal vaccines
Read this. Then imagine how your world as a hospitalist would change if we had an adult pneumococcal vaccine that actually worked.
Monday, April 27, 2009
A double evidentiary standard
If it’s a drug or a surgical procedure insist on a randomized clinical trial. If it’s a system of care (e.g. rapid response teams) go with your passions and instincts, says Donald Berwick in this keynote address from somewhere.
I respectfully disagree.
I respectfully disagree.
DB on comparative effectiveness research
DB was recently blogging from the ACP national meeting. His post on the keynote, about comparative effectiveness research (CER), opens with:
I am one of the med bloggers who has been less than enthusiastic about the new CER agenda and I am a political conservative. While I don’t know if I am one of the bloggers referenced by DB as being opposed to CER I think this would be a good time for me to clarify my views and pose some questions.
First, I don’t know of any med bloggers or politicians who are truly opposed to CER. If they were they would have raised objections to the CER that has been going on for decades long before it became a political agenda.
In over 30 years of clinical practice I have taken advantage of a great deal of CER to help me make decisions. Ever aware that science is a work in progress and that we will always need more and more research at many levels it never occurred to me that we needed a special agenda. I have never been opposed to CER, but I am suddenly very skeptical now that it has become politicized.
So, I don’t think this discussion is mainly about CER. I think it’s about an agenda for more government largesse based in part on distrust of the pharmaceutical industry. I had to laugh when I read this paragraph from Harold Sox’s keynote at the ACP meeting (italics mine):
Again I'll remind readers that we've already spent about a billion on research sponsored by a subsidiary of the NIH which by any reasonable account has been a tremendous waste.
DB concludes with:
No one that I know of is objecting to more unbiased data. But CER is not inherently unbiased. Moreover, it is inherently susceptible to design flaws for reasons I pointed out here, with several examples. Bias has more to do with who’s sponsoring the research than the type of research. There’s no reason to think that the government would introduce less bias. In fact, the government policy makers who are pushing CER are explicitly very biased. If you don’t believe me just read the Congressional Budget Office paper which was pushing for CER, which I cited here.
Many med bloggers do not appear to support CER. Many "conservatives" appear to oppose CER. I truly believe that opposition is not based on an understanding of CER’s importance.
I am one of the med bloggers who has been less than enthusiastic about the new CER agenda and I am a political conservative. While I don’t know if I am one of the bloggers referenced by DB as being opposed to CER I think this would be a good time for me to clarify my views and pose some questions.
First, I don’t know of any med bloggers or politicians who are truly opposed to CER. If they were they would have raised objections to the CER that has been going on for decades long before it became a political agenda.
In over 30 years of clinical practice I have taken advantage of a great deal of CER to help me make decisions. Ever aware that science is a work in progress and that we will always need more and more research at many levels it never occurred to me that we needed a special agenda. I have never been opposed to CER, but I am suddenly very skeptical now that it has become politicized.
So, I don’t think this discussion is mainly about CER. I think it’s about an agenda for more government largesse based in part on distrust of the pharmaceutical industry. I had to laugh when I read this paragraph from Harold Sox’s keynote at the ACP meeting (italics mine):
In summary, the public isn’t getting its money’s worth from our system of industry sponsored clinical research. The public pays the costs of drug trials through higher drug prices drugs but gets research with tells us everything we need to know to make good decisions. We get more for our money with the NIH-sponsored trials that we support with our taxes.
Again I'll remind readers that we've already spent about a billion on research sponsored by a subsidiary of the NIH which by any reasonable account has been a tremendous waste.
DB concludes with:
CER will provide more unbiased data - I do not understand how that could be bad.
No one that I know of is objecting to more unbiased data. But CER is not inherently unbiased. Moreover, it is inherently susceptible to design flaws for reasons I pointed out here, with several examples. Bias has more to do with who’s sponsoring the research than the type of research. There’s no reason to think that the government would introduce less bias. In fact, the government policy makers who are pushing CER are explicitly very biased. If you don’t believe me just read the Congressional Budget Office paper which was pushing for CER, which I cited here.
Saturday, April 25, 2009
What’s going on with swine flu?
Over the last couple of days I’ve been trying to cut through the hype about swine flu. It’s been difficult because media reports are coming at a dizzying pace. Here follows the result of my attempt in Q&A format:
Is this the same swine flu that caused the 1976 scare? Although both are of the H1N1 subtype, apparently this one is different. Officials have indicated that this is a strain never before isolated. Recall that fears that the 1976 Fort Dix swine flu outbreak would morph into a pandemic were unfounded.
This virus is of the H1N1 subtype. So was the virus that caused the 1918 pandemic. Are they the same virus? No. Again, officials say this virus has never been seen before, and it has elements of three animal strains and one human strain. The 1918 pandemic virus resulted from a direct mutation of a pure avian strain.
What is the pandemic risk? The World Health Organization believes the threat of a pandemic exists. The finding of elements of three animal strains and one human strain suggests that it developed by genetic reassortment rather than a direct mutation. In the past, strains created by genetic reassortment have resulted in milder pandemics (1957, 1968) than that created by direct mutation (1918). The 1957 and 1968 strains, however, were the result of reassortment between one human and one animal strain. The new swine flu strain contains elements from three animal strains and could conceivably be more virulent than the 1957 and 1968 strains. For background information on genetic reassortment as opposed to direct mutation causing pandemic flu consult this reference.
What is the relationship between the U.S. and the Mexico cases? Of the much larger number of cases of severe influenza like illness in Mexico only a small minority are thus far confirmed as swine flu. From the WHO report:
I don’t usually appeal to the popular media for perspectives in health issues but this piece by Dr. Marc Siegel seemed helpful.
Here’s more from Kevin MD.
Follow CDC Twitter updates here.
Here is CDC’s main swine flu page with additional links.
WHO information here.
Disclaimer: This post is the result of the efforts of a non-expert to make some sense of the media hype by going to primary sources. Don’t accept what I say uncritically. Check the links above. This story is changing rapidly and much of what is stated here may be wrong in a few days.
Is this the same swine flu that caused the 1976 scare? Although both are of the H1N1 subtype, apparently this one is different. Officials have indicated that this is a strain never before isolated. Recall that fears that the 1976 Fort Dix swine flu outbreak would morph into a pandemic were unfounded.
This virus is of the H1N1 subtype. So was the virus that caused the 1918 pandemic. Are they the same virus? No. Again, officials say this virus has never been seen before, and it has elements of three animal strains and one human strain. The 1918 pandemic virus resulted from a direct mutation of a pure avian strain.
What is the pandemic risk? The World Health Organization believes the threat of a pandemic exists. The finding of elements of three animal strains and one human strain suggests that it developed by genetic reassortment rather than a direct mutation. In the past, strains created by genetic reassortment have resulted in milder pandemics (1957, 1968) than that created by direct mutation (1918). The 1957 and 1968 strains, however, were the result of reassortment between one human and one animal strain. The new swine flu strain contains elements from three animal strains and could conceivably be more virulent than the 1957 and 1968 strains. For background information on genetic reassortment as opposed to direct mutation causing pandemic flu consult this reference.
What is the relationship between the U.S. and the Mexico cases? Of the much larger number of cases of severe influenza like illness in Mexico only a small minority are thus far confirmed as swine flu. From the WHO report:
24 April 2009 -- The United States Government has reported seven confirmed human cases of Swine Influenza A/H1N1 in the USA (five in California and two in Texas) and nine suspect cases. All seven confirmed cases had mild Influenza-Like Illness (ILI), with only one requiring brief hospitalization. No deaths have been reported.
The Government of Mexico has reported three separate events. In the Federal District of Mexico, surveillance began picking up cases of ILI starting 18 March. The number of cases has risen steadily through April and as of 23 April there are now more than 854 cases of pneumonia from the capital. Of those, 59 have died. In San Luis Potosi, in central Mexico, 24 cases of ILI, with three deaths, have been reported. And from Mexicali, near the border with the United States, four cases of ILI, with no deaths, have been reported.
Of the Mexican cases, 18 have been laboratory confirmed in Canada as Swine Influenza A/H1N1, while 12 of those are genetically identical to the Swine Influenza A/H1N1 viruses from California.
I don’t usually appeal to the popular media for perspectives in health issues but this piece by Dr. Marc Siegel seemed helpful.
Here’s more from Kevin MD.
Follow CDC Twitter updates here.
Here is CDC’s main swine flu page with additional links.
WHO information here.
Disclaimer: This post is the result of the efforts of a non-expert to make some sense of the media hype by going to primary sources. Don’t accept what I say uncritically. Check the links above. This story is changing rapidly and much of what is stated here may be wrong in a few days.
Friday, April 24, 2009
PE is common in patients hospitalized with COPD exacerbation
---as noted in this recent paper. Another study a couple of years ago found the same thing, and I cited it here.
Authors of the recent paper conclude:
Testing in these patients needs to be individualized and based on careful clinical assessment. Inappropriate knee-jerk CT scanning may result in a spike in renal failure.
