Thursday, March 29, 2007
In brief, the February 13 issue of JACC contains this report of a randomized double blind trial of nesiritide after coronary artery bypass in patients with left ventricular systolic dysfunction, showing that nesiritide was associated with improved renal function, decreased length of stay and lower 180 day mortality.
This meta-analysis from American Heart Journal (posted on Medscape February 7), arguably methodologically stronger than the aforementioned JAMA meta-analysis, showed no difference in mortality between nesiritide and comparison groups in 7 studies. For an analysis of the strengths and weaknesses of the two meta-analyses read the discussion section of the American Heart Journal paper particularly in reference to the heavier use of inotropes in the neseritide treated patients in the JAMA paper. (It’s well known that inotropes increase mortality in heart failure).
I’m lukewarm on neseritide and there are enough remaining questions about its efficacy and safety to keep it off the front line, at least for now. For acute cardiogenic pulmonary edema I prefer an approach utilizing nitroglycerine, loop diuretics and CPAP or NPPV. (A randomized controlled trial of nesiritide to evaluate for mortality, renal function and cost effectiveness will begin this year).
Wednesday, March 28, 2007
Monday, March 26, 2007
The post in question, in essence, applauded the new IDSA guidelines and suggested that Lyme disease can be quack fodder. Why quack fodder? Diagnostic guidelines from the International Lyme and Associated Disease Society, recently cited by Dinosaur, allow a diagnosis of “chronic Lyme disease” in the absence of any abnormal physical or laboratory findings. And the symptoms on which the diagnosis can be made are vague, overlapping sufficiently with other diseases or even the normal population to be meaningless. So, you have statements like this: Available data suggest that objective evidence alone is inadequate to make treatment decisions, because a significant number of chronic Lyme disease cases may occur in symptomatic patients without objective features on examination or confirmatory laboratory testing. Well, in the absence of objective findings how do we know those patients have Lyme disease in the first place?
That’s just another way of saying the diagnosis of chronic Lyme disease is subjective, isn’t it? That’s why it’s potential quack fodder. Any patient with vague symptoms can be declared to have chronic Lyme disease and be subjected to all sorts of woo.
The Infectious Disease Society of America (IDSA) recognizes that there are some patients who “remain unwell” following completion of standard courses of antibiotic treatment for Lyme disease. I’m willing to reserve judgment about such patients, currently the subject of randomized controlled trials. I will not summarily dismiss the notion of chronic Lyme disease as long as it is under investigation. Unfortunately such patients, until the condition is better defined, are all too vulnerable to the purveyors of woo.
Sunday, March 25, 2007
Sir Godfrey Hounsfield, whose BMJ obit is here, worked as an engineer for EMI and was the inventor of the CT scan (PubMed citation here). According to this article from Whittington Hospital: Having sold 200 million of the Fab Four’s singles, (at seven inches, almost enough vinyl to stretch the length of the equator) the Beatles’ record company, EMI, was able to fund Hounsfield to do his research and the scanner was ready be used in hospitals in the 1970’s.
Image source: The Library of Congress
Thursday, March 22, 2007
So what’s happened in the ensuing year? CMAJ is still doing very well, thank you. If the journal is indeed on life support you wouldn’t know it from this optimistic piece featuring the new Editor-in-Chief. And the new journal? It has a web site and a title but no content.
Tuesday, March 20, 2007
A more recent example is the pro-motility drug cisapride (Propulsid, or Prepulsid in Canada) withdrawn from the market a few months after a well publicized case of fatal cardiac arrhythmia (presumably torsade de pointes) despite the fact that the drug was being taken against product labeling. As reviewed in this article form CMAJ Johnson and Johnson, facing huge lawsuits regarding adverse cisapride related events, contended that physicians improperly used the drug. That contention was evidence based (as it is for many drugs); nevertheless, the company settled for $90 million.
