Dr. Bobbs has written a skeptical post on EMRs, citing an AAFP blog post and the Medical Economics article I referenced here.
Although the EMR is widely touted as an important part of the solution for much of what ails health care, evidence and experience suggest it ain’t so, at least in its present state of development. The AAFP post cites a recent WSJ article by Groopman and Hartzband. It opens:
Last week, President Barack Obama convened a health-care summit in Washington to identify programs that would improve quality and restrain burgeoning costs. He stated that all his policies would be based on rigorous scientific evidence of benefit. The flagship proposal presented by the president at this gathering was the national adoption of electronic medical records -- a computer-based system that would contain every patient's clinical history, laboratory results, and treatments. This, he said, would save some $80 billion a year, safeguard against medical errors, reduce malpractice lawsuits, and greatly facilitate both preventive care and ongoing therapy of the chronically ill.
That’s generous serving of Obama Kook-Aid.
The article deserves to be read in its entirety. The authors go on to review the evidence:
A study of orthopedic surgeons, comparing handheld PDA electronic records to paper records, showed an increase in wrong and redundant diagnoses using the computer -- 48 compared to seven in the paper-based cohort…
A 2008 study published in Circulation, a premier cardiology journal, assessed the influence of electronic medical records on the quality of care of more than 15,000 patients with heart failure. It concluded that "current use of electronic health records results in little improvement in the quality of heart failure care compared with paper-based systems." Similarly, researchers from the Brigham and Women's Hospital and Harvard Medical School, with colleagues from Stanford University, published an analysis in 2007 of some 1.8 billion ambulatory care visits. These experts concluded, "As implemented, electronic health records were not associated with better quality ambulatory care." And just this past January, a group of Canadian researchers reviewed more than 3,700 published papers on the use of electronic medical records in primary care delivered in seven countries. They found no solid evidence of either benefits or drawbacks accruing to patients. This gap in knowledge, they concluded, "should be of concern to adopters, payers, and jurisdictions."
It’s worse than a gap in knowledge. It’s a complete lack of supporting evidence. Why, then, the rush for adoption?
Dr. Bobbs quotes from the Medical Economics Article:
In April 2008, a study published in the New England Journal of Medicine reported similar problems, pointing out that “Notes that are meant to be focused and selective have become voluminous and templated, distracting from the key cognitive work of providing care. Such charts may satisfy the demands of third-party payers, but they are the product of a word processor, not of physicians’ thoughtful review and analysis. They may be ‘efficient’ for the purpose of documentation but not for creative clinical thinking.”
The study also reported an example of the consequences of these problems: “A colleague at a major cancer center that recently switched to electronic medical records said that chart review during rounds has become nearly worthless. He bemoaned the vain search through meaningless repetition in multiple notes for the single line that represented a new development . . .
That came from this NEJM perspective piece by Groopman and Hartzband. I think “pimp my note" may be appropriate here to refer to electronically generated documentation that looks fancy and is long on text but devoid of substance. (In reference to the MTV show Pimp My Ride in which a car in poor condition gets a fancy make over which is mainly cosmetic, with little attention to the engine and other essentials).
It’s been over 16 years since the notion of EBM was popularized. You’d think in those 16 years we’d have come a long way. What once took an entire afternoon to find in the archives of a traditional print library (remember the Index Medicus?) can now be accessed in mere moments on line. Yet, the penetration of best evidence into clinical practice remains low, ranging from 10% to 50% in surveys. In spite of all the progress we’ve made there remain barriers.
In the February 15 installment of American Family Physician’s series on this topic Mark H. Ebell, MD, MS discusses some of these barriers. One of the most important barriers, he says, in spite of the improved speed that internet technology has delivered, is still time. Filtered resources (secondary sources) help save time by removing from the end user the steps of searching and critical appraisal. That’s a mixed blessing. In some situations there’s no substitute for searching and critically appraising the primary sources. Over reliance on secondary sources may lead to a loss of these skills. Secondary sources vary in quality and some are very expensive. It’s a work in progress.