Authors of the recent paper conclude:
A diagnosis of PE should be considered in patients with exacerbation severe enough to warrant hospitalization, especially in those with an intermediate-to-high pretest probability of PE.
Testing in these patients needs to be individualized and based on careful clinical assessment. Inappropriate knee-jerk CT scanning may result in a spike in renal failure.
Why use CT contrast in the evaluation for appendicitis?
Accumulating evidence suggests it’s not necessary. Emergency Medicine professor Richard Bukata went on a rant about it in a recent issue of Emergency Medicine News. Concerning oral contrast he said:
Concerning IV contrast:
He cited a couple of papers favoring non-contrast, the older of which I noted here.
Many radiologists insist on it even when emergency physicians don't want it, it adds hours to the patient evaluation, and it dumps a large oral fluid load on a patient who may be having surgery, increasing the risk of aspiration, at least theoretically. All sorts of literature on this topic indicate that oral contrast adds little if anything to the evaluation when compared with noncontrast CTs, but this topic seems to be highly resistant to the evidence.
Concerning IV contrast:
IV contrast?! What possible reason could there be for using IV contrast in the patient with suspected appendicitis? I thought IV contrast was about the evaluation of solid organs such as liver, spleen, and kidneys. …. Using oral contrast is bad enough, but IV contrast is not without risks, particularly if there are issues regarding renal compromise.
He cited a couple of papers favoring non-contrast, the older of which I noted here.
Thursday, April 23, 2009
Pitfalls in EMR documentation
Recently I’ve posted a couple of anecdotal reports of documentation and coding fraud driven by electronic medical record documentation tools. I could just see the Medicare auditors licking their chops when I read those reports. Now those fears are confirmed. A recent Medical Economics article reports:
So how does an auditor know whether or not you actually did a twelve system review? From my read here are some ways EMRs get docs in trouble:
1) The EMR tools drive (sometimes almost force) documentation that is excessive for the severity of the presenting problem. The patient who comes in for a sprained ankle gets a twelve system review and family history because the EMR automatically imports such text, then the folks in your coding department bill accordingly. Medicare looks to see whether the severity of the patient’s problem matches the documentation, and if it doesn’t it’s a red flag.
2) The EMR tools generate implausible documentation, e.g. the one year old who is oriented times three, or whose pupils react to accommodation.
3) The templates generate multiple records with nearly identical text. This is a red flag which may cause the Medicare recovery auditor to cast a deeper and wider net.
4) The templates default to multisystem reviews and exams whether you do them or not, and it takes time and trouble to edit them out. If too many of your notes are so rich in documentation the auditor will look askance.
Not long ago a physician pitching a certain EMR product showed how to generate a complete H&P with a few mouse clicks. Very little editing was necessary, he told us, because almost all patients who presented with that particular problem had similar findings.
Unfortunately doctors are being held to a double standard regarding the old maxim: if you didn’t document it you didn’t do it. So don’t expect the Medicare auditor to believe that just because you did document it you did do it.
Although the article focused on coding and documentation, other downsides of the EMR were mentioned:
One of the commenters noted:
I frequently review records faxed from outside hospitals on patients admitted to my service. The ones which are electronically generated, including those from the VA, are generally so full of electronic clutter that I have a difficult time deciphering what really happened to the patient let alone what the docs were thinking. It’s electronic illegibility, often much worse than doctors’ handwriting.
H/T to Kevin MD.
Recent audits by federal agencies confirm the warnings about E/M compliance dangers accompanying documentation shortcuts introduced by many current EHR software designs. These audits are a clarion call for stakeholders to eliminate the problems they have created, however unintended.
So how does an auditor know whether or not you actually did a twelve system review? From my read here are some ways EMRs get docs in trouble:
1) The EMR tools drive (sometimes almost force) documentation that is excessive for the severity of the presenting problem. The patient who comes in for a sprained ankle gets a twelve system review and family history because the EMR automatically imports such text, then the folks in your coding department bill accordingly. Medicare looks to see whether the severity of the patient’s problem matches the documentation, and if it doesn’t it’s a red flag.
2) The EMR tools generate implausible documentation, e.g. the one year old who is oriented times three, or whose pupils react to accommodation.
3) The templates generate multiple records with nearly identical text. This is a red flag which may cause the Medicare recovery auditor to cast a deeper and wider net.
4) The templates default to multisystem reviews and exams whether you do them or not, and it takes time and trouble to edit them out. If too many of your notes are so rich in documentation the auditor will look askance.
Not long ago a physician pitching a certain EMR product showed how to generate a complete H&P with a few mouse clicks. Very little editing was necessary, he told us, because almost all patients who presented with that particular problem had similar findings.
Unfortunately doctors are being held to a double standard regarding the old maxim: if you didn’t document it you didn’t do it. So don’t expect the Medicare auditor to believe that just because you did document it you did do it.
Although the article focused on coding and documentation, other downsides of the EMR were mentioned:
Physicians have long been counseled that a well-documented medical record provides the best defense in the event of a claim of medical liability. The June 2008 issue of the Journal of AHIMA quoted EHR legal expert Patricia Trites on the potential danger of electronic systems that permit copying of near-identical documentation into large numbers of patient records: "From a medical-legal standpoint, what would [lawyers] do when they [see] this chart?" she asks. "They are going to rip it apart."
One of the commenters noted:
I have personally been an expert witness in 5 malpractice case in two years caused directly by EHR's. The Veterans Agency EHR, touted by many as one of the top systems was involved in 2 of them. I counted 1012 pages of template heavy notes in one simple 8 month long chart and 157 times that this patient was supposedly screened for PTSD. Who are they kidding?
I frequently review records faxed from outside hospitals on patients admitted to my service. The ones which are electronically generated, including those from the VA, are generally so full of electronic clutter that I have a difficult time deciphering what really happened to the patient let alone what the docs were thinking. It’s electronic illegibility, often much worse than doctors’ handwriting.
H/T to Kevin MD.
The changing face of infective endocarditis
It’s more often an acute disease, and more often due to S. aureus.
Via Archives of Internal Medicine.
Via Archives of Internal Medicine.
Which patients with fever need anti-staphylococcal coverage?
This study adds to our understanding:
(BTW: you can translate S. aureus as MRSA).
Of 1015 patients enrolled, 181 patients (17.8%) had clinically significant bacteremia, including 77 patients (7.6%) with S. aureus bacteremia. Clinical characteristics associated with S. aureus bacteremia were the presence of a hemodialysis graft or shunt (odds ratio [OR] 3.22; 95% confidence interval [CI], 1.85-5.61), chills (OR 2.38; 95% CI, 1.43-3.98), and a history of S. aureus infection (OR 2.68; 95% CI, 1.38-5.20). Peripheral vascular catheters were inversely associated with S. aureus bacteremia (OR 0.42; 95% CI, 0.26-0.69). Clinical characteristics associated with any bloodstream infection were central venous access, chills, history of S. aureus infection, and hemodialysis access.
(BTW: you can translate S. aureus as MRSA).
Wednesday, April 22, 2009
A world without industry support
ACP Advocate Blog author Bob Doherty is reporting from ACP convention headquarters in Philadelphia. He’s pumped up about the annual meeting, Internal Medicine 2009. He writes:
But this year the looming ban on industry support for CME brings new concerns. He goes on:
He’s probably wondering if this year’s premier internal medicine conference will be the last.
The moderate players in this debate would be content to bolster the existing safeguards and firewalls for industry supported CME and find a way to provide more resources of the ACCME so they can do a better job of evaluating content. The more likely scenario, unfortunately, is that the agitators will continue to demagogue this issue in the popular media until there’s nothing left of industry support.
H/T to DB’s Medical Rants.
Today and for the rest of the week, I will be blogging from the Philadelphia Convention Center, where ACP will be holding its annual scientific meeting. Convention center workers are now doing all of the prep work for a successful medical convention, including setting up the exhibit hall.
But this year the looming ban on industry support for CME brings new concerns. He goes on:
A premier scientific meeting like ACP's clearly services a public good (helping doctors keep up-to-date in their clinical knowledge and skills), and drug industry support, within strict guidelines, helps keep the meeting affordable. If industry support for CME was to be prohibited, I wonder where the money would come from to allow internists to continue to have access to CME at a price they can afford.
He’s probably wondering if this year’s premier internal medicine conference will be the last.
The moderate players in this debate would be content to bolster the existing safeguards and firewalls for industry supported CME and find a way to provide more resources of the ACCME so they can do a better job of evaluating content. The more likely scenario, unfortunately, is that the agitators will continue to demagogue this issue in the popular media until there’s nothing left of industry support.
H/T to DB’s Medical Rants.
Allergic bronchopulmonary aspergillosis
---is underappreciated in asthma patients. Review here. From the abstract:
Because many patients with ABPA may be minimally symptomatic or asymptomatic, a high index of suspicion for ABPA should be maintained while managing any patient with bronchial asthma whatever the severity or the level of control. This underscores the need for routine screening of all patients with asthma with an Aspergillus skin test.