Now cisapride’s in the news again as a class action suit gets underway against Canada’s Johnson and Johnson subsidiary. Again the company maintains, correctly, I believe, that “the drug ‘is a safe and effective medicine when prescribed appropriately.’" But, doctors, worry not. They’ll settle.
I wrote about this very problem in our fourth Medscape Roundtable Discussion on how to stay current on prescription drugs. So, doctors, it ain’t rocket science. Just read the product labeling. (If you got your copy of the product labeling from a drug rep be sure and wash your hands 10 times after handling).
DB’s Medical Rants – thought provoking discussions on teaching, learning and health policy.
Retired Doc – critical discussions of issues in Internal Medicine which often challenge popular simplistic assumptions.
Orac – incisive criticism of pseudoscientific woo---and some really funny stuff.
Kevin MD – something intriguing just about every day. How does he do it?
Clinical Cases and Images – a great repository of Web based resources that challenge me on my quest of lifelong learning.
OK, consider yourself tagged. You know the drill.
Sunday, March 18, 2007
It’s an important clinical lesson (always think of coarct when you’re looking for secondary hypertension) but there’s a little something wrong with this story. Either the NYT account is simplistic or the folks at Yale made some sophomoric mistakes. (I suspect the former).
When I read a story like this I’m in the “quiz mode.” It’s different in the hectic, mind numbing, day to day clinical world. But it’s not rocket science to check for radiofemoral delay and take upper and lower extremity blood pressures. It’s hypertension 101 to perform these maneuvers and think of coarctation. And this was a specialty clinic. Equally strange is that she had had all these tests including rennin profiling, magnetic resonance imaging and angiography before getting a simple echo.
I can hardly imagine this happened at Yale’s hypertension clinic. Did the New York Times feel the need to dumb the presentation down for the lay public?
Now that timeline, showing methadone deaths to rise 7 times faster than all poison deaths, is an interesting one. It speaks volumes. A Substance Abuse and Mental Health Services Administration report concluded that it reflects increased use of methadone as a prescription analgesic rather than a treatment for opiate addiction.
1999 was about the time pain management became politicized and activists were beating up on doctors for under treating pain. They pummeled us with arguments based 90% on dogma and 10% on science. They told us that the patient’s numeric rating of pain was “the fifth vital sign.” They redefined the concept of addiction to suit their agenda and told us that most instances of drug seeking behavior were in fact “pseudo addiction”, supposedly an indication to give more narcotics. A stable patient verbalizing “eight out of ten” pain was a medical emergency and a mandate for narcotics. Respiratory hazards were downplayed.
Around the time Joint Commission launched their pain initiative they held a panel discussion with Q&A. A pulmonologist asked “Aren’t you concerned about an increased incidence of respiratory depression?” The panel’s answer was, in effect, “It’s your problem. Your hospital needs to draft policies and procedures for respiratory assessment.”
Methadone seemed appealing for chronic pain management because it was cheap and its pharmacokinetic profile was thought to limit its abuse potential. Now we’re seeing the consequences of our zeal. True, not many years ago we under treated pain, but the pendulum has swung too far.
Many of us anticipated respiratory deaths from methadone, but the problem of cardiotoxicity was below the radar screen until the drug began enjoying heavy use as an analgesic.
Methadone’s proarrhythmic effects reviewed.
Methadone’s new FDA warning.
Methadone and the death of Anna Nicole Smith’s son.
Friday, March 16, 2007
Everyone remembers the fabled BMJ paper demonstrating how Google helped lead doctors to the correct NEJM case record diagnosis in 15 of 26 cases. As interesting as that is one has to ask how it would compare with other on line differential diagnosis resources such as Isabel or Dxplain.
Dr. Eamon Armstrong, a teacher of EBM, expressed concern about the imprecision of Google and noted “’I can't think of a single person in the EBM field who would use Google on a regular basis.’”