Some of the barriers, Ebell points out, are cultural. One cultural barrier he didn’t mention is that of patients’ perceptions (or misperceptions) about searching for answers at the point of care. Some patients admire and respect the doctor who goes to the trouble to look up answers. Others, thinking that doctors should “know it all”, may look askance. Doctors should be concerned about patients’ perceptions. Should they look up answers in front of the patient or should they leave the room?
Perhaps the ultimate advance to help improve penetration of evidence into practice is the embedding of best evidence pathways into computerized physician order entry systems. This technology is in its infancy.
A major downside to all these advances is that they de-emphasize background reading, pathophysiologic rationale, critical appraisal and judgment. Sixteen years after the launch of the EBM movement our biggest challenge moving forward is to increase the application of EBM to everyday practice without diminishing the physician’s role.
OASIS-5 showed fondaparinux (Arixtra) to be non-inferior in efficacy to enoxaparin (Lovenox) and to be associated with a decreased risk of bleeding in the treatment of unstable angina and NSTEMI. A new study in the American Heart Journal confirms these observations.
Fondaparinux has some unique risks but seems to cause less bleeding when used in the treatment of ACS. The findings cannot be extrapolated to the treatment VTE, in which higher doses of fondaparinux are used.
The greater ease, compared to older insulins, in the implementation of basal/bolus regimens, is appealing. According to this meta-analysis, though, the benefits in terms of HbA1C levels were modest and of questionable clinical significance.
This analysis in the same issue of CMAJ looked at cost effectiveness and found that among short and long acting insulin analogues for type 1 and type 2 diabetes only the short acting analogues for type 1 diabetes were cost effective.
· The improved glycemic control, reduced risk of hypoglycemia and improved quality of life achieved with insulin analogues versus conventional insulins are at best minor and of clinically debatable relevance. · Insulin analogues should be reserved for use in selected patients, such as those with nocturnal hypoglycemia. · Efforts should be focused on offering structured educational programs to help patients manage their diabetes and improve glycemic control.
Many patients receive their initial diagnosis of diabetes during hospitalization. Basal/bolus regimens are started in such patients in order to maintain inpatient glycemic control. Protocols and order sets for glycemic control tend to favor insulin analogues. Newly diagnosed diabetics are often discharged on insulin analogues as a continuation of their hospital regimens, and because basal/bolus treatment is easier to understand and teach using analogues. The down side is that for patients with limited financial resources such a regimen may be a recipe for “noncompliance.”
These papers will cause me to rethink my discharge planning for newly diagnosed diabetics, particularly those with limited finances.
In issue 1 of 2009 the journal American Family Physician launched a series on the application of evidence based medicine: how to put best evidence into practice. (I don’t know why I bothered to link to the issue. In a reversal of today’s trend towards open access publication AFP has recently gone from open access to controlled access. Worse yet, you can’t even view the table of contents on line, let alone the abstracts. You can access the content if you are a member of AAFP, you have your own subscription, you or your hospital library has access to the MD Consult Core Collection or you get your own “throw away” copy in the mail).
Traditional teaching on EBM held that doctors should do PubMed searches to find answers to clinical questions. Because PubMed is cumbersome and time consuming for unskilled users, recent trends favor filtered resources or, as the writer of the introductory editorial calls them, secondary literature:
There is a rich body of literature advising physicians on how to ask and answer questions. Too often, though, it has encouraged physicians to focus on PubMed searches and the original research literature, a time–consuming and sometimes frustrating process. This is not unlike trying to encourage people to use e–mail and the Internet by teaching them how to write Javascript code, or encouraging people to bake bread but forcing them to grow their own wheat. Hardly a recipe for success!
Family physicians are busier than ever and have limited time to keep current with the literature. Reading lengthy and detailed original research studies is hardly the best use of that time. Practicing physicians, and even most academic physicians, do not have the training or time to critically appraise all of the articles needed to answer clinical questions or stay current.