Adding a drug to improve hypertension control
---worked better than doubling the dose of the initial drug in this meta-analysis:
Blood pressure reduction from combining drugs from these 4 classes can be predicted on the basis of additive effects. The extra blood pressure reduction from combining drugs from 2 different classes is approximately 5 times greater than doubling the dose of 1 drug.
Tuesday, April 21, 2009
Dissecting quality
In a recent post Bob Wachter discusses the growing backlash against the measurement and public reporting of performance metrics. Research reports over the last few years (some of which I compiled here and elsewhere) have shown that implementation of performance measures is generally ineffective, for a variety or reasons.
According to Bob’s postmortem what we really need is better science and a more circumspect approach, and that those who call for a moratorium on the performance movement have gone too far:
Ouch. I kind of liked the Groopman and Hartzband piece. Yes, we need better quality. Yes, there is a huge gap between evidence and practice. The question is what should we do? That’s where Bob and I part company. I don’t believe the performance movement will get us there. I’ll go a step further and question what appears to be a basic premise of his, which is that the measurement and public reporting of performance has anything at all to do with real quality.
So why is the performance movement a failure? Let’s count the ways.
First, what about the science? In his post Bob notes:
But the problem is not the science. The problem is its misappropriation by policy mavens many of whom, I dare say, understand little about real world application of such science.
The science, for example, which informs us that the effectiveness of adult pneumococcal vaccine is somewhere between slim and zilch is just fine, thank you. What about the blood sugar debacle? Here the rush to clamp every hospitalized patient’s glucose between 80 and 110 was based on the misinterpretation of perfectly sound science. But in their enthusiasm for a single study the misguided policy wonks ignored one of the first principles of critical appraisal: ask yourself whether your patient was in that study. Most hospitalists and intensivists working in the real world knew right off the bat that their patients were not represented by that study. In the case of perioperative beta blockers the policy wonks extended the findings of good science far beyond what appropriate critical appraisal warranted.
In some cases science gave us an important, generalizable lesson for real world care but the policy wonks couldn’t see the utter folly of translating the evidence into a “metric.” Such was the case with the four hour antibiotic rule.
Some performance measures were based on science that was strong, generalizable, mature and straightforward to implement, yet they still failed. What could be more evidence based and easy to implement, we thought, than the heart failure measures? So some were more than a little surprised when, in the Optimize-HF database, those measures turned out to be a bust! Why? I dissected the reasons here. The short version of that analysis is that while there’s no doubt the measures are evidence based and underutilized, promulgating them as performance metrics may do all sorts of things that negate their effectiveness.
So what can we do about the horribly low uptake of evidence into practice? Bob cites data suggesting that it’s only around 50%. For many conditions it’s much lower than that. Multiple systemic and cultural barriers exist. Some of the barriers have been created by the performance movement itself! (I explain here, here, and here). The enormous number and complexity of those barriers should make it obvious that no easy fix exists. If any effective fix exists it will be multifaceted and complex. It will involve education and the development of better tools to help doctors put evidence into practice. It won’t come from Washington in the form of more “metrics.”
Bob concludes his post with:
I agree. But I wouldn’t stop at two. I’d add performance metrics to that list of failures.
According to Bob’s postmortem what we really need is better science and a more circumspect approach, and that those who call for a moratorium on the performance movement have gone too far:
And now we have Groopman and Hartzband arguing that we should take a “time out” on quality measures, leaving it to doctors to make their own choices since only they truly know their patients. Do we really believe that the world will be a better place if we went back to every doctor deciding by him or herself what treatment to offer, when we have irrefutable data demonstrating huge gaps between evidence-based and actual practice? Even when we KNOW the right thing to do (as in handwashing), we fail to do it nearly half the time! Do the authors really believe that the strategy should remain “Doctor Knows Best"; just stay out of our collective hair? Pullease...
Ouch. I kind of liked the Groopman and Hartzband piece. Yes, we need better quality. Yes, there is a huge gap between evidence and practice. The question is what should we do? That’s where Bob and I part company. I don’t believe the performance movement will get us there. I’ll go a step further and question what appears to be a basic premise of his, which is that the measurement and public reporting of performance has anything at all to do with real quality.
So why is the performance movement a failure? Let’s count the ways.
First, what about the science? In his post Bob notes:
Some critics have even suggested that we put a moratorium on new quality measures until the science improves.
But the problem is not the science. The problem is its misappropriation by policy mavens many of whom, I dare say, understand little about real world application of such science.
The science, for example, which informs us that the effectiveness of adult pneumococcal vaccine is somewhere between slim and zilch is just fine, thank you. What about the blood sugar debacle? Here the rush to clamp every hospitalized patient’s glucose between 80 and 110 was based on the misinterpretation of perfectly sound science. But in their enthusiasm for a single study the misguided policy wonks ignored one of the first principles of critical appraisal: ask yourself whether your patient was in that study. Most hospitalists and intensivists working in the real world knew right off the bat that their patients were not represented by that study. In the case of perioperative beta blockers the policy wonks extended the findings of good science far beyond what appropriate critical appraisal warranted.
In some cases science gave us an important, generalizable lesson for real world care but the policy wonks couldn’t see the utter folly of translating the evidence into a “metric.” Such was the case with the four hour antibiotic rule.
Some performance measures were based on science that was strong, generalizable, mature and straightforward to implement, yet they still failed. What could be more evidence based and easy to implement, we thought, than the heart failure measures? So some were more than a little surprised when, in the Optimize-HF database, those measures turned out to be a bust! Why? I dissected the reasons here. The short version of that analysis is that while there’s no doubt the measures are evidence based and underutilized, promulgating them as performance metrics may do all sorts of things that negate their effectiveness.
So what can we do about the horribly low uptake of evidence into practice? Bob cites data suggesting that it’s only around 50%. For many conditions it’s much lower than that. Multiple systemic and cultural barriers exist. Some of the barriers have been created by the performance movement itself! (I explain here, here, and here). The enormous number and complexity of those barriers should make it obvious that no easy fix exists. If any effective fix exists it will be multifaceted and complex. It will involve education and the development of better tools to help doctors put evidence into practice. It won’t come from Washington in the form of more “metrics.”
Bob concludes his post with:
From where I sit, of all our options to meet the mandates to improve quality and safety, tenaciously clinging to a Marcus Welbian (and demonstrably low quality) status quo or creating tests that can be passed by appearing to be working on improvement seem like two of the worst.
I agree. But I wouldn’t stop at two. I’d add performance metrics to that list of failures.
Metformin added to insulin
---improves macrovascular outcomes in DM 2, NNT 16.1 according to this study. Given that so many treatments are macrovascular neutral or even associated with macrovascular harm, this is important information. Since metformin is a generic drug this is a pretty good bang for the buck.
How useful is Wikipedia as a drug information resource?
Not very, according to this study.
I use it occasionally to check brand names, manufacturer names and as a starting point to find primary sources, but that’s about it.
Wikipedia has a more narrow scope, is less complete, and has more errors of omission than the comparator database. Wikipedia may be a useful point of engagement for consumers, but is not authoritative and should only be a supplemental source of drug information.
I use it occasionally to check brand names, manufacturer names and as a starting point to find primary sources, but that’s about it.
Monday, April 20, 2009
The expected turf battles between hospitalists and intensivists over ICU care
---have never really materialized due in large part to shortages in both specialties. Fierce competition over closed ICUs has given way to team work and collaboration. An article in Today’s Hospitalist discusses the latest trends.
Which patients in the ER with chest pain need a triple rule out CT?
Not every one, according to Robert D. Glatter, MD in a Medscape Ask the Experts piece:
Clinical assessment and simple initial testing usually narrows it down to one or two of the “big three.” Yet, there are those occasional patients with severe, undifferentiated and unrelenting pain who may benefit from the triple rule out protocol.
Although this triple-rule out technique may exclude deadly causes of chest pain from 3 different anatomic vascular locations, the higher radiation dose delivered with current techniques is a valid clinical concern. Therefore, the triple rule-out protocol should be limited to selected patients in which there is "weighted" support for the diagnosis of either PE or AD, as well as suspicion for ACS.
Clinical assessment and simple initial testing usually narrows it down to one or two of the “big three.” Yet, there are those occasional patients with severe, undifferentiated and unrelenting pain who may benefit from the triple rule out protocol.
Friday, April 17, 2009
Key issues in stroke care
Today’s Hospitalist’s coverage of S. Andrew Josephson’s talk at Bob Wachter’s hospital medicine course last fall addresses the hot issues in stroke care including the new time window and safety data for thrombolytic therapy, the choice of anti-platelet agent, the use of statins, the optimal use of imaging studies and more.
ACC 2009---statins in patients with ESRD on hemodialysis
This ACC presentation was published in NEJM:
This is in line with what was known before and was the subject of my inaugural blog post in 2005.
