Wednesday, November 28, 2007

Rapid response teams in perspective

I don’t have anything against rapid response teams (RRTs) although I’ve long suspected that they are promoted way beyond what the evidence supports. Yesterday saw some thoughtful blogging on the subject. Bob Wachter, though somewhat of a skeptic on RRTs, notes that the appeal is undeniable:

Don’t get me wrong. The concept of a Rapid Response Team is attractive. It isn’t hard to find patients who die in hospitals or require emergent transfer to the ICU in whom evidence of deterioration was present for hours – sometimes days – before the crash.

Indeed. Wachter goes on to mention Joint Commission’s 2008 National Patient Safety Goals number 16 of which states:

The organization selects a suitable method that enables health care staff members to directly request additional assistance from a specially trained individual(s) when the patient’s condition appears to be worsening. [Critical Access Hospital, Hospital]

This is rather vague, to Joint Commission’s credit, in that it allows individual institutions to fashion a method that meets their individual needs in this area. Wachter’s interpretation is that each hospital have a system in place to identify deteriorating patients and intervene. Such a system may or may not take the form of a RRT in the usual sense.

California Medicine Man, acknowledging the scarcity of data in support of RRTs, notes that some of the things such teams can do, such as administration of fluid boluses and respiratory treatments, just make sense. Moreover, the nurses feel more confident when such teams are available.

If RRTs are such a good idea who cares if they aren’t “evidence based?” If a RRT suits your hospital’s needs maybe you don’t need a study to justify it. It’s all well and good up to a point. It becomes problematic when unsupported claims are made (“we’re saving lives”) or rigid mandates are promulgated. That’s when I’ll say “show me the evidence.”

So, what does the evidence say? I’ve previously noted the lack of evidence in support of RRTs. Last month I blogged about a more recent systematic review which again failed to support RRTs. Wachter cited some more recent studies. Just out in JAMA is a paper showing a reduction in mortality associated with a RRT in a children’s hospital. Can such results be extrapolated to adult hospital medicine? Probably not. Things move faster in pediatrics. Compared to adult medicine everything in pediatrics is stat.

Perhaps the most interesting study Wachter mentioned was this one which demonstrated a remarkable reduction in mortality. In fact, the authors estimated that by the end of the study period the NNT to save one life was 3! Astounding! But take a closer look at what they really did. It wasn’t a RRT as we generally think of it. It was really early goal directed therapy.

So it all depends on what we really mean when we speak of RRTs. I suspect for many hospitals RRTs meet an important need. For others they may be no more than a promotional gimmick, an exercise in symbol over substance.

Tuesday, November 27, 2007

Coronary slow flow phenomenon (CSFP): an emerging cause of chest pain with “normal” coronary arteries

A case report and review of the literature appeared in Clinical Cardiology.

Key points:

This poorly understood disorder is not cardiac syndrome X and is not always a benign disorder.

Abnormal QT interval dispersion and life threatening cardiac arrhythmias may be associated.

Dipyridamole is a potential treatment.

Cooley and DeBakey make amends

A 40 year clash of surgeons’ egos apparently ends. Fascinating stuff.

Via Kevin M.D.

Monday, November 26, 2007

Pulmonary edema: Is it cardiogenic or non-cardiogenic?

Mesurement of BNP can help differentiate. From Chest.

New findings on VTE prophylaxis in hospitalized patients

A meta-analysis published in Archives of Internal Medicine found that both UFH and LMWH reduced VTE but neither agent reduced mortality. LMWH was superior to UFH with respect to prevention of DVT and occurrence of injection site hematoma.

Myasthenia gravis

This is one of the better reviews I’ve seen on the topic. From the Orphanet Journal or Rare Diseases.

D-dimer testing in pregnancy: helpful if normal

Since pregnancy is associated with elevated D-dimer levels clinicians have been hesitant to use the test in pregnant patients. Its usefulness in the diagnostic evaluation of pregnant patients for VTE had not been systematically reported, however, until publication of this study in Annals of Internal Medicine.

It turns out that the test is helpful when normal, and is normal often enough to make it worth while.

Avoiding geriatric medication nightmares

This article in Internal Medicine World Report, featuring Peter A. Boling, MD, director of the MCV Campus Geriatric Section at Virginia Commonwealth University, has several excellent clinical pearls on polypharmacy in geriatric patients.

Sunday, November 25, 2007

Trying to be fair and balanced

Lest I come across as always defending the pharmaceutical companies I’ll note here a couple of industry shenanigans reported last week which are---well, indefensible.

First a ghost writing offer. Now I’ve been a little skeptical of all these claims about journal articles ghost written by pharmaceutical companies. I’ve never seen a specific article cited and verified as ghost written. (I’m from Missouri and would still like for some one to “show me” by citing a ghost written article!). But now the WSJ Health Blog reports on an offer by a pharmaceutical consulting firm to ghost write an abstract for a big name in hypertension, Jean Shealey. She declined. One of the Health Blog commenters wrote:

So, this is some new revelation for the WSJ?
There are plenty of studies in the medical literature which have been ghost written by an industry-sponsored medical writer, that was then submitted under the name of a highly-recognizable leader in the field–always at a steep price.

To which I say: documentation, please!

H/T to Kevin M.D.

Then there’s this update (via Medscape/Heartwire) on GlaxoSmithKline (GSK) applying pressure to silence Dr. John Buse, a diabetes expert who raised early concerns about the cardiovascular safety of rosiglitazone (Avandia). California Medicine Man discusses it here. The full report of the Senate Committee on Finance is here. Suppression of debate does not serve the cause of science.

The pharmaceutical industry has interests in common with those of the medical profession, but abuses exist. Our profession can collaborate with industry to the benefit of patients, but doctors need to aware of the possibility of abuse, and to be skeptical.

Chantix and suicide---what’s going on?