I propose a different skill set that prioritizes making the practicing family physician an informed consumer of the secondary literature (e.g., evidence–based guidelines, systematic reviews, critical appraisals, validated decision–support tools).
I only partially agree. While secondary sources are indispensable, there are situations where there’s no substitute for the primary source. And while some secondary sources like UptoDate have the advantage of greater speed, PubMed can be used very efficiently with a little training and practice.
While this series is directed toward family physicians the information should be useful to general internists and hospitalists as well. If time constraints and lack of computer searching skills are barriers to the application of EBM this series should help. I’ll be commenting on various installments in future posts.
This small series was published in Mayo Clinic Proceedings:
Most patients aged 90 years or older who received intravenous tPA for acute ischemic stroke had poor 30-day functional outcomes or died. Intravenous tPA treatment in this age group does not improve the outcome of ischemic stroke.
The first piece, by Alan M. Garber, M.D., Ph.D., and Sean R. Tunis, M.D., addresses concerns by some groups that CER could impede the progress of individualized medicine if it drives a one size fits all approach. I view genomic medicine the way I view the electronic medical record. I believe it is the wave of the future but it may be decades before the science matures enough for it to be clinically useful on a broad scale. I agree with the authors that it’s difficult to know the impact of genomic medicine in any given time frame and even more difficult to know the impact of CER on genomic medicine. The Partnership to Improve Patient Care (PIPC), cited by the authors, expresses concern and skepticism but is not opposed to CER. Their web site says:
Used appropriately, comparative effectiveness research can play a valuable role in supporting good decision-making in health care. Moreover, improved quality is the best path to greater health care affordability….
While CER can play a positive role in improving patient care and health care delivery, it also can be misapplied in ways that unintentionally undermine patient access to care and physician-patient decision-making.
That's because comparative effectiveness research results typically are based on broad population averages that don't reflect the differences in needs of individual patients. Any research results need to be considered along with the broader body of evidence, the patient's individual needs and preferences, and the physician's clinical expertise.
That last statement (italics mine) merely urges the application of one of the fundamental principles of EBM (it’s straight out of David Sackett’s definition) to the findings of CER. The drug and device companies, who have been accused of opposing CER, are key players in PIPC. Clearly there’s no opposition to CER there.
The next piece, by Jerry Avorn, M.D., accuses skeptics of mounting a “vigorous and well-coordinated backlash” against CER. The problem is that the skeptics he cites, including Betsy McCaughey and Rush Limbaugh, were objecting to a hidden agenda in the stimulus package to increase government control over health care. That debate had nothing to do with CER. The whole piece was a straw man attack against legitimate skepticism towards the government’s plan for health care.
Aanand D. Naik, M.D., and Laura A. Petersen, M.D., M.P.H. discuss the problem of poor translation of evidence into practice and cite tools developed by the VA and AHRQ.
Finally, Daniel Carlat weighs in on the NEJM pieces and adds to the confusion in a post here by, again, suggesting there’s opposition to CER when in fact no such opposition exists. I have tried to read extensively about CER. In my reading, while I’ve encountered lively debate and opposition to Obama’s political agenda for health care I’ve yet to read any opposition to the pure notion of comparative effectiveness research. We all seem to agree it’s worthwhile.
First a link to Medscape’s Alert Center. It looks like a pretty good resource and features some interesting video blogs, most notably by John Bartlett, “the bomb” when it comes to emerging infectious diseases.
Now a word or two about the name. Apparently it’s now officially Influenza A H1N1. Swine flu was unsatisfactory because of the mistaken reference to the 1976 scare. Not the same bug. But Influenza A H1N1 seems even worse because not only the 1976 Swine flu but also the 1918 flu were H1N1 strains. In fact, Influenza A H1N1 signifies nothing. Why not a geographic name such as the three previous pandemics were given? The 1918 pandemic was called Spanish flu (which didn’t originate in Spain, BTW); the 1957 pandemic was named Asian flu; the 1968 pandemic was Hong Kong flu. H1N1 is not very informative but, as Dr. Bartlett suggests in one of his video blogs, at least it's politically correct.