Conclusions In patients undergoing hemodialysis, the initiation of treatment with rosuvastatin lowered the LDL cholesterol level but had no significant effect on the composite primary end point of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke.
This is in line with what was known before and was the subject of my inaugural blog post in 2005.
The lactate level in the ICU patient
---is a powerful predictor. One of the rules of the House of God (if they had done lactate levels back then) might have been “Mortality=lactate x 10.” That’s not far from accurate according to this study.
Thursday, April 16, 2009
Optimal vancomycin use
One of these days we’ll be saying good bye to our old friend vanco. Until then, here is a new consensus statement for optimal use of a dying drug. Although there has been extensive published experience with vancomycin there are few available prospective randomized trials. Thus, this consensus statement draws heavily on “lower level” evidence.
The document is available as free full text. It is an excellent review of vancomycin use and deserves to be read in the original. Any highlights I would post here would not do it justice.
The document is available as free full text. It is an excellent review of vancomycin use and deserves to be read in the original. Any highlights I would post here would not do it justice.
BNP (and proBNP): Are they useful in the evaluation of patients presenting with acute dyspnea?
According to this Annals study testing did not affect ER treatment, admission rates or length of stay. Test discrimination, however, was good, so the test still appears to have diagnostic utility. I believe it is useful in appropriately selected patients, used with appropriate clinical judgment.
ACC 2009---ADMIRE-HF
This probably won’t make prime time soon (due to low commercial interest) but it should. A simple and readily available nuclear scan is a powerful prognostic tool for patients with heart failure. According to a Medscape-Heartwire report on the presentation at ACC 2009:
What’s the radiotracer? It’s 123I meta-iodobenzylguanidine (MIBG) aka AdreView, the agent that’s been recommended for years for imaging of occult pheochromocytoma. As an analog of norepinephrine, it is taken up by cardiac sympathetic nerves and serves as an indicator of cardiac sympathetic nervous activity.
…the composite end point, the first occurrence of NYHA heart-failure class progression, potentially life-threatening arrhythmic event, or cardiac death, as determined by an independent adjudication panel, occurred significantly more frequently in patients who had low uptake of the tracer.
…there were 51 cardiac deaths in the low-uptake group and just two in the higher-uptake group, and the negative predictive value of a high uptake for cardiac death over two years was 98.8%.
…the test was particularly effective in identifying those with the worst prognosis, with the group who were in the lowest 10% for uptake having a death rate 10 times those in the highest 20%.
What’s the radiotracer? It’s 123I meta-iodobenzylguanidine (MIBG) aka AdreView, the agent that’s been recommended for years for imaging of occult pheochromocytoma. As an analog of norepinephrine, it is taken up by cardiac sympathetic nerves and serves as an indicator of cardiac sympathetic nervous activity.
Wednesday, April 15, 2009
The abyss of post-hospital care
An important study recently published in NEJM examined Medicare hospital readmission rates. You can read Bob Wachter’s take here. Among the findings:
It was the first paper to look at all cause Medicare readmission rates since this paper which looked at readmissions in the pre-DRG era. Its findings:
Those authors presciently warned:
Although direct comparisons of the two studies are difficult it does indeed appear that the problem has gotten worse in the DRG era, as the 30 day readmission rate in the current study almost equals the 60 day rate from the pre-DRG data. That should surprise no one. I was early in my career during the enactment of Medicare’s prospective payment system. The changes in the way patients were cared for and the sudden administrative pressures to limit hospitalization of Medicare beneficiaries were dramatic. Medicare no longer paid for the care hospitals delivered. Hospitals lost money on Medicare admissions. This resulted in more selective admission criteria for hospitals such that only more severely ill patients were hospitalized. In addition, widespread anecdotal reports of Medicare patients being discharged “quicker and sicker” were confirmed in research reports such as this one:
Although increased mortality has not, as far as I am aware, been attributed to the enactment of DRG’s, probably due to progressive improvements in the overall quality of care over time, it is highly likely that the prospective payment system has resulted in increased readmission rates.
This is why I disagree with Bob on one point. He likes DRG’s. I don’t. I believe the PPS was an ill-conceived and reactionary move against the largesse and massive inefficiencies of the first 20 years of Medicare’s existence as I pointed out here.
At any rate, we’re stuck now with a perverse system of negative cost incentives that we must make the best of. We can all agree that we have an unacceptable readmission rate and hospitals are doing a lousy job of transitions care. What to do about it? A proposal which is gaining momentum (which will accelerate as a result of the new NEJM paper) is to bundle payment for episodes of care over the 30 days following hospitalization. A part of me rebels at this strategy; it is nothing more than an extension of the perverse cost incentives that got us in this fix in the first place. On the other hand we have to live with these incentives. We can’t dismantle the PPS in 2009. And we have to do something about the horrible transitions process. We know from experience that performance measures won’t cut it. They’ll result in cosmetic improvements only. It may well be that our only recourse now is to make it all about money.
Almost one fifth (19.6%) of the 11,855,702 Medicare beneficiaries who had been discharged from a hospital were rehospitalized within 30 days, and 34.0% were rehospitalized within 90 days; 67.1% of patients who had been discharged with medical conditions and 51.5% of those who had been discharged after surgical procedures were rehospitalized or died within the first year after discharge. In the case of 50.2% of the patients who were rehospitalized within 30 days after a medical discharge to the community, there was no bill for a visit to a physician's office between the time of discharge and rehospitalization.
It was the first paper to look at all cause Medicare readmission rates since this paper which looked at readmissions in the pre-DRG era. Its findings:
In order to examine the proportion of Medicare expenditures attributable to repeated admissions to the hospital, we assessed the frequency with which 270,266 randomly selected Medicare beneficiaries were readmitted after hospital discharge between 1974 and 1977. Twenty-two per cent of Medicare hospitalizations were followed by a readmission within 60 days of discharge.
Those authors presciently warned:
Even a small decrease in the readmission rate could result in substantial savings for the Medicare program. The recently enacted prospective-payment legislation, however, creates economic incentives that could increase readmission rates.
Although direct comparisons of the two studies are difficult it does indeed appear that the problem has gotten worse in the DRG era, as the 30 day readmission rate in the current study almost equals the 60 day rate from the pre-DRG data. That should surprise no one. I was early in my career during the enactment of Medicare’s prospective payment system. The changes in the way patients were cared for and the sudden administrative pressures to limit hospitalization of Medicare beneficiaries were dramatic. Medicare no longer paid for the care hospitals delivered. Hospitals lost money on Medicare admissions. This resulted in more selective admission criteria for hospitals such that only more severely ill patients were hospitalized. In addition, widespread anecdotal reports of Medicare patients being discharged “quicker and sicker” were confirmed in research reports such as this one:
Instability at discharge (important clinical problems usually first occurring prior to discharge) predicted the likelihood of postdischarge deaths. At 90 days postdischarge, 16% of patients discharged unstable were dead vs 10% of patients discharged stable. After the PPS introduction, instability increased primarily among patients discharged home. Prior to the PPS, 10% of patients discharged home were unstable; after the PPS was implemented, 15% were discharged unstable, a 43% relative change.
Although increased mortality has not, as far as I am aware, been attributed to the enactment of DRG’s, probably due to progressive improvements in the overall quality of care over time, it is highly likely that the prospective payment system has resulted in increased readmission rates.
This is why I disagree with Bob on one point. He likes DRG’s. I don’t. I believe the PPS was an ill-conceived and reactionary move against the largesse and massive inefficiencies of the first 20 years of Medicare’s existence as I pointed out here.
At any rate, we’re stuck now with a perverse system of negative cost incentives that we must make the best of. We can all agree that we have an unacceptable readmission rate and hospitals are doing a lousy job of transitions care. What to do about it? A proposal which is gaining momentum (which will accelerate as a result of the new NEJM paper) is to bundle payment for episodes of care over the 30 days following hospitalization. A part of me rebels at this strategy; it is nothing more than an extension of the perverse cost incentives that got us in this fix in the first place. On the other hand we have to live with these incentives. We can’t dismantle the PPS in 2009. And we have to do something about the horrible transitions process. We know from experience that performance measures won’t cut it. They’ll result in cosmetic improvements only. It may well be that our only recourse now is to make it all about money.
ACC 2009---effects of statins in patients undergoing acute intervention
Whether your patient is statin-naive or already on a statin, acute pre- and post-procedure loading with atorvastatin may improve outcomes according to presentations at ACC 2009. While such loading is not considered the standard of care statin use is moving “upstream” in the treatment of acute coronary syndrome:
In practice, said Cannon, clinicians should start intensive statin therapy in acute coronary syndrome patients on hospital admission and potentially the night prior to the procedure in elective PCI.
ACC 2009---proBNP to guide heart failure treatment
Via Medscape-Heartwire:
In this study protocol an algorithmic approach triggered an immediate intensification of heart failure treatment any time a patient’s proBNP value exceeded an individualized target. This result is in line with previous research.