The news about a possible link between Chantix (varenicline) and suicide has started making its way around the blogosphere. Chantix binds to a4b2 nicotinic receptors in the brain providing weak agonism while at the same time blocking nicotine. Although this prevents complete nicotine (and consequently dopamine) withdrawal by providing a low level of receptor stimulation it blocks those dopamine rushes people get from cigarettes. That may not only take the fun out of smoking but it may also take away your patient’s antidepressant. In some hard core smokers those dopamine surges have powerful antidepressant and anxiolytic effects.

Friday, November 23, 2007

Taking advantage of patient complaints to reduce malpractice risk and enhance professionalism

Dr. Gerald Hickson, director of the Center for Patient and Professional Advocacy at Vanderbilt University Medical Center, has conducted extensive research on why people sue doctors. His findings? Patient and family perception, not medical error, drives most malpractice suits:

He has found that 85 percent of malpractice claims are invalid, and that neither technical competence nor patient severity is a significant determinant of the risk of malpractice suit. “All doctors have patients who experience adverse events,” Hickson said. “What sends people to lawyers are perceptions, not necessarily medical facts.”

His research also suggests a correlation between the number of complaints from patients and the physician’s risk of being sued. Physicians with high numbers of complaints account for a disproportionate share of lawsuits and may benefit from intervention. Everybody wins if identification of patterns of patient complaints and timely intervention promotes professionalism and loss prevention.

Hickson is the lead author of a paper in the current issue of Academic Medicine which describes Vanderbilt’s non-punitive system for identifying and correcting patterns of unprofessional behavior based on analysis of patterns of patient complaints.

Must read DIC review

I recently ran across this review of DIC (via CCJM). Though a bit dated it’s the best review of the topic I’ve seen for its elucidation of basic concepts and clinical pearls.

This review is important for another reason: it illustrates that expert narrative reviews, decried by some EBM enthusiasts, are still useful.

MEN type 2

Reviewed in the Orphanet Journal of Rare Diseases.

Wednesday, November 21, 2007

Docs don’t know stats?

Dr. Helen and California Medicine Man tipped me off to this fascinating paper in JAMA. House staff, fellows and faculty with research backgrounds were given a basic skills test on biostatistics and quantitative interpretation of medical research articles. Test performance was surprisingly poor:

The overall mean percentage correct on statistical knowledge and interpretation of results was 41.4% (95% confidence interval [CI], 39.7%-43.3%) vs 71.5% (95% CI, 57.5%-85.5%) for fellows and general medicine faculty with research training (P < .001).

Read Dr. Helen’s and California Medicine Man’s commentaries on the study. I’ll offer a few random observations here.

According to the study author:

In her own teaching, Windish had seen that trainees often read only the abstracts, or "ignored the statistics and skipped right to the results." This practice turns out to be common throughout the medical profession -- and potentially troubling.

Heck, if you think that’s bad, how many docs settle for the New York Times?

You can take the test here. It was eye opening for me. I don’t know as much as I thought I did although I scored substantially better than the residents. It’s been a self teaching exercise for me through the years and I’m still on the learning curve.

This dovetails with the concerns of the No Free Lunchers, who never have given docs much credit for their ability to critically appraise the medical literature. What’s the answer? For me it’s an ongoing self study (there are plenty of free on line resources) of EBM and medical literature analysis as part of one’s commitment to lifelong learning.

Tuesday, November 20, 2007

Additional thoughts on chelation death

Here are a couple of additional points I should have made in last night's rant on the chelation related death of Abubakar Tariq Nadama.

1) It is alleged that the chelation mixture was given IV push. The labeling for Endrate, the drug which was apparently used, indicates that such rapid injection increases the possibility of fatal toxicity due to a precipitous fall in the serum calcium. Although rapid injection of Endrate, if it occurred, would be relevant to the case, it remains my considered opinion that the emphasis of the CDC, the prosecution and the prosecution’s expert witness sends the implicit message that it’s OK to use chelation therapy for everything under the sun so long as you don’t give the “wrong” drug or administer it “inappropriately”. It would be foolish for me to suggest how the prosecution should spin their arguments but I’d personally rather see wording to the effect that Dr. Kerry “engaged in scientifically unfounded treatment and, moreover, administered such treatment in a manner which enhanced its toxicity”.

2) I noted that Endrate is indicated for the treatment of hypercalcemia and digitalis toxic ventricular ectopy. However, it deserves mention that newer and safer treatments for these conditions have been available for decades, effectively rendering Endrate obsolete.

Death by chelation

Orac recently posted an update on the story of Abubakar Tariq Nadama and noted that the wheels of justice are finally turning as Dr. Roy Kerry faces charges in the death of the 5 year old autistic boy. I join Orac and others in the hope that justice prevails. But, while lacking any legal training, I am bothered about this case. One of the roles of the execution of criminal justice is to set examples and thereby send appropriate messages to society. If this case plays out as it has so far the wrong message will be sent. Dr. Kerry may “go down” but justice will not have been fully served.

What’s wrong with the case? From The Washington Post (italics mine):

A doctor was ordered on Thursday to stand trial on charges he caused the death of a 5-year-old autistic boy by incorrectly administering a controversial chemical treatment.

Dr. Roy Kerry, 69, used the wrong drug and administered it incorrectly while trying to use chelation therapy on Abubakar Tariq Nadama…

As I pointed out in some detail over a year ago, this is not a case of the wrong drug or the wrong method of administration. No, it’s a case of total woo. In that post I called it a matter of “wrong indication”, implying merely off label use, but it’s really much worse than that. Most off label use is evidence based to some degree. The use of chelation as a treatment for autism is even worse than non-evidence based---it isn’t based on anything.

If chelation for the treatment of autism is baseless in the first place how can you talk about the wrong drug or even the wrong method of administration? There has to be a right alternative before you can talk about a wrong drug. Logically, at least, the prosecution appears to be on thin ice in pursuing this line.