First some definitions. Diastolic heart failure is the syndrome of heart failure due to impaired left ventricular filling in the context of a normal or near normal ejection fraction. Recently the term has been used interchangeably with “heart failure with preserved ejection fraction “(HFPEF). Such usage is not always appropriate, since some syndromes of HFPEF may be due to valvular dysfunction or systemic disease and need not involve diastolic dysfunction. (Personal observation: virtually all patients presenting to the hospital with acute decompensated heart failure have diastolic dysfunction and many have coexisting systolic dysfunction).
Key points from the article:
A vast body of evidence is available to guide treatment of systolic dysfunction. This is not true for diastolic dysfunction.
The evidence summary for pharmacologic therapies in the long term management of diastolic heart failure cited in the CMAJ review is shown here. Not impressive.
Guidelines for management, then, have been based largely on expert opinion and pathophysiologic rationale. They emphasize treatment of comorbidities and are summarized here. (Here’s an important JAMA paper emphasizing treatment of comorbidities in patients with HFPEF).
Though not exactly his ideological twin I agree with a lot of what Dr. Rich has to say and would consider myself among his camp of “classical liberals” (go and read carefully what he means by that term before you draw any conclusions). Dr. Rich’s writings reflect considerable insight and skepticism of simplistic ideas about medicine and health care. So I’m a little surprised to find him arguing for CER. My problem with this is that the need for such an argument presupposes opposition to CER. Dr. Rich writes:
And now, despite the fact that it will further alienate many of those who might otherwise be his conservative brethren, DrRich formally endorses Comparative Effectiveness Research (CER).
Conservatives, everyone must know by now, have taken a formal position on CER - they’re against it.
OK, stop. Where are these people, conservatives or those of any ilk, who have taken a position against CER? Dr. Rich cites groups who are skeptical and very concerned about the new political agenda for CER, not CER itself. The popular claim that there’s all this opposition to CER seems like a straw man argument to me.
If all these folks are against CER per se why their silence up to now, about the large amount of CER we’ve already had for decades? Those who claim that doctors have no research evidence upon which to draw to decide which treatments are best for their patients are either disingenuous, extremely cynical or just plain ignorant. (I don’t accuse Dr. Rich of taking that position, by the way).
I am a hospitalist and respect outpatient internists and family practitioners too much to consider myself as noble as them. But I am an internist and today, a pain management specialist paged me for a consult, I mean, comanagement, I mean, “take care of all the paperwork under the guise of controlling her already under control chronic illnesses”.
DB tells of another hospitalist who had to do some job hopping before he found professional satisfaction:
At Internal Medicine 2009, I ran into a former resident (from the 1980s when I was a program director.) I asked him about his career, and he told me of 15 years in private practice. He then left to become a hospitalist. He is finally happy in his 3rd hospitalist job.
These stories illustrate problems in the hospitalist movement which I’ve written about many times before. Here are the main points:
The original appeal of hospital medicine was that it was an opportunity for a clinician to focus on and ascend the unique clinical learning curve of hospital based internal medicine.
But because the role has not been carefully defined it is morphing into that of a jack-of-all-trades house doctor, a career few of us signed up for.
Uncritical enthusiasm for some nebulous notion of “comanagement” has blurred the boundaries of responsibility among hospitalists and other specialists and forced hospitalists into clinical encounters way beyond the scope of their training, pushing them out of their comfort zones and creating liability concerns.
Under the rubric of comanagement some hospitalist programs are being made to function as H&P and discharge planning services in which they perform the clerical scut work on surgical and subspecialty patients who have no need of their clinical expertise.
Hospitalists are increasingly coming to be viewed as administrative and business solutions more than clinicians. Not exactly what a candidate looks for in a career.
These factors may increase the risk of burnout, increase turnover in hospitalist programs and exacerbate the shortage in the work force.
Given this climate candidates who seek hospitalist jobs are increasingly likely to be short timers---docs who are moonlighting, are between jobs or are waiting to grab a fellowship.