Although the study did not validate the use of proBNP as a direct trigger for intervention it did confirm its usefulness as a prognostic marker, as patients who stayed in their target range had better outcomes.
This study does not negate proBNP as a marker to follow in heart failure. What it does tell us is that we are not sure how to optimally use it.
Using individualized levels of the biomarker NT-proBNP to guide the treatment of patients with chronic heart failure did not improve their morbidity or mortality over standard clinical management, according to results of the Can Pro-Brain-Natriuretic Peptide Guided Therapy of Chronic Heart Failure Improve Heart Failure Morbidity and Mortality? (PRIMA) study presented here at the American College of Cardiology 2009 Scientific Sessions.
In this study protocol an algorithmic approach triggered an immediate intensification of heart failure treatment any time a patient’s proBNP value exceeded an individualized target. This result is in line with previous research.
Although the study did not validate the use of proBNP as a direct trigger for intervention it did confirm its usefulness as a prognostic marker, as patients who stayed in their target range had better outcomes.
This study does not negate proBNP as a marker to follow in heart failure. What it does tell us is that we are not sure how to optimally use it.
Tuesday, April 14, 2009
ACC 2009: ACTIVE A
This ACC presentation was also published in NEJM:
The major event reduction was for stroke. The benefit over and above the bleeding risk was fairly slim.
Given that anti-platelet therapy does not address the mechanism of stroke induced by atrial fibrillation, how does this strategy work? Probably by reducing platelet mediated events at the surface of atherosclerotic plaques, which has nothing to do with atrial fibrillation.
In patients with atrial fibrillation warfarin remains the drug of choice absent contraindications.
Medscape-Heartwire’s report is here.
Conclusions In patients with atrial fibrillation for whom vitamin K–antagonist therapy was unsuitable, the addition of clopidogrel to aspirin reduced the risk of major vascular events, especially stroke, and increased the risk of major hemorrhage.
The major event reduction was for stroke. The benefit over and above the bleeding risk was fairly slim.
Given that anti-platelet therapy does not address the mechanism of stroke induced by atrial fibrillation, how does this strategy work? Probably by reducing platelet mediated events at the surface of atherosclerotic plaques, which has nothing to do with atrial fibrillation.
In patients with atrial fibrillation warfarin remains the drug of choice absent contraindications.
Medscape-Heartwire’s report is here.
How important is it to diagnose the specific cause of a patient’s chest pain
---after they have ruled out for MI, PE and aortic dissection? Coders always want us to diagnose a specific cause. “Chest pain due to gastroesophageal reflux disease” pays more than “chest pain cause undetermined”, we’re told.
J. Willis Hurst, Professor of Medicine at Emory, once said that to tell patients what they don’t have without giving them a specific diagnosis is a crotchet:
I wonder if this is the right approach. If you’re a hospitalist discharging a patient, once you’ve ruled out ACS, PE, dissection, pneumothorax and pneumonia is it realistic to think you can make a specific and accurate diagnosis? Patients with obvious musculoskeletal pain get sent home from the ER. Cases which get admitted are usually less clear. Once all the serious conditions are ruled out the clinician is under pressure to come up a diagnosis. The coders don’t want to see “chest pain cause undetermined.” The patient and family, eager to “get to the bottom” of what’s wrong, may be resentful or disappointed if you say “we don’t know what was wrong.”
Under such pressure the clinician often resorts to the default diagnosis of ”gastroesophageal reflux disease.” Most patients with non cardiac chest pain do not have GERD, so the “diagnosis” at discharge is mere guesswork. (Try convincing administration or an insurance company to let you keep a stable patient in the hospital for endoscopy or radiographic studies). So the diagnosis of GERD at discharge in patients who “rule out” for cardiac disease is a wastebasket.
This has significant unintended consequences. What happens when you label patients with “GERD”? You are declaring that they are at risk for adenocarcinoma of the esophagus and may need future endoscopic surveillance. Moreover, you, explicitly or implicitly, are committing them to long term treatment, often with a proton pump inhibitor, a regimen not without adverse effects.
When we discharge patients with unexplained chest pain we are under pressure to pull a diagnosis out of thin air. Sometimes it’s more intellectually honest and better for patients to simply recognize that they often have unexplained symptoms.
J. Willis Hurst, Professor of Medicine at Emory, once said that to tell patients what they don’t have without giving them a specific diagnosis is a crotchet:
Some physicians believe they have solved their patients’ problems by stating what the patients do not have. This is a crotchet. I recognize that it is not always possible to state the exact cause of a patient’s chest pain. Despite this, the goal should be to learn as much as possible about the causes of chest pain and not to be satisfied with stating what a patient does not have.
I wonder if this is the right approach. If you’re a hospitalist discharging a patient, once you’ve ruled out ACS, PE, dissection, pneumothorax and pneumonia is it realistic to think you can make a specific and accurate diagnosis? Patients with obvious musculoskeletal pain get sent home from the ER. Cases which get admitted are usually less clear. Once all the serious conditions are ruled out the clinician is under pressure to come up a diagnosis. The coders don’t want to see “chest pain cause undetermined.” The patient and family, eager to “get to the bottom” of what’s wrong, may be resentful or disappointed if you say “we don’t know what was wrong.”
Under such pressure the clinician often resorts to the default diagnosis of ”gastroesophageal reflux disease.” Most patients with non cardiac chest pain do not have GERD, so the “diagnosis” at discharge is mere guesswork. (Try convincing administration or an insurance company to let you keep a stable patient in the hospital for endoscopy or radiographic studies). So the diagnosis of GERD at discharge in patients who “rule out” for cardiac disease is a wastebasket.
This has significant unintended consequences. What happens when you label patients with “GERD”? You are declaring that they are at risk for adenocarcinoma of the esophagus and may need future endoscopic surveillance. Moreover, you, explicitly or implicitly, are committing them to long term treatment, often with a proton pump inhibitor, a regimen not without adverse effects.
When we discharge patients with unexplained chest pain we are under pressure to pull a diagnosis out of thin air. Sometimes it’s more intellectually honest and better for patients to simply recognize that they often have unexplained symptoms.
Monday, April 13, 2009
ACC 2009---the IRIS trial
This is one of several posts with my take on some presentations at ACC 2009 that interested me.
The IRIS trial: no survival benefit from early ICD implantation following risk stratification after myocardial infarction. This adds little to what we already knew and does not suggest changes in current guideline recommendations for device therapy.
Sudden cardiac death was reduced but there was a corresponding increase in non-arrhythmic death so that all cause mortality was unaffected. These discordant findings are poorly understood but it was suggested that these patients stratified early on were at high risk for both arrhythmic death and pump failure, and device therapy merely exchanged one mode of death for another. Also, as is apparent from the Medscape-Heartwire report, selection criteria were unusual, resulting in a mixed bag of study patients which differed from those for whom device therapy is currently recommended based on MADT II and other trials that support current guidelines.
Finally and perhaps most importantly, IRIS, which looked at patients one month or less post MI, confirms what we previously learned several years ago from DINAMIT, which showed no reduction in all cause mortality by device therapy in patients selected for treatment within 40 days post MI. That was the basis for the current guideline recommendations:
The IRIS trial: no survival benefit from early ICD implantation following risk stratification after myocardial infarction. This adds little to what we already knew and does not suggest changes in current guideline recommendations for device therapy.
Sudden cardiac death was reduced but there was a corresponding increase in non-arrhythmic death so that all cause mortality was unaffected. These discordant findings are poorly understood but it was suggested that these patients stratified early on were at high risk for both arrhythmic death and pump failure, and device therapy merely exchanged one mode of death for another. Also, as is apparent from the Medscape-Heartwire report, selection criteria were unusual, resulting in a mixed bag of study patients which differed from those for whom device therapy is currently recommended based on MADT II and other trials that support current guidelines.
Finally and perhaps most importantly, IRIS, which looked at patients one month or less post MI, confirms what we previously learned several years ago from DINAMIT, which showed no reduction in all cause mortality by device therapy in patients selected for treatment within 40 days post MI. That was the basis for the current guideline recommendations:
ICD therapy is indicated in patients with LVEF less than 35% due to prior MI who are at least 40 days post-MI and are in NYHA functional Class II or III. (Level of Evidence: A).
ICD therapy is indicated in patients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF less than 30%, and are in NYHA functional Class I (Level of Evidence: A).
Refeeding syndrome
Many hospitalized patients are at risk for this. Although under recognized as a clinical entity it is often averted unwittingly by daily chemistry profiles which are commonplace in very ill patients. Dieticians and clinical pharmacists snooping in patients’ charts also may help prevent some cases.
Once the exclusive province of the surgeons, nutritional support is increasingly falling into the lap of the hospitalist who may not be well trained in the complications.
Once the exclusive province of the surgeons, nutritional support is increasingly falling into the lap of the hospitalist who may not be well trained in the complications.
Recombinant Human Activated Protein C for Severe Sepsis---is the product labeling strict enough?