The article drew my attention to one Google enhancement I hadn’t noted before which is the category links at the top of the results page. (This may be under development, as I found the feature for some, but not all medical searches I tried). A search of Brugada syndrome, for example, yielded this page displaying the first of 261,000 hits.
That’s too large a number to be very useful, but by using the category links at the top you can narrow the search. Clicking on “for health professionals” narrows the results down to a more manageable 386 hits.
Also note that the health professionals page provides additional categories of interest to doctors such as “CME” and “practice guidelines.”
Still, it’s imprecise. Because you never know exactly what you’re getting or how the results are chosen Google can never be better than “pretty darn good” as termed by internist and Google product manager Roni Zeiger. Because Google’s searching methods are proprietary there’s a lack of transparency, and although there are books written about numerous “hacks” you never quite know. There’s always something dark and mysterious about Google.
That’s why for more scholarly work or any search which needs to be exhaustive (e.g., has this or that type of case ever been reported in the world’s literature?) Pub Med is better. Pub Med, like Google, is powerful. But unlike Google there are no Pub Med secrets, so no hacks are necessary. It’s all out in the open and if you’re among the Pub Med uninitiated you can take their tutorial which will teach you formal search strategies. If you haven’t taken the tutorial you can still enter a simple free text search. Although that sacrifices searching power you can still know exactly what you got and how by viewing the strategy Pub Med used to retrieve your results. That’s done by clicking the details tab. Search results using the free text search syncope in patients with brugada syndrome are shown here. (I would not recommend this sloppy search statement for actual use of Pub Med but is it illustrative of how it works).
Clicking the details tab reveals what search strategy Pub Med actually used to get the results.So which search engine is best? It depends on your objectives. Google doesn’t offer the precision of Pub Med but there are advantages, such as ability to search blogs, Wikis and emedicine. The two search engines are best viewed as complementary.
At the Cleveland Clinic Heart-Brain Summitt Gordon Ewy, M.D., Chief of Cardiology at the University of Arizona College of Medicine and expert on resuscitation spoke on CPR and the 2005 AHA and ILCOR guidelines and made this statement: “An important reason for these continued poor outcomes is that both sets of guidelines, despite being updated in 2005, recommend an approach to out-of hospital cardiac arrest that is far from optimal.”
Ewy and his colleagues in Tucson have been telling us for years that our approach to CPR is fundamentally wrong. I first cited the evidence here and made follow up posts here and here. Simply put, the Arizona investigators recommend elimination of rescue breathing for adult out of hospital cardiac arrest (unless circumstances such as drowning or choking indicate a respiratory cause) and, for unwitnessed arrest, emphasize compressions rather than AED protocols as the initial modality of treatment. These new procedures have been implemented in public education programs and EMT protocols in Tucson. Ewy’s presentation summarizes and updates the evidence and is an excellent review of the topic.
Sometimes the wheels of EBM turn too slowly. The 2005 guideline authors, dutifully and painstakingly trying to be “evidence based”, largely ignored this evidence because it didn’t meet the EBM standard of randomized clinical trials. Nevertheless, the evidence is compelling, and subsequent studies continue to show marked survival improvement when the new protocols are used. I discussed this topic as an example of a failing of evidence based medicine in the last Medscape Roundtable Discussion on EBM.
Thursday, March 15, 2007
I’m not surprised by the decline in procedures but I found the ABIM editorial’s recommendations odd concerning what procedures general internists should be able to do versus merely talk about. I appreciate the comments by letter writer and Annals Associate Editor Michael LaCombe, who decries the committee approach to procedural competencies and calls for research on what procedures general internists should be trained to do. He concludes (italics mine) “Finally, a caveat to you young students out there: if such research is not funded, if this profound question is not answered by funded clinical research, if the question is sent to committee and therefore to certain death, continue to avoid general internal medicine at all costs, as you have been.”