The Nadama family’s attorney in praising the judge’s decision to order Kerry to stand trial displays his misunderstanding of the issue in stating “He did something no doctor in the world would do”. But, truth is, the non-indicated non-evidence based non-anything based use of chelation is widespread, and it’s apparently done without rhyme or reason as to the choice of chelation agent.

A little background on the two chelation agents--- Endrate, the drug apparently used by Dr. Kerry, has two indications: hypercalcemia and digitalis toxic ventricular ectopy. Versenate, the other available chelation agent, has one indication: lead poisoning. Although the prosecution’s expert witness seems to be following the CDC’s faulty analysis of the case in implying that Versenate would have been the “right” drug, neither drug can be applied to the treatment of autism on any basis other than absolute and total woo.

Endrate, the purported “wrong drug”, is frequently administered by chelation practitioners for the bogus indication of atherosclerosis and is in fact the agent being used in the NCCAM sponsored Trial to Assess Chelation Therapy. In a recent post to the Health Fraud List, quackbuster Robert S. Baratz, MD, PhD, DDS noted that “Chelationists regularly conflate Endrate (R) (disodium EDTA) and Verseanate (R)”. Something “no doctor in the world would do”? Uh huh. And if the indoctrination of current medical students is any indication, the woo based use of chelation may become more widespread. Here’s what the American Medical Student Association’s Complementary Therapies Primer says on page 20 about chelation:

Since it improves blood flow, it is also helpful in gangrene, intermittent claudication caused by peripheral vascular disease, and poor memory due in part to insufficient cerebral blood flow. Reduction in metal ions reduces inflammation caused by free radicals, and makes chelation therapy helpful in arthritis, scleroderma, and lupus. Chelation therapy has also been used to normalize cardiac arrhythmias, improve vasculogenic vision loss, reduce cancer mortality, protect against iron poisoning and detoxification of snake and spider bites.

Sunday, November 18, 2007

Chronic eosinophilic pneumonia

It was reviewed in the Orphanet Journal of Rare Diseases. The review distinguishes it from other eosinophilic diseases with pulmonary manifestations. A couple of points are of particular interest. Chronic eosinophilic pneumonia responds dramatically well to corticosteroids. Its characteristic chest radiographic pattern (the “photographic negative” of pulmonary edema), though not entirely sensitive or specific, may at times enable a “look see” diagnosis (making it potential fodder for board exams).

An evidence based medicine toolkit

---is now on line at American Family Physician.

Hospital medicine CME conference: final reflections

The 4th annual Mayo Clinic Update in Hospital Medicine was completed today. It was my first time to attend this particular conference and the first hospital medicine course I’ve attended that was not affiliated with the Society of Hospital Medicine. I had high expectations for the course (after all it’s Mayo Clinic, right?) and was not disappointed. This course was comparable in quality to Bob Wachter’s excellent and very popular course in San Francisco and I would recommend it highly to hospitalists and other health care professionals interested in hospital medicine.

There is currently a groundswell of sentiment which seeks to ban this type of lecture based CME (a subject many of you probably think I’ve already beaten to death in the pages of this blog). The naysayers seem to occupy one of two camps. One maintains that lecture based CME is worthless, and wants all future CME to consist of case based interactive programs with built in mechanisms to measure how much the activity resulted in changed physician “behavior”. The other camp seeks to block the accreditation of all programs that receive support from the pharmaceutical industry. That would mean the end of the program I attended this week, the end of Bob Wachter’s program and the end of CME as we now know it.

To the agitators I say rubbish. What makes them think they know my learning style and educational needs better than I do? And I’m more than a bit rankled by the paternalistic arrogance of those who want to tell me what medical literature I should and should not read. I’m an adult. I graduated from medical school quite some time ago. The responsibility for life long learning lies with me and I take it very seriously.

Yes, I need occasional feedback about the strengths and weaknesses of my fund of knowledge. For that purpose there are plenty of self assessment tools (e.g. MKSAP) I can choose and on which I have spent hundreds of dollars through the years. For most physicians the external requirements for maintenance of licensure and certification are already onerous enough.

Trips to lecture based CME activities, although they constitute just one of several types of CME I participate in, have helped me to be a more effective physician though often in intangible ways which can’t be “measured”. Many important content areas such as basic clinical skills, pathophysiology and certain abstract concepts (one of today’s sessions dealt with heuristics and other cognitive traps in medical decision making) could never reasonably be expected to result in direct, measurable changes in physician behavior because they impact intangible attributes such as judgment and skill.

But those who want some form of verification of the educational impact of my activities this week can read my last few posts about some of the content areas. Moreover, rest assured that for the next several weeks while pouring over the course syllabus I’ll be looking up primary sources of information and background material. And I’ll be reflecting and thinking extensively on ways to put the information to the most appropriate use for the benefit of hospitalized patients.

Saturday, November 17, 2007

More clinical pearls from the hospital medicine CME conference

Continuing from my last post---

How should doctors decide whether to administer corticosteroids to patients with septic shock in the wake of the surprising findings of CORTICUS, which failed to show benefits from such therapy? This and related questions were discussed by Dr. Charles Abboud of the endocrinology section at Mayo Clinic. First it must be remembered that CORTICUS did not address “classic” adrenal failure which can occur in critical illness as a result of bilateral adrenal hemorrhage, bilateral adrenal infarction or, most commonly, suppression of the HPA axis as a result of prior corticosteroid therapy. Instead, CORTICUS applies to the concept of relative adrenal insufficiency, also known as “adrenal exhaustion” more recently termed “critical illness related corticosteroid insufficiency” (CIRCI). There is no dispute about the need to identify and treat classic adrenal insufficiency, either primary or secondary, in acutely ill patients. But in view of the recent CORTICUS results the treatment of CIRCI has become controversial.