Here’s a concerning small study from Critical Care Medicine:
“Baseline bleeding precautions” refers to patient characteristics under the “warnings and precautions” category of the Xigris product labeling. Patients under not only the “contraindications” category but also under the “warnings and precautions” category of the product labeling were excluded from the PROWESS trial. Thus, the exclusion criteria in PROWESS were stricter than the contraindications in the FDA approved labeling.
Study design and small numbers limit the conclusions we can draw from this paper but here’s what’s interesting: Including patients under the “warnings and precautions” category resulted in high bleeding rates and more than twice the mortality of the placebo patients in PROWESS. On the other hand, patients who would have been allowed to participate in PROWESS had bleeding rates and mortality almost identical to the treatment arm of PROWESS!
Clinicians may want to consider going beyond the labeling restrictions and treat only those patients who lack PROWESS exclusion criteria. Medscape reports that the FDA is monitoring the situation but has not decided whether to take regulatory action.
Measurements and Main Results: Seventy-three patients received recombinant human activated protein C. Serious bleeding events occurred in 7 of 20 patients (35%) with any baseline bleeding precaution vs. only 2 of 53 patients (3.8%) without any bleeding precautions (p less than 0.0001). More patients with a baseline bleeding precaution died compared with patients without any bleeding precautions (65% vs. 24.5%, p = 0.0015).
“Baseline bleeding precautions” refers to patient characteristics under the “warnings and precautions” category of the Xigris product labeling. Patients under not only the “contraindications” category but also under the “warnings and precautions” category of the product labeling were excluded from the PROWESS trial. Thus, the exclusion criteria in PROWESS were stricter than the contraindications in the FDA approved labeling.
Study design and small numbers limit the conclusions we can draw from this paper but here’s what’s interesting: Including patients under the “warnings and precautions” category resulted in high bleeding rates and more than twice the mortality of the placebo patients in PROWESS. On the other hand, patients who would have been allowed to participate in PROWESS had bleeding rates and mortality almost identical to the treatment arm of PROWESS!
Clinicians may want to consider going beyond the labeling restrictions and treat only those patients who lack PROWESS exclusion criteria. Medscape reports that the FDA is monitoring the situation but has not decided whether to take regulatory action.
Friday, April 10, 2009
Homeopathy versus conventional medicine and patient satisfaction
From BioMed Central Complementary and Alternative Medicine:
On examination of the body of the paper, these differences can only be attributed to differences in side effects.
Take home message: water has fewer side effects than real medicine.
Results: A total of 6778 adult patients received the questionnaire and 126 responded(46.1%). Statistically significant differences were found with respect to health status (higher percentage of chronic and severe conditions in the homeopathic group), perception of side effects (higher percentage of reported side effects in the conventional group) and patient satisfaction (higher percentage of satisfied patients in the homeopathic group).
Conclusion: Overall patient satisfaction was significantly higher in homeopathic than in conventional care. Homeopathic treatments were perceived as a low-risk therapy with two to three times fewer side effects than conventional care.
On examination of the body of the paper, these differences can only be attributed to differences in side effects.
Take home message: water has fewer side effects than real medicine.
Stroke outcomes and the pleiotropic effects of statins
Thursday, April 09, 2009
Leapfrog’s performance scores are meaningless
According to a recently published JAMA analysis:
The measures surveyed included, but were not limited to: (1) creating a safety culture, (2) ensuring an adequate nursing workforce, (3) ensuring that a pharmacist is active in medication use, (4) not providing patient care summaries from memory, (5) providing patient care information and orders to all clinicians, (6) requiring patient readback of informed consent, (7) documenting resuscitation or end-of-life directives, (8) preventing mislabeled radiographs, (9) providing risk assessment and prevention for deep vein thrombosis/venous thromboembolism, (10) providing anticoagulation services, (11) preventing aspiration, (12) preventing central venous line sepsis, and (13) requiring hand washing.
Public reporting has hospitals scrambling to do all sorts of things to buff their profiles. Unfortunately these “improvements” are largely cosmetic and have little beneficial impact on patient outcomes. That’s just one reason the performance movement is a failure.
On the Internet, hospital performance on the Safe Practices Survey is ranked by quartiles, which may suggest to consumers that hospitals in higher quartiles are safer than hospitals in lower quartiles. In this first study of the relationship between survey scores and hospital outcomes, we studied a national sample of hospitals and found no relationship between quartiles of score and in-hospital mortality, regardless of whether we adjusted for expected mortality risk and certain hospital characteristics.
The measures surveyed included, but were not limited to: (1) creating a safety culture, (2) ensuring an adequate nursing workforce, (3) ensuring that a pharmacist is active in medication use, (4) not providing patient care summaries from memory, (5) providing patient care information and orders to all clinicians, (6) requiring patient readback of informed consent, (7) documenting resuscitation or end-of-life directives, (8) preventing mislabeled radiographs, (9) providing risk assessment and prevention for deep vein thrombosis/venous thromboembolism, (10) providing anticoagulation services, (11) preventing aspiration, (12) preventing central venous line sepsis, and (13) requiring hand washing.
Public reporting has hospitals scrambling to do all sorts of things to buff their profiles. Unfortunately these “improvements” are largely cosmetic and have little beneficial impact on patient outcomes. That’s just one reason the performance movement is a failure.
Typhilitis
If you’re doing comanagement on the oncology service you’ll see this.
Caution: In this case report the treating physicians, after finding Aspergillus species in the surgical specimen, began treatment with fluconazole. I have no idea why. To the best of my knowledge fluconazole is not effective against Aspergillus.
Caution: In this case report the treating physicians, after finding Aspergillus species in the surgical specimen, began treatment with fluconazole. I have no idea why. To the best of my knowledge fluconazole is not effective against Aspergillus.
Test characteristics of physical exam maneuvers in pleural effusion
Via JAMA Clinician’s Corner.
Percussion dullness had a positive LR of 8.7. Lack of reduced fremitus has a negative LR of 0.21.
Percussion dullness had a positive LR of 8.7. Lack of reduced fremitus has a negative LR of 0.21.
Wednesday, April 08, 2009
PubMed searching
For point of care searching PubMed has been supplanted for many users, in the interest of time, by UptoDate and other filtered resources. Nevertheless, for certain searching tasks, I continue to find PubMed’s unique features useful. Occasionally I find useful tips to share with readers.
A question that often arises is “How useful is a free text search in PubMed?” Free text searching is fine for some searching purposes but does not take full advantage of PubMed’s features. I experimented by comparing a free text search with a search using Boolean operators for the topic “heparin induced thrombocytopenia”. The results?
Free text:
Boolean:
Identical.
You can find out exactly how the search was done by clicking the details tab which, in the case of our searches, reveals the exact same strategy for both:
(No other popular medical search engine that I know of allows you to do this, by the way).
These strategies, however, yield 2908 hits. This illustrates the disadvantage of free text searching which is that it usually produces an unmanageable number of citations. A more restrictive search strategy is often needed. One method is to restrict search terms to the title field. Without the title restriction PubMed searches throughout the entire citation including the abstract. The results will include many articles in which heparin induced thrombocytopenia is incidental to the main topic---articles you probably don’t want. By applying the title restriction you confine your results to articles that have all three words in the title. Type [ti] after each search term:
A question that often arises is “How useful is a free text search in PubMed?” Free text searching is fine for some searching purposes but does not take full advantage of PubMed’s features. I experimented by comparing a free text search with a search using Boolean operators for the topic “heparin induced thrombocytopenia”. The results?
Free text:
Boolean:
Identical.
You can find out exactly how the search was done by clicking the details tab which, in the case of our searches, reveals the exact same strategy for both:
(No other popular medical search engine that I know of allows you to do this, by the way).
These strategies, however, yield 2908 hits. This illustrates the disadvantage of free text searching which is that it usually produces an unmanageable number of citations. A more restrictive search strategy is often needed. One method is to restrict search terms to the title field. Without the title restriction PubMed searches throughout the entire citation including the abstract. The results will include many articles in which heparin induced thrombocytopenia is incidental to the main topic---articles you probably don’t want. By applying the title restriction you confine your results to articles that have all three words in the title. Type [ti] after each search term:
A clinical score to predict Legionella
---had good test characteristics in patients with community acquired pneumonia.
Via BMC Pulmonary Medicine.
Via BMC Pulmonary Medicine.
The natural history of bicuspid aortic valve
This Medical Economics piece is about a physician’s personal battle with the complications of bicuspid aortic valve. It is compelling reading from the human interest side but also contains an important clinical lesson: bicuspid aortic valve is a disease not only of the valve but also of the aortic wall. An aortic ejection sound is non specific but may be an important first clue.