DB goes on to say:
I have cautioned frequently in essays that the title does not define the job. I know of outstanding hospitalist jobs, and I know of jobs that represent semi-advanced resident positions.
Indeed. If you’re looking at hospitalist jobs ask tough questions. Find out what comanagement really means in the program you’re considering. In today’s market you can be picky. There are some good programs out there that will provide you with professional satisfaction. And there are some that will burn you out.
He concludes with:
Internists tend to say yes. We become the "least common denominator" for patient care - we get the patients who others "refuse." We are the nice guys and gals.
The best hospitalist programs set clear limits on their responsibilities. As hospital medicine evolves, it needs strong leadership based upon sound principles.
Does hospital medicine have the leadership it needs to address these issues? Hospital Medicine 2009, our national meeting, is about to start. We’ll see what our leaders have to say. If Hospital Medicine 2008 is any indication I’m not optimistic.
The laundry list of precautions to take starts with things which, if not evidence based, are at least plausible---get plenty of rest, stay away from hospitals and doctors’ offices if you can---then devolves into total woo: reflexology, tapping (especially those critical areas between certain chakras), homeopathy and various Yoga techniques.
She even offers some of the “mechanisms” of the Yoga postures:
Halasana - all plough variations - massages the internal organs, stimulates the spinal nerves and brings increased blood supply in the region, nourishing many essential internal organs
Pashimottanasana…stimulates and tones the digestive organs and detoxifies the body
Sarvangasana - Shoulder Stand -As the chin presses on the throat it brings a rich blood supply, the thyroid gland is massaged and brought to its proper level of activity,…
Bhujangasana - baby cobra and all cobra variations, the arching of the spine stimulates the thymus gland and boosts the immunity of the body,…
Sirsasana - Headstand - reverses the flow of gravity, allows the hypothalamus to secrete hormones and stimulates total glandular secretion, boosts the immunity by catalyzing the thymus gland functions
Ustrasana - Camel - opens the heart, expands the lung capacity and stimulates the thymus gland,…
(Digression: I have been smacked down, here and elsewhere, for my characterization of the religious and pseudoscientific underpinnings of Yoga with the rejoinder “Hey, lighten up, it’s just relaxation, stretching and balance exercise.” Almost all the explanations of Yoga I come across contain language like that above. It’s total woo).
The common thread in these remedies is the claim that they “boost the immune system.” Now, given that immunity exists on many levels, comprising diverse mechanisms and effector elements, any simple mention of an “immune system” can pretty nebulous. So what do the woosters really mean (assuming they even know what they mean) when they talk about the immune system? They must mean innate immunity rather than adaptive immunity because the former is the only type you could “boost” in a non-specific way absent vaccines or prior infection. But, given that it’s probably those innate immune mechanisms which caused the cytokine storm purported to make the 1918 pandemic so lethal in young healthy individuals I’m not sure I even want to boost my immune system in a non-specific manner!
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.
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:
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.
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.
DB was recently blogging from the ACP national meeting. His post on the keynote, about comparative effectiveness research (CER), opens with:
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.
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:
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.
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.
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.
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:
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.
Recently I’ve posted a couple of anecdotalreports 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:
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.
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.
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:
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.
---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.
---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.
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:
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.
---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.
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.
---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.
Not every one, according to Robert D. Glatter, MD in a Medscape Ask the Experts piece:
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.
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.
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.
---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.
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.
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.
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:
…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.
An important study recently published in NEJM examined Medicare hospital readmission rates. You can read Bob Wachter’s take here. Among the findings:
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.
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.
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.
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.
---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:
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 adverseeffects.
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.
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:
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).
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.
Here’s a concerning small study from Critical Care Medicine:
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.
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.
Two patients come in with stroke and an LDLC of 100. One patient got there with the help of a statin. The other by diet, exercise or genetics. Which one is better off?
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.
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.
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:
1363 is still too many citations. Additional strategies will be explored in future posts.
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.
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.
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.