CORTICUS was recently reviewed at the 72nd Annual International Scientific Assembly of the American College of Chest Physicians and at the Society of Critical Care Medicine 36th Critical Care Congress. The CORTICUS patients were less ill than those in other studies showing benefits of corticosteroid treatment. Also the study was halted before its enrollment target was met. From the Medscape report of the ACCP presentations:

Clinicians, nonetheless, must choose if and how to utilize corticosteroids. Hence, restricting their employment to persons who resemble those studied by Annane and colleagues might be the most prudent course as there are clinical trial findings to support this. Broad, routine administration of corticosteroids in severe sepsis and shock seems unwarranted at present.

Acknowledging the controversy raised by CORTICUS, Dr. Abboud believes that over 60% of patients with septic shock have CIRCI and recommends treating with corticosteroids if appropriate testing indicates its presence. His testing criteria seem to me more rigorous than other recommendations I’ve seen for evaluating CIRCI (any cortical value over 20 rules it out; subtract 5 from this cutoff value to account for decreased cortical binding if the serum albumin is below 2.5) and may select more severely ill patients, and hence those more likely to benefit. Dr. Abboud advises clinicians to closely follow the evidence in this evolving controversy.

Although guidelines now exist to help determine the duration of warfarin treatment following VTE there are controversies and gray areas. For such patients, measurement of D dimer levels 3-4 weeks following discontinuation of warfarin can help determine the risk of recurrent VTE. This enables a quantitative estimate which can be weighed against the estimated bleeding risk.

In a single center study of patients admitted with unexplained severe COPD exacerbation, with no initial suspicion of PE, PE was found in 25%.

Random observations from the hospital medicine CME conference

Before heading down for the final day of sessions I thought I’d mention a few noteworthy items from the course content that particularly impressed me (now that we’ve gotten the woo out of the way). These were little ah ha moments for me and are not necessarily representative of the best of the course content:

In its checkered history hospital medicine has gone through many transformations but three lessons seem to have endured the test of time: Wash your hands. Seek the evidence. Examine the patient.

Acute phosphate nephropathy, thought to be rare, is now an emerging issue in hospital medicine. Associated with sodium phosphate based bowel cleansing products, it can result in permanent renal failure.

Enoxaparin dosing guidelines do not call for renal adjustment until the creatinine clearance drops below 30ml/min. However, bleeding complications with enoxaparin begin to rise precipitously as GFR falls below 80ml/min/1.73m2.

The colloid/crystalloid debate is still unresolved. We lack high level evidence to favor colloid over crystalloid.

Almost every hospital medicine conference contains a talk on in patient pain management, including this one. Having listened to many such lectures and noting the widely varying opinions and biases of the speakers it is my considered opinion that current recommendations regarding pain management are based 45% on the art of medicine, 45% on dogma and 10% on science.

Enough for now. I’ll post additional impressions and a wrap up, time permitting, after today’s sessions.

Fondaparinux and HIT---the bubble has burst

It only takes one counter-example to disprove an absolute statement like “fondaparinux (Arixtra) never causes HIT”. We now have a counter-example in the form of a letter to the editor of NEJM which documents a case of HIT due to fondaparinux. So much for its emergence as a treatment for HIT!

H/T to the Mayo Hospital Medidine update!

Friday, November 16, 2007

Alternative medicine promoted to hospitalists attending CME course

I revealed in last night’s post that the Mayo Clinic CME conference in hospital medicine I’m attending had “integrated” some woo into an otherwise excellent assemblage of “hard core” scientific content. I decided to reserve judgment until after the two lectures in question were delivered today. My verdict? Mixed. Some valid points and eye opening statements were made. But much of the content, from where I sat, consisted of uncritical promotion of non-evidence treatments, suggestions of biologically implausible mechanisms and a certain amount of bobbing and weaving. Let me explain.

There were two speakers. The first one discussed general issues of CAM in hospital medicine. He opened his talk declaring that, like it or not, CAM is now very much a part of our health care system and went on to present data on the recent “CAMbrian explosion” (my words) in hospital medicine. Some interesting data on the demographics of CAM use were presented (it’s really high, as one would expect, in cancer patients) along with some discussion of the hazards of herbal medicine (St. John’s wort is a big inducer of metabolism of many drugs---watch those antiretrovirals, antirejection meds and warfarin!).

He also touched on stress medicine. The study of stress and its effects on health (brain-body medicine) is not total woo although it is plagued by methodologic obstacles. From the point of view of scientific validation brain-body medicine is not ready for prime time. On the other hand do we really need a study (the speaker dutifully cited many) to know that if music or a nice massage relaxes you it probably does some good in some way?

The second speaker, who focused on acupuncture, was more problematic. When pinned down he allowed that we don’t really know how acupuncture “works”, although spoke of the existence of the vital energy Qi and the meridians through which it flows as undisputed facts. It’s the blockage of Qi, he said, that causes illness and pain.

He made the claim that the body’s 400 and some odd acupuncture points can be verified by changes in electrical resistivity and are reproducible in location from one person to another. The history of how the locations of these points were determined, however, leads me to suspect that the science behind such a claim is dubious. According to Dr. Wallace Sampson, professor emeritus of medicine at Stanford:

First, most people assume that it's an ancient Chinese cure that has existed, unchanging, for centuries. Not so, says Sampson, noting that "acupuncture was formalized in a complex way over the past 100 years, mostly in Europe and France and after the Communist takeover in China. Before that time there was no consistent formalization of acupuncture points or what each place was supposed to do. It was largely regional, and the thinking varied from city to city."

According to an article from Quackwatch, the purported acupuncture points were at one time 365 in number, corresponding to the days of the year!

Treatment is applied to "acupuncture points," which are said to be located throughout the body. Originally there were 365 such points, corresponding to the days of the year, but the number identified by proponents during the past 2,000 years has increased gradually to about 2,000 [1].

With such confusion about where the “real” acupuncture points are supposed to be the claims of “sham acupuncture”, the new and sexy standard for research reports, become meaningless. Sham acupuncture studies are blinded to the patient but not the therapist. What’s the actual difference, then, between sham and “real” acupuncture? Do the sham therapy sessions apply the same personal touches and TLC as the real ones?