Tuesday, April 07, 2009
Comparative effectiveness research and the problem of rigged design
As proponents of comparative effectiveness research (CER) point out, we have many treatments for the same illness which are known to work because in clinical trials they work better than placebo. The clinician wants to know which among these treatments is best for a given condition. Although such questions are simplistic in the real clinical world they serve as starting points for CER, of which we have many examples. But the wealth of CER studies already at our disposal contains lessons in clinical trial design which should sound a note of caution about an inherent vulnerability: CER is uniquely susceptible to design rigging.
Here’s how it works. Say you want to compare drug A with drug B. Suppose you have a conflict of interest that biases you towards drug A, and you have an incentive to make drug A look better than drug B. There are several easy ways to rig the design and accomplish this and, as I will illustrate, it has been done many times. The simplest way is to give the wrong (or a suboptimal) dose of drug B.
Take, for example, the RECORD studies on VTE prophylaxis in patents undergoing hip and knee arthroplasty. In these studies rivaroxaban, developed by Bayer, the company which funded the trials, came out looking superior to enoxaparin. But look at the study design. The dose of enoxaparin given in the trials was 40 mg once daily. Dosing of enoxaparin for VTE prophylaxis following hip and knee surgery is somewhat controversial but by most accounts 40 mg daily is below the optimal dose. Thus the design appears to have favored rivaroxaban.
Here’s another example. In a comparative effectiveness study concluding that enoxaparin was superior to unfractionated heparin for VTE prophylaxis in stroke patients the investigators, who had ties to Sanofi-Aventis, the makers of enoxaparin, apparently forgot to give the optimal dose of unfractionated heparin.
Besides suboptimal dosing there are other ways to stack the deck in comparative effectiveness research. ALLHAT, which was spun as positioning thiazides as the unequivocal starting drugs of choice in hypertension, was designed to place lisinopril at a disadvantage compared to chlorthalidone. (Rather than elaborate myself I’ll let you read hypertension expert and ALLHAT investigator Michael Weber’s analysis here).
I could go on and on but will give just a couple more examples. Two comparative effectiveness megatrials of thrombolytic therapy in myocardial infarction, GISSI 2 and ISIS 3, designed adjunctive heparin use in a manner which placed TPA at a disadvantage.
Of course comparative studies are important. They answer a type of clinical question not addressed by placebo studies. Placebo controlled trials, on the other hand, tend to have cleaner and simpler designs for the reasons I point out above.
I believe clinical researchers are basically honest. I don’t believe most of the design flaws in these studies resulted from deliberate, thoughtful efforts on the part of the investigators. But I do believe biases and conflicts creep in, especially when given opportunity by the unique vulnerabilities of comparative effectiveness research. And we know there are conflicts of interest, huge conflicts, in the new government funded program.
Here’s how it works. Say you want to compare drug A with drug B. Suppose you have a conflict of interest that biases you towards drug A, and you have an incentive to make drug A look better than drug B. There are several easy ways to rig the design and accomplish this and, as I will illustrate, it has been done many times. The simplest way is to give the wrong (or a suboptimal) dose of drug B.
Take, for example, the RECORD studies on VTE prophylaxis in patents undergoing hip and knee arthroplasty. In these studies rivaroxaban, developed by Bayer, the company which funded the trials, came out looking superior to enoxaparin. But look at the study design. The dose of enoxaparin given in the trials was 40 mg once daily. Dosing of enoxaparin for VTE prophylaxis following hip and knee surgery is somewhat controversial but by most accounts 40 mg daily is below the optimal dose. Thus the design appears to have favored rivaroxaban.
Here’s another example. In a comparative effectiveness study concluding that enoxaparin was superior to unfractionated heparin for VTE prophylaxis in stroke patients the investigators, who had ties to Sanofi-Aventis, the makers of enoxaparin, apparently forgot to give the optimal dose of unfractionated heparin.
Besides suboptimal dosing there are other ways to stack the deck in comparative effectiveness research. ALLHAT, which was spun as positioning thiazides as the unequivocal starting drugs of choice in hypertension, was designed to place lisinopril at a disadvantage compared to chlorthalidone. (Rather than elaborate myself I’ll let you read hypertension expert and ALLHAT investigator Michael Weber’s analysis here).
I could go on and on but will give just a couple more examples. Two comparative effectiveness megatrials of thrombolytic therapy in myocardial infarction, GISSI 2 and ISIS 3, designed adjunctive heparin use in a manner which placed TPA at a disadvantage.
Of course comparative studies are important. They answer a type of clinical question not addressed by placebo studies. Placebo controlled trials, on the other hand, tend to have cleaner and simpler designs for the reasons I point out above.
I believe clinical researchers are basically honest. I don’t believe most of the design flaws in these studies resulted from deliberate, thoughtful efforts on the part of the investigators. But I do believe biases and conflicts creep in, especially when given opportunity by the unique vulnerabilities of comparative effectiveness research. And we know there are conflicts of interest, huge conflicts, in the new government funded program.
Hospital infection control
This review discusses infection control for the big three: C diff, MRSA and VRE.
What is the optimal role for hospitalists in the care of surgical patients?
The jury is still out. Options range from consulting hospitalists only when medical complications occur to a broad net of comanagement of all patients. Another approach is to screen for high risk patients who stand to benefit most. A hospitalist group from the University of Chicago Medical Center presented their data on this approach at the 2009 Cleveland Clinic Perioperative Medicine Summit.
Monday, April 06, 2009
What does the evidence say about the value of the hospitalist model?
A while back I suggested that it was unlikely there would be any more studies on the effects of the hospitalist model on outcomes and resource utilization because there were no longer enough practitioners in the traditional model of hospital care against which to compare. I also suggested that despite the hype, good quality evidence in favor of the value of the model was lacking. Although I stand by that premise the latest systematic review, published in Mayo Clinic Proceedings, warrants a revisit to the issue.
The review concluded, in line with popular belief, that the hospitalist model results in improved efficiency of resource utilization. Although it will be greeted with fanfare among boosters of the model (read Happy Hospitalist’s take here) there is a big problem with this paper which the author hints at (italics mine):
It turns out that there are very important unpublished data on this topic, and those data are not friendly to supporters of the movement. A very large and methodologically sound study was presented at the 2005 national meeting of the Society of Hospital Medicine. When it first came out it received a lot of attention in the blogs. DB said of the study:
California Medicine man observed:
The study was never published in any Medline indexed journal, which is why it was soon forgotten and didn’t make it into the systematic review. (There just might be a lesson here on the effect of publication bias from within our own ranks). The presentation abstract, though, was reported in the summer 2005 issue of The Hospitalist which you can access here. As far as I can tell it was the highest quality study ever done. It was a large (the second largest ever done), prospective, randomized multicenter study. It showed no difference between hospitalists and non-hospitalists in any efficiency metric or in patient outcomes.
But back to the Mayo Clinic Proceedings paper. The abstract says:
This was not a meta-analysis so we can’t do sensitivity testing. It’s not difficult to imagine, though, how the conclusion might read had the 2005 SHM study been included in the review. It would have been much more circumspect and might have gone something like this:
So if the evidence doesn’t support the present day hospitalist hype what does it tell us? I think the following:
For mortality and other patient outcomes it’s value neutral. For efficiency metrics (length of stay and charge per case) at least we know it’s not detrimental. It may be beneficial but evidence is mixed and will remain controversial.
What’s the harm in hyping the evidence? For one thing it may lead to inflated economic expectations of hospitalist groups, causing administrators to view hospitalists as business solutions. Back in the early days of my hospitalist program there was an excellent, tightly run traditional internal medicine group which admitted patients to our hospital. We compared efficiency metrics but try as we might we could not beat theirs. In measured value we offered nothing over them. Fortunately, in spite of that fact, demand for our services grew rapidly and our niche was secured. But with today’s economic woes and all the hospitalists-as-business-solutions hype I can imagine administration saying “all the studies show that hospitalists can deliver more efficient care, so why aren’t you guys more efficient than your local non-hospitalist peers?” (Now as it turns out horrible reimbursement and deteriorating professional satisfaction in general internal medicine led many of those excellent docs to look for greener pastures, often in hospital medicine, causing that internal medicine group to dissolve).
So what, other than the need to fill a growing niche, is the value of hospitalists? For me it’s largely subjective. My group members and I feel good about the work we do. Our physician colleagues in the community appreciate it, as do our hospital staff and administration. But the economic benefits, if any, of hospitalist care vary from one community to another. If your group can make a difference in your hospital’s bottom line, great. Measure it. But I’m afraid we’ll never be able to make a general evidentiary claim for the hospitalist model over any other.
The review concluded, in line with popular belief, that the hospitalist model results in improved efficiency of resource utilization. Although it will be greeted with fanfare among boosters of the model (read Happy Hospitalist’s take here) there is a big problem with this paper which the author hints at (italics mine):
Systematic reviews may be hampered by difficulties related to publication bias, in which articles are more likely to be published if they show positive findings. This limitation is not confined to this review but is a potential problem for any review. I am unaware of any unpublished data on the topic of this review. Whether to include unpublished data should be an important consideration in conducting a systematic review. Investigators need to remember, however, that bias against negative results is not the only reason why a manuscript may be unpublished; a manuscript may have any of a number of inadequacies that disqualify it from consideration for publication.