Wednesday, March 14, 2007
Tuesday, March 13, 2007
The Cleveland Clinic Journal of Medicine recently published the Proceedings of its Brain-Heart Summit. Cleveland Clinic’s heart-brain institute bears the name of Earl and Doris Bakken. Earl Bakken is the founder of Medtronic and is credited with development of the first wearable (a precursor to implantable) artificial pacemaker. Bakken co-authored the introduction.
Bakken also gave some opening remarks which, let’s hope, won’t define the focus of the brain-heart institute. Here are a few:
The mind is not in the brain. The mind is throughout the whole body and external to the body.
The sun and the moon have great impact on the function of parts of our body, including the heart and brain.
There are important roles for Ho`oponopono and naturopathic, homeopathic,
chiropractic, and blended medicine.
Energy medicine has an important role: reiki, chi gong, guided imagery, massage, taichi, yoga,healing touch, prayer, aloha.
(One has to wonder if Baaken, like Linus Pauling, is another example of a brilliant mind and humanitarian turned to the dark side).
But I digress. There was some good stuff presented.
Dr. Martin Samuels, Neurologist-in-Chief at Brigham and Women’s Hospital, reviewed the field of neurocardiology. The spectrum of neurocardiac conditions encompasses electrocardiographic abnormalities (e.g. cerebral T waves), segmental disease (takotsubo cardiomyopathy) and sudden death. The common denominator is catecholamine cardiotoxicity producing a characteristic histologic lesion known as contraction band necrosis, aka coagulative myocytolysis. This lesion is to be distinguished from coagulation necrosis which is the lesion of myocardial infarction.
The most dramatic example of neurocardiac toxicity is death following an intense emotional experience, sometimes termed “Voodoo death.” The degree of fright necessary to induce a fatal autonomic storm cannot ethically be induced in the laboratory, limiting researchers’ ability to test the model for neurocardiac death. Anecdotal evidence from antiquity to modern times, however, can be found in literature, anthropology research, medical journals and even the popular media (was neurocardiac toxicity the precipitating cause of Ken Lay’s death?). The evidence is compelling, and animal experiments coupled with observations of human cases, along with the help of some “experiments of nature” such as earthquakes and pheochromocytoma, have enabled scientists to better understand the neurocardiac pathway (which begins in the insular cortex) and gain some understanding of the biochemical mechanisms.
Some of the pioneering work on the model, as cited, for example, here, here, here, here, and here was done by Dr. Robert Eliot. His early interest in this problem was spurred by field observations on aerospace workers at NASA at the height of the space race. These engineers, who were under extreme occupational stress, suffered an increased rate of sudden cardiac death despite their youth and an absence of traditional cardiac risk factors. At autopsy contraction band necrosis was found much more frequently than coronary atherosclerosis. Eliot, who devoted much of his career to stress management as a means of reducing cardiovascular risk, was fond of saying “The brain talks to the body. The body talks back. Sometimes it’s a fatal conversation.”
Dr. Ilan S. Wittstein of the division of Cardiology at Johns Hopkins elaborated on one of the clinical forms of neurocardiac disease, takotsubo cardiomyopathy. This condition has, until recently, been mistaken for acute myocardial infarction and currently has several other names including stress cardiomyopathy, broken heart syndrome and transient LV apical ballooning. Patients most commonly present with chest pain and/or dyspnea following severe emotional stress. Pulmonary edema and cardiogenic shock may be present. Cardiac imaging reveals a peculiar apical wall motion abnormality which does not conform to a vascular territory. The name takotsubo derives from this characteristic pattern of apical ballooning despite preserved function of the basilar segments which gives the left ventricle the appearance of a takotsubo, a Japanese octopus trapping pot with a narrow neck. Although ECG changes which can be mistaken for ischemia as well as troponin leak often accompany the syndrome, myocardial ischemia is not the principal mechanism, with many patients being free of demonstrable coronary disease. Recovery in several weeks is the rule. Although there has been some controversy as to the mechanism of this syndrome, endomyocardial biopsies have revealed that the lesion is contraction band necrosis, thus warranting inclusion of takotsubo cardiomyopathy in the spectrum of neurocardiac disease.