This speaker, in my view, was inappropriately and uncritically promotional of acupuncture.

Attendance at these lectures afforded me a unique opportunity. My knowledge of the woo invasion of mainstream medicine, up to now, was based on reading---reading of medical journals, medical school web sites and a few blogs. Today, by experiencing it first hand, I came to appreciate the problem on several new levels. I was amazed, for example, at the utter lack of audience reaction, even during the presentation of the worst of the woo---no snickers, groans or shaking heads and no skeptical audience questions (except for mine!).

Most eye opening for me was my interaction with the faculty during Q&A. Remember, these are Mayo Clinic faculty members, not woomeisters from the community. As such, their responses represent the official academic “party line” on CAM. I asked the acupuncture speaker if the energy flowing through the meridians could be measured, and in what form it was transported (e.g. as heat, phosphate bonds, etc.). He answered, without explanation or elaboration, merely that yes it had been measured, and smoothly deflected the question of how or in what form the energy was transferred.

The other presenter had mentioned Yoga and I asked him, in effect, what the placebo should be. In other words, to what extent has Yoga research employed comparison groups using sham postures and mantras with reasonably equivalent relaxation and conditioning value. The speaker, who is the director of Mayo’s complementary and integrative medicine program, indicated that little if any of the Yoga research has been conducted according to this rigorous standard. In fact, control groups in Yoga research have consisted of patients on waiting lists for Yoga classes!

The responses of these faculty members, the best and brightest in the field of CAM who are trying to put the best foot forward, convinced me more than ever before how faulty present day “research” in CAM actually is.

And I shouldn’t be surprised that Mayo is promoting this sort of thing. After all, they’re on Orac’s list.

Thoughts and impressions on hospital medicine CME

When scheduling conflicts prevented me from attending Bob Wachter’s Hospital Medicine Conference I consoled myself by signing up for Mayo Clinic’s Update in Hospital Medicine which I have been attending in Tucson for the last few days. Although it’s my first time at this course (the 4th annual) I’ve had prior experience with other Mayo CME and found that they have a knack putting together quality activities, exceptional in every detail. From my experience so far this meeting (but for one possible concern which I’ll explain below) is no exception.

Although singular in quality this program is like a lot of others. It has the traditional didactic lecture format and receives support from the pharmaceutical industry. Recently some extreme critics have called for the end of such programs. For me, though, this type of activity (parade of stars faculty, relaxed setting away from distractions) provides a uniquely effective learning experience.

And my concern about this meeting? It appears they’ve thrown in a little woo! I’ll reserve judgment at this point---the woo based content will be presented tomorrow. For all I know the lectures will be appropriately critical. If not, the course directors will get a piece of my mind on the evaluation form.

Time permitting I’ll post my observations tomorrow.

Thursday, November 15, 2007

Panic attacks and heart disease

I read with interest this post from the Clinical Cases and Images blog which points to a paper in the Archives of General Psychiatry demonstrating a link between panic attacks and cardiovascular disease in postmenopausal women. But Dr. Wes in a blistering attack cites the study’s flaws and asks whether these women were in fact exhibiting heart disease symptoms misdiagnosed as panic attacks.

So what’s going on? From where I sit the study makes a contribution (albeit a weak one) to the growing body of evidence of a relation between panic disorder and heart disease. I previously posted evidence that myocardial perfusion abnormalities occur during panic attacks and cited an epidemiologic association.

A question remains. How many of the episodes of heart disease cited in the paper were actually examples of takotsubo cardiomyopathy, an under appreciated entity with a demonstrated preponderance in postmenopausal females strongly suspected to be a brain-heart disorder?
For a broader view of brain-heart disorders see my post here.

Wednesday, November 14, 2007

Orac’s med school woo aggregator

Over the last couple of years Orac and I along with a few other bloggers have posted innumerable examples of uncritical promotion and teaching of non-evidence based woo in medical schools. Although we’ve marshaled plenty of evidence of the encroachment of woo into med school curricula, up to now it’s been fragmented, widely scattered and buried in archives of our blogs. This, of course, is not conducive to quick reference. Today Orac has remedied the problem by compiling a list of links to academic medical woo all in one post! (I had thought about doing something similar but had not yet found the time or energy).

I knew such a list would be large, but seeing it all in one post was overwhelming. As the list grows it will need updating frequently to keep it current and near the top of our blogs, an effort to which I hope to contribute from time to time.

Panda Bear continues his series of posts on CAM

In today’s post Panda Bear likens the patient to a person seeking automotive repairs:

And yet I am not so confident in my intelligence that I don’t think I can be fooled. Because, for example, I having nothing but a polite interest in automotive technology I am pretty much at the mercy of my mechanic when he describes the repairs needed by our aging pair of automobiles. I trust the guy because nothing he has ever suggested sounds too outrageous and on a couple of occasions he replaced a three-dollar fuse when he could have taken me for an alternator. I am however at his mercy unless I want to study car repair or haul the thing to more than one mechanic.

That is, the consumer’s only real option is to accept the findings and recommendations of the professional since he/she lacks the expertise needed to independently verify the professional’s findings. The analogy between auto repairs and medical treatment, as Panda Bear points out, isn’t perfect because medicine is far more complex. It comes down to a level of trust, to which the patient has no viable alternative. In other words there’s no caveat emptor in medicine. This puts doctors in the position of fiduciary duty. I used this same analogy to raise the principle of fiduciary duty last year.

The ethical questions posed by this analysis may differ between proponents of non-evidence based CAM within and outside of mainstream medicine. Many CAM practitioners outside of conventional medicine honestly believe in their methods. By contrast, mainstream practitioners purport to adhere to scientific principles and evidence based medicine and know, or should know, that water does not possess memory and that acupuncture meridians have not been documented to exist. Their credentials attest to scientific integrity and are the basis for public expectations. Thus, for mainstream medical institutions or their representatives to promote non-evidence based and biologically implausible claims is a violation of fiduciary duty. It’s the most egregious form of woo.