It turns out that there are very important unpublished data on this topic, and those data are not friendly to supporters of the movement. A very large and methodologically sound study was presented at the 2005 national meeting of the Society of Hospital Medicine. When it first came out it received a lot of attention in the blogs. DB said of the study:
Much of the fire behind the rapid growth of the hospitalist movement comes early studies which suggested that hospitalists made a large difference in cost and quality of care. This study suggests that we must be careful in attributing benefits. I do believe that there is a valid volume efficacy curve, but the big question is how we determine it. Having the title does not make one a better inpatient doctor.
California Medicine man observed:
Great. It was for my expertise as a hospitalist that I received my academic appointment at UCLA. I can imagine my department head at the next budget meeting. 'Now remind me, why did we hire Ford?'In fact, I'm giving a grand rounds lecture on the benefits of the hospitalist paradigm in a few weeks. I guess I can make it a very brief one. I'm reminded of Gilda Radner's line while playing character Emily Litella: "Never mind!"
The study was never published in any Medline indexed journal, which is why it was soon forgotten and didn’t make it into the systematic review. (There just might be a lesson here on the effect of publication bias from within our own ranks). The presentation abstract, though, was reported in the summer 2005 issue of The Hospitalist which you can access here. As far as I can tell it was the highest quality study ever done. It was a large (the second largest ever done), prospective, randomized multicenter study. It showed no difference between hospitalists and non-hospitalists in any efficiency metric or in patient outcomes.
But back to the Mayo Clinic Proceedings paper. The abstract says:
The reports that were included (N=33) show general agreement that hospitalist care leads to shorter length of stay and lower cost per stay.
This was not a meta-analysis so we can’t do sensitivity testing. It’s not difficult to imagine, though, how the conclusion might read had the 2005 SHM study been included in the review. It would have been much more circumspect and might have gone something like this:
Most studies comparing models of care are of low methodologic quality. Although evidence from these studies suggests reduced length of stay and charges per case attributable to the hospitalist model the only large randomized, prospective multicenter study showed no significant difference between models in any efficiency metric.
So if the evidence doesn’t support the present day hospitalist hype what does it tell us? I think the following:
For mortality and other patient outcomes it’s value neutral. For efficiency metrics (length of stay and charge per case) at least we know it’s not detrimental. It may be beneficial but evidence is mixed and will remain controversial.
What’s the harm in hyping the evidence? For one thing it may lead to inflated economic expectations of hospitalist groups, causing administrators to view hospitalists as business solutions. Back in the early days of my hospitalist program there was an excellent, tightly run traditional internal medicine group which admitted patients to our hospital. We compared efficiency metrics but try as we might we could not beat theirs. In measured value we offered nothing over them. Fortunately, in spite of that fact, demand for our services grew rapidly and our niche was secured. But with today’s economic woes and all the hospitalists-as-business-solutions hype I can imagine administration saying “all the studies show that hospitalists can deliver more efficient care, so why aren’t you guys more efficient than your local non-hospitalist peers?” (Now as it turns out horrible reimbursement and deteriorating professional satisfaction in general internal medicine led many of those excellent docs to look for greener pastures, often in hospital medicine, causing that internal medicine group to dissolve).
So what, other than the need to fill a growing niche, is the value of hospitalists? For me it’s largely subjective. My group members and I feel good about the work we do. Our physician colleagues in the community appreciate it, as do our hospital staff and administration. But the economic benefits, if any, of hospitalist care vary from one community to another. If your group can make a difference in your hospital’s bottom line, great. Measure it. But I’m afraid we’ll never be able to make a general evidentiary claim for the hospitalist model over any other.
Using a simple clinical assessment tool and CT coronary angiography
---we could send more chest painers home from the ER according to this study.
Friday, April 03, 2009
Medical textbooks are not legal documents
Say you’re a defendant in a malpractice suit giving your deposition. Plaintiff’s attorney holds up your favorite medical textbook and asks “Doctor, would you consider this an authoritative source of information in your specialty?” Answer yes if you want to help send that attorney’s kids to college.
The correct answer, as your risk management folks will tell you, is that no textbook is authoritative and that treatment must be individualized, applying the best available evidence with judgment, tailored to the patient’s individual circumstances.
Recently the editors of several leading emergency medicine textbooks made this answer official in a position statement. It opens:
The editors of the textbooks listed below strongly believe that the complex practice of medicine, the vagaries of human diseases, the unpredictability of pathologic conditions, and the functions, dysfunctions, and responses of the human body cannot be defined, explained, or rigidly categorized by any written document. It is neither the purpose nor intent of our textbooks to serve as a final authoritative source on any medical condition, treatment plan, or clinical intervention, nor should our textbooks be used to rigorously define a rigid standard of care that should be practiced by all clinicians.
The correct answer, as your risk management folks will tell you, is that no textbook is authoritative and that treatment must be individualized, applying the best available evidence with judgment, tailored to the patient’s individual circumstances.
Recently the editors of several leading emergency medicine textbooks made this answer official in a position statement. It opens:
The editors of the textbooks listed below strongly believe that the complex practice of medicine, the vagaries of human diseases, the unpredictability of pathologic conditions, and the functions, dysfunctions, and responses of the human body cannot be defined, explained, or rigidly categorized by any written document. It is neither the purpose nor intent of our textbooks to serve as a final authoritative source on any medical condition, treatment plan, or clinical intervention, nor should our textbooks be used to rigorously define a rigid standard of care that should be practiced by all clinicians.
ICU family conferences---practical aspects
Evidence suggests that certain methods of communication lead to more rational decisions and greater family satisfaction. This topic was recently reviewed in Chest.
Lay people don’t know Jack about sepsis
---according to this study:
Why is this important? Because the two most important dimensions of sepsis are time dependent: early goal directed therapy (you’ve got 6 hours or it doesn’t work) and antibiotics (mortality rises by the hour of delay).
With things like point of care lactate levels and ER protocols we’re doing better. Public awareness is another link in the chain of survival.
In Italy, Spain, the United Kingdom, France and the United States, a mean of 88% of interviewees had never heard of the term sepsis. In Germany 53% of people knew the word sepsis. In Italy, Spain, United Kingdom, France, and United States, of people who recognized the term sepsis, 58% did not recognize that sepsis is a leading cause of death.
Why is this important? Because the two most important dimensions of sepsis are time dependent: early goal directed therapy (you’ve got 6 hours or it doesn’t work) and antibiotics (mortality rises by the hour of delay).
With things like point of care lactate levels and ER protocols we’re doing better. Public awareness is another link in the chain of survival.
Thursday, April 02, 2009
ICU Medicus
The welcome message says:
Free stuff, looks promising. Access it here.
Whether you are a resident preparing for the internal medicine board examination, an internist who is keeping up with his skills or an intensivist who wants excellent teaching materials for his residents and fellows, we believe that you will enjoy and benefit from the efforts of our carefully selected, high quality educational materials.
Free stuff, looks promising. Access it here.
Hospital medicine CME
---sponsored by Johns Hopkins. There are 18 hours of offerings available so far. I haven’t examined the content in detail but the titles look promising. This stuff is pharma supported, so if you spot any bias let me know, and I’ll try and do the same.
History of a failed performance measure: perioperative beta blockers
There many reasons why the performance movement has been a train wreck. The reasons vary with different measures. For preoperative beta blockers it was a matter of policy wonks and opinion leaders taking low quality evidence beyond what it warranted. Read the story here.
The Newseum
Wednesday, April 01, 2009
Cognitive dysfunction after recovery from ARDS
---was common, mainly in the form of depression, in this study. This sort of thing is increasingly being recognized, and is one of several factors driving increased attention toward minimization of sedation during mechanical ventilation.
CT is us
This is an educational site from Johns Hopkins on CT scanning covering new advances, protocols, image interpretation and contrast issues.
Via Clinical Cases and Images blog.
Via Clinical Cases and Images blog.
Acute management of atrial fibrillation
Hospitalized patients go into a fib often. It’ll drive you crazy when you’re on call. This review in Chest is timely.
Which medical students pass out in the OR and why?
From a paper in BMC Medical Education:
Of the 630 clinical students surveyed, 77 responded with details of at least one near or actual operating theatre syncope (12%). A statistically significant gender difference
existed for syncopal/near-syncopal episodes (male 12%; female 88%), p less than 0.05. Twenty-two percent of those affected were graduate entry medical course students with the remaining 78% undergraduate. Mean age was 23-years (range 20 - 45). Of the 77 reactors, 44 (57%) reported an intention to pursue a surgical career. Of this group, 7 (9%) reported being discouraged by syncopal episodes in the operating theatre. The most prevalent contributory factors were reported as hot temperature (n= 61, 79%), prolonged standing (n=56, 73%), wearing a surgical mask (n=36, 47%) and the smell of diathermy (n=18, 23%).
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