Dr. Stephen Oppenheimer discussed in greater detail the role of the insular cortex in neurocardiac disease, noting that left insular strokes are associated with adverse cardiovascular outcomes.
This presentation deals with sudden unexpected death in epilepsy (SUDEP). Although some cases have a neurocardiac etiology, multiple mechanisms including neurogenic pulmonary edema and central apnea may be at play. It is worth remembering that cardiac channelopathies such as Brugada syndrome have been mistaken for epilepsy.
Dr. Cathy A. Sila discussed the strong association of heart failure and cognitive impairment due to multiple mechanisms. (AKA cardiac encephalopathy).
Brain-body medicine has biologic plausibility. But, because of the complex systems and unique methodologic issues that exist it is a popular form of quack fodder. In discussing this fascinating field we must be careful to make the difficult distinctions between science and pseudoscience.
Monday, March 12, 2007
Although the ethics of hospital and physician practice advertising are, to say the least, problematic, the practice is widespread---every bit as widespread as pharmaceutical company advertising. And let’s face it: many of the outreach and “educational” programs put on by hospitals are little more than promotional events.
This survey from Archives of Internal Medicine a couple of years ago (cited in Oxman’s article) looked at the 17 “America’s Best Hospitals” and concluded “Advertising to attract patients is common among top academic medical centers but is not subjected to the oversight standard for clinical research. Many of the ads seemed to place the interests of the medical center before the interests of the patients.” All but one of the institutions advertised. Commonly the ads appealed to patients’ emotions or emphasized institutional prestige. Over half mentioned a symptom or a disease and many offered introductory free or discounted services.
In other words, the investigators found evidence of conflicts of interest, disease promotion (or what some might call “medicalization”), non-evidence based claims and free “samples.” Does this sound familiar at all? Isn’t it interesting how doctors rail about pharmaceutical ads while remaining silent about the equally pervasive and questionable promotions coming from their own practices and institutions? Our profession’s ethical stance on this issue is disingenuous. We have no credibility in criticizing DTC advertising until we put our own house in order.
Sunday, March 11, 2007
I was taken to task on the one hand for listing all the things Internal Medicine is not without addressing what it is, and on the other hand for claiming that Internal Medicine is everything Family Practice is, only better. One would think I was talking out of both sides of my mouth.
Emmy commented “OK, well you have told us what Internal Medicine doctors are not. Would you now tell us what they are? Because I'm kind of confused. You see, I go to an Internal Medicine doctor as my primary care physician, and if that's not her role then I can't see what else her practice would be described as.“ A broad range of adult problems comprises Internal Medicine. Internists do in fact practice primary care when it is defined as that care which is given by the first doctor the patient sees for a problem. But I agree with DB that the term has been hijacked by so many people with agendas that it has become meaningless. It’s not useful in defining Internal Medicine as a specialty. While Internal Medicine and Family Practice are overlapping circles in a Venn diagram there is a difference in focus and there are distinctions.
Internal Medicine and Family Practice are overlapping, though not identical, specialties. There are problems (and I’m not just referring to Ob/Gyn and Peds) in the realm of expertise of Family Practice for which internists are not particularly well trained and vice versa. As I once explained, Internal Medicine stresses the care of patients with multiple complex problems. As DB said in his postulates internists have more training in the care of severely ill patients. Internists are (or should be!) uniquely, more than other specialists, interested in the basic scientific underpinnings---the how and why---of both normal function and disease. (Note that the word “internal” is apt here).
This concept of multiple complex medical problems as a defining attribute of the Internal Medicine patient is evidently difficult for some, but Emmy of all people should understand. Just look at her profile. (Emmy, by all means, stick with your internist!).
