Thursday, October 28, 2010

The changing profile of nephrogenic systyemic fibrosis

According to this summary post at the Clinical Correlations blog:

Since NSF’s identification as a disease entity, there has been a marked shift in radiological standards and practices, as well as rapid growth of literature regarding the disease.

Among other things the incidence appears to have fallen sharply since widespread adoption of safety protocols.

Acid base slide show

From Slideshare.

Wednesday, October 27, 2010

Idiot's guide to capnography

You might as well get used to wave form capnography because it's now in the main cardiac arrest algorithm. As illustrated in this video, it has uses beyond cardiac arrest.

Tuesday, October 26, 2010

Should I read White Coat, Black Hat?

I'm not in the habit of reviewing other people's book reviews but two articles on the book in question, one by Thomas Sullivan and the other by Sally Satel, are worth mentioning here because they nicely address the broader controversy about the relationship between the medical profession and industry. Now that I've read those two articles I think I'll pass on White Coat, Black Hat. The book, based on those two articles and another positive review I recently read seems to be anything but a balanced treatment of the issue. In fact, it comes across as a knee-jerk, intellectually lazy collection of anecdotes designed to appeal to popular animosity against the pharmaceutical industry.

Sullivan and Satel offer a nuanced view of physician-industry relationships. Sullivan makes this point, with which I partially disagree:

For now, there is no data suggesting any harm to patients from working with industry because no studies have used clinical outcomes.

It's true that there are no data suggesting harm to patients from working with industry. The pharmascolds have no data in support of their position. All they can do is appeal to a set of popular beliefs. What I disagree with is the statement that no studies have looked at clinical outcomes. One study did look at clinical outcomes following an industry sponsored campaign