Tuesday, November 13, 2007

Grand Rounds 4.8 hosted by Dr. Anonymous

Dr. Anonymous hosts for the second time. (His first hosting was about this time last year and can be found here).

That’s not all! Dr. Anonymous and Grand Rounds custodian Nick Genes recently took turns interviewing each other. To get a double fix of musings and ruminations about blogging listen to Dr. Anonymous interview Nick Genes on Dr. Anonymous Live then check out Nick Genes’s Medscape Pre-Rounds interview of Dr. Anonymous.

This week’s edition was special because Dr. A performed the finishing touches and launched GR 4.8 live during the performance of his Internet radio show.

I’ve followed Dr. A’s activities with interest the last few days because he’s been in Tucson. I’m there now to attend the Mayo Clinic Hospital Medicine course and wondered if Dr. A was attending the same meeting. Listening to last night’s show, it turns out not to be. He left for home about the same time I arrived.

Anyhow, I’ll be blogging from Tucson for the next few days and sharing my impressions of the meeting as time permits.

Sorry I missed you, Dr. A!

Monday, November 12, 2007

Stress echocardiography review

Published in the British Journal of Cardiology, via Medscape. The free access full text article (made possible with the help of your friendly pharmaceutical companies) discusses indications, contraindications and comparison with other stress imaging modalities.

Don’t forget primary aldosteronism

---in your patient with resistant hypertension. It’s more common than formerly believed. (Via Medscape).

More evidence on erythropoietin agonists in critical illness

A meta-analysis published in CMAJ. I recently posted similar evidence here.

Palliative care

This web site from Medical College of Wisconsin is THE resource for palliative care. Some subsections, such as the one on patient controlled analgesia, have broader applicability.

Sunday, November 11, 2007

Treatment of pulmonary embolism in critical illness

A very helpful review appeared recently in Chest. Key points follow:

Get a bigger bang for the buck with CT by measuring RV and LV diameters. RV/LV diameter ratios over 0.9 are concerning for right ventricular dysfunction.

Echocardiography is useful in the assessment of RV function.

Biomarkers (troponin, BNP, ProBNP) are potentially useful indicators of RV damage and wall stress. Given the shorter half life of BNP and ProBNP these markers are more useful than troponin for assessment of patient progress in real time. Q 12 hour determinations are suggested by the authors.

Assessment of RV function by any means is useful for assessing risk. Negative predictive power exceeds positive predictive power.

Hemodynamic support
Judicious volume infusion can improve RV function. Theoretical adverse effects of RV over distension are cited.

Norepinephrine is favored for vasopressor support. However, this is based largely on animal data. High level comparative clinical studies are not available.

Antithrombotic and antiembolic strategies
Intravenous anticoagulants are favored over subcutaneously administered anticoagulants if the patient is critically ill.

Concerning contraindications the authors state: Only rarely is anticoagulant treatment flatly contraindicated (eg, active hemorrhage in the brain or another vital organ, uncontrolled bleeding threatening tissue perfusion); but in those situations, consideration of prompt placement of a vena cava filter (see below) and clot removal (see above) should be undertaken.

The established indication for intravenous thrombolytic therapy is PE causing shock. Potential indications are deterioration despite standard treatment and normotensive patients with RV dysfunction.

Update on intra-abdominal infections

From Cleveland Clinic Journal of Medicine.

Fondaparinux for HIT?

This pentasacharide anticoagulant (Arixtra) does not cross react with HIT antibodies. Early experience with its use in HIT patients is favorable. It’s not approved for such use at present, and not recommended in guidelines. I predict it will eventually emerge as a treatment for HIT. The topic is reviewed here. (Pharmacotherapy, via Medscape).

See update here!

Fibromuscular dysplasia

Reviewed in the Orphanet Journal of Rare Diseases.

Saturday, November 10, 2007

November is CAM month

---over at Panda Bear. He responds to some of the tired arguments of his detractors in the latest installment.

Ohio State University under the influence of woo

Orac beat me to it, thanks to an anonymous tip.

Where medicine is headed

I laughed watching Homeopathic ER. For some in academic medicine, though, this is serious business. Orac said it well:

I don't think we're too far from this point, at least in some medical centers. If current trends continue, give it a decade or two. Something to look forward to when I get old and start to need more medical care.

Friday, November 09, 2007

Update on skin and soft tissue infections

An excellent and thorough review of this topic recently appeared in CCJM as part of its supplement on Infections in Hospitalized Patients. With the increasing severity of illness of hospitalized patients and the rise of community associated MRSA, clinicians must be vigilant for necrotizing infections and the need for surgical consultation. The review covers clinical assessment for necrotizing infections and cites this study from Critical Care Medicine describing a scoring system of laboratory parameters to assess for necrotizing fasciitis. Although the scoring system is not detailed in the abstract of the Critical Care Medicine paper it can be accessed in this open access full text paper from Current Opinion in Infectious Diseases.

Sepsis update

From Current Opinion in Infectious Diseases.

New and noteworthy:

If appropriate antibiotics are given within the first hour of hypotension the survival rate in one study was 79.9% and declined by 7.6% per hour of delay.

While elevated lactate levels may result from acceleration of glycolysis due to hypermetabolism rather than tissue hypoxia, levels of 4 meq/l or above are concerning and indicate need for aggressive hemodynamic support.

New data from the CORTICUS study were cited regarding the use of corticosteroids in patients with shock. No benefit was found. Corticosteroids can be considered in selected cases, but routine use is no longer warranted.

EGTD, activated protein C and other bundle components are discussed

Pyoderma gangrenosum review

Via the Orphanet Journal of Rare Diseases.