Some medical students read my blog and commented over at the Student Doctor Network Forum. Their comments suggest that they too misunderstand what general IM is supposed to be:
I suppose if the public expects you to act like a family physician, it only makes sense to train as one.
…the people who don't go on to fellowships will have a hard time.
There is nothing that IM covers that there is not a specialty for (Intensive Care, Pulmonology, Cardiology... etc etc etc) so how can you call them a specialty.
Why? They can be hospitalists...
Wow. No wonder it’s difficult to get students to choose general Internal Medicine.
Friday, March 09, 2007
Why these disappointing results? One reason may be that the advantages of the model are neutralized by its weakest point: discontinuity between hospital and ambulatory care. The problem was highlighted by a recent JAMA review documenting poor information transfer between hospital and ambulatory physicians at hospital discharge. Discharge summaries were available to clinic physicians at the time of the first follow up visit at a disturbingly low rate and often lacked critical information about medications, follow up needs and test results.
The authors note the potential adverse impact on patient safety and resource utilization. They suggest standards for quality and timeliness of discharge summaries as well as the use of templates and computer generated summaries. Somehow I’m not sure that will be enough. Such measures have been in place for a while. My suggestion is for a hospitalist group to hire a liaison who would be responsible for filling in the communication gaps. This person could call patients after discharge to make sure instructions were properly communicated, call PCPs to make sure vital information was received and track down missing documents. In busy hospitalist programs it would be a full time job for a nurse case manager or could be part of the responsibility of a physician extender. As far as I know this approach is not yet evidence based and could be studied. It could potentially improve efficiency and outcomes. Its impact on patient and referring physician satisfaction would be a no brainer.
Whatever the solution, I expect this to be a major initiative for the Society of Hospital Medicine. Hospitalist thought leader Robert Wachter, interviewed last summer by Internal Medicine World Report, said communication was key, and the quality of communication is an attribute that separates good hospitalist programs from bad ones.
Background: Retired Doc and DB comment.
Thursday, March 01, 2007
The hypertension section, largely off topic with its focus on an anecdote about a former Seattle Times reporter who was placed on an ACE inhibitor and experienced a frightening episode of angioedema, accused the JNC-7 panel of designating a systolic blood pressure of 120 as “unsafe”. Although the panel cited evidence that with lower and lower blood pressures there is a continuum of decreasing cardiovascular risk down to 115/75 there was no statement that 120 was “unsafe”. In fact, the panel’s recommendation for a blood pressure of 120/80, the lowest reading in the prehypertension category, was “no antihypertensive drug indicated.”
Several paragraphs later the article states “More people visit doctors for hypertension than for any condition other than the common cold. And no wonder, as the threshold for hypertension has dropped from 160/100 to 140/90 and now, with prehypertension, to 120/80.” Well, not exactly. The threshold for JNC-7’s designation of hypertension is indeed 140/90, but not 120/80. And who in their right mind thinks 160/100 is an acceptable target? The article even mentions the old saw that “100 plus your age” is an acceptable systolic blood pressure. That went out 30 years ago. Disease mongering?
The section on deep vein thrombosis (DVT) profiles an ad campaign by Aventis, the maker of Lovenox, to raise awareness about DVT and encourage prevention. When anticoagulant drugs such as Lovenox are used for DVT prevention the typical duration of treatment is a matter of days and in unusual circumstances a few weeks. But the article makes this statement about the campaign (italics mine): “It was powerful marketing, tapping primal fears of death and disease, targeting the healthy for life-long use of blood thinners.” Well, wrong. What the campaign actually did was suggest that patients who are laid up with injury, surgery or illness ask their doctors about DVT prophylaxis. Maybe that’s not such a bad idea since research has repeatedly shown that this evidence based, potentially life saving treatment is underutilized.
There’s been a lot of screaming about disease mongering and medicalization, little of which is evidence based.