Thursday, November 08, 2007

Pioglitazone (Actose) vs rosiglitazone (Avandia)

Ever wonder why the two drugs seem to have opposite effects on macrovascular outcomes? Well, just look at what happened to lipid levels when patients were switched form one to the other. (Via Baylor University Medical Center Proceedings).

Real world experience with early goal directed therapy for sepsis

Here’s how they did it at the Carolinas Medical Center. Although the investigators observed a 33% RRR similar to that reported in the original study by Rivers, their study was time limited and not powered to reach statistical significance.

The Carolinas Medical Center protocol was an ER based protocol. That is, the initial assessment for patient eligibility, insertion of the central venous catheter, initial hemodynamic management and antibiotic initiation were done by ER personnel before admission to the ICU.

What kind of diabetes does Halle Berry have, anyway?

When I was lurking over at Diabetes Mine preparing for my post on diabetes technology I ran across this little rant on the controversy sparked by Halle Berry’s claim that she weaned herself off insulin thus transitioning from type 1 to type 2 diabetes. That’s some serious misinformation. The dangerous message this sends to anyone who really does have type 1 diabetes is obvious.

But I think maybe Amy and other bloggers are being unfair to Berry. Maybe she doesn’t know any better. I fault the media. They should know better. If they don’t they have no business covering the story. Even the news reports that purported to debunk the idea were faulty.

So, what type of diabetes does Berry really have? Type 1? Can’t be. She’s alive. Is it type 2? Well, she doesn’t really fit the profile. According to reports the presenting manifestation of her diabetes was coma. Besides, look at her. Type 2 doesn’t immediately come to mind!

We don’t really have enough information, but given that Berry’s father is African American and that her diabetes appears to have transitioned from type 1 to “something else” she could have an under appreciated condition that I blogged about early last year which has gone by various names including Flatbush diabetes, diabetes 1.5 and, more recently, ketosis prone type 2 diabetes, something of a misnomer since it’s not really type 2 diabetes at all.

If this is the disease Berry has her days of taking insulin may not be over. Diabetes 1.5 is a form of intermittent, reversible beta cell failure that can cause the diabetes to appear to flip-flop like John Kerry from type 1 to type 2 and back.

Image source: U.S. Government Via Wikipedia.

Wednesday, November 07, 2007

Type 1 diabetes, gadgets, and evidence based medicine

A recent keynote speech by Richard Kahn, Chief Scientific Officer of the American Diabetes Association (ADA), seems to have raised the ire of Amy and numerous commenters over at Diabetes Mine. Kahn spoke about where we’ve been and where we’re going with technological advances in diabetes care. So what’s controversial about that, you ask?

The post and comments that followed covered several related issues---inappropriate lumping of type 1 and type 2 diabetes, failure to advocate for patients, not enough emphasis on a cure---but I will focus on one. It seems Dr. Kahn is being accused of “dissing” diabetes technology:

It is frightening that someone like Kahn, who in his position with the ADA is arguably the most visible spokesperson for diabetes in this country, would deliver a speech essentially dissing the value of new diabetes technologies -- and at the country's top gathering of D-tech experts, no less!

OK, so did Kahn really dis new technology? Here’s an excerpt from the speech:

The ‘90s also gave birth to many other advances in technology without which we would have made little progress in controlling the ravages of the disease. Laser photocoagulation, insulin pumps, angioplasty and by-pass procedures, mono filaments for foot exams, sophisticated glucose meters, and many more technological advances, have given people with diabetes a far better life than was imagined even a decade or two earlier. They have certainly saved lives, improved many more lives, and made diabetes manageable for millions of people.

Kahn suggests a healthy skepticism towards new technology. He raises questions of evidence. But he’s not dismissive, at least in my reading. He’s not even suggesting technologies be subjected to the same scrutiny we apply to new drugs. I can think of many gadgets, bells and whistles, both in and outside the field of diabetes, which have survived such scrutiny despite a lack of proof of improvement in clinical outcomes. The proliferation in the 1980s of programmable functions in cardiac pacemakers and new modes in mechanical ventilators are just two examples. Many of these advances, while never passing the rigorous tests of evidence based medicine, remain available today to the benefit of individual patients.

Amy goes on:

Think of the ramifications. If the ADA comes out with an official position that there's no value in using an insulin pump, or a CGM system, or even a fingerstick meter if you're a Type 2 not on insulin, the Powers That Be will listen.

The ADA should follow the evidence. Although insulin pumps have no proven superiority over newer insulins they represent an alternative which should be available to patients with type 1 diabetes. I can understand patients’ concerns. I hope we never see the day when the patient has to wait a year after the doctor fills out a ream of paper in order to get a pump. That may happen if we go to a single payer system---not as a result of any influence of Richard Kahn or the ADA.

H/T to Kevin MD.

Frontotemporal dementias

This group of dementias was formerly called Pick’s disease. Some patients are mislabeled as Alzheimer’s disease. The topic is reviewed here in the Annals of General Psychiatry.

Emergency treatment of warfarin associated intracranial hemorrhage

This review in Emergency Medicine News is full of pearls. Given current controversies and the almost universally dismal outcome in patients presenting with warfarin associated ICH, no particular regimen for reversal can be held up as the standard of care. A practical approach taking into account recent guidelines and the relevant physiology and pharmacology is presented.

Tuesday, November 06, 2007

The Orphanet Journal of Rare Diseases

Don’t be deceived by the title. Some of the diseases covered in this journal, launched early last year, are not so rare. Others are rare in real world practice but not so rare on Internal Medicine boards. These high quality, thoroughly referenced expert reviews (the EBM Nazis are gasping) should prove useful for clinical reference, background reading and board review. I’ll be linking to some of the articles, which are available as free full text, in future posts.

Early goal directed therapy five years later

Five years after the seminal paper of Rivers, et al. establishing the efficacy of early goal directed therapy (EGDT) for severe sepsis and septic shock this review was published in the November 2006 issue of Chest. It reviews evidence on EGDT since the original paper and covers multiple theoretical and practical aspects of EGDT. The following points are noteworthy:

Experience accumulated since the Rivers study has confirmed the benefits of EGDT.

Treatment modalities for sepsis are time dependent. Goal directed therapy must be given in the first 6 hours. Older studies demonstrated that, when given later in the course of sepsis, goal directed therapy was not efficacious and possibly harmful.

Arrival to the ER of a patient with suspected sepsis carries the same urgency as does the arrival of a patient with suspected stroke, MI or trauma.

Each hospital must have its own plan for implementation. Three options were suggested for those patients presenting to the ER with sepsis: 1) EGDT is carried out entirely in the ER, by ER personnel. This is how it was done in the original study, in which ICU personnel were uninvolved in EGDT and were, in fact, blinded to the initial therapy. 2) Patients who meet criteria after an initial rapid assessment are taken directly to the ICU, and EGDT is initiated there. 3) As soon as assessment indicates severe sepsis, resources are mobilized by calling a rapid response sepsis team which could be assembled from multiple hospital departments. (Option 1 seems logical, but may not be appropriate for ERs that are burdened by overcrowding and understaffing. Option 2 would probably work only in ICUs staffed around the clock by dedicated intensivists. Option 3 might be best for many hospitals).

EGDT must not supplant or in any way diminish the importance of timely administration of appropriate antibiotics.

Applying different methods to the Avandia meta-analysis yields uncertainty

This paper is old news because of the media splash that resulted when it was released ahead of print, but it’s in the current print issue of Annals of Internal Medicine. Diamond point out one of the hazards of meta-analysis: conclusions may be sensitive to methodologic choices made by the authors. Based on their use of alternative methods of analysis: “We conclude that the risk for myocardial infarction and death from cardiovascular disease for diabetic patients taking rosiglitazone is uncertain: Neither increased nor decreased risk is established.”

Sepsis review from Hospital Physician

This review on the diagnosis and management of sepsis from the June 2007 issue of Hospital Physician covers multiple aspects of treatment including practical application of the Surviving Sepsis Guidelines.

Of special note, the section on early goal directed therapy (EGDT, the Rivers protocol) emphasizes the underappreciated point that EGDT is time dependent. As such it is an emergency department protocol which commences as soon as severe sepsis or septic shock is recognized, and is carried out during the first 6 hours. The article appropriately cautions that EGDT should not wait until arrival in the ICU.

This caveat is supported by largely forgotten evidence that goal directed therapy which commenced in the ICU (late goal directed therapy, when a pulmonary artery catheter could be inserted) was ineffective.

Monday, November 05, 2007

47 million uninsured?

Dr. Wes offers some healthy skepticism.

None dare call it quackery

(With apologies to John A. Stormer). In yesterday’s edition of an ongoing series on alternative medicine Panda Bear compares and contrasts alternative and mainstream methods on several levels. Both traditions, for example, construct models to describe the how and why of biological processes. The difference, of course, is that conventional medicine refines its models over time to conform to new scientific observations while much of alternative medicine does not. As Panda Bear notes:

“Meridians” make sense when your knowledge of the body is based on religious superstition and mysticism. Once you discover the true function of blood vessels and nerves, however, it is time to put away your belief in qi, a spiritual construct that as a metaphor for disease has no basis in real physiology.

Is academic medicine listening? Almost a century ago Abraham Flexner urged medical education to get rid of the woo. Nowadays, though, the leaders (well, maybe there are two or three exceptions) in medical education seem unwilling to take a stand. The task is left to a few bloggers who choose to call quackery what it is at the risk of being labeled narrow minded fuddy-duddies or Pharma shills.

Friday, November 02, 2007

The up and coming Rush Limbaugh of medical talk?

Who knows? Listen to Dr. Anonymous Live! There are a few technical difficulties to iron out. Nice bumper music, though.

Via Clinical Cases and Images.

Panda Bear joins the chorus against quacky promotions by academic medicine

Not only that, he’s launching a month long series on the subject. Here are some excerpts from the inaugural post:

Actually, by the time I had finished the eighth grade I had a sufficient background in chemistry and biology to recognize that these things cannot possibly work.

This is literally third grade stuff and the fact that many prestigious medical centers lack the institutional courage to point it out should make you cringe in shame, either at their gullibility or their venality.

“Well, we’re just being open-minded,” is the formula used to justify spending large sums of money to investigate therapies that even my ten-year-old son could instantly recognize as not only impossible but also somewhat ridiculous.

Glucocorticoid replacement during surgery and acute illness

Hospital physicians frequently encounter patients with decreased adrenal reserve (iatrogenic adrenal insufficiency due to long term corticosteroid therapy or, rarely, adrenal or pituitary disease) who undergo invasive procedures or become acutely ill. The physician must be familiar with the indications for steroid replacement as well as the appropriate dosing schedule. A recent article in The Hospitalist (p. 12) discussed this issue and cited two important primary sources.

A JAMA Clinicians Corner piece published in the January 9, 2002 issue made these procedure specific recommendations:

Minor procedure (endoscopy, inguinal hernia repair): 25 mg hydrocortisone or its equivalent on day of procedure only.

Moderate procedure (abdominal surgery): 50-75mg hydrocortisone on day of procedure and taper quickly over 2-3 days to patient’s maintenance dose.

High risk procedure (cardiovascular surgery, extensive abdominal): 100-150 mg hydrocortisone initially, then taper over 1-2 days to patient’s maintenance dose.

Similar recommendations apply to mild, moderate or severe illness, respectively. For critical illness, 50-100 mg hydrocortisone every 6-8 hours for the duration of critical illness is recommended, along with mineralocorticoid replacement, with slower taper after critical period has resolved.

The above regimens may need to be modified according to the patient’s clinical response.

Superficial procedures under local anesthesia lasting one hour or less require continuation of the patients maintenance regimen but no additional supplementation.

Similar recommendations appeared in a review in Bulletin on the Rheumatic diseases, freely available in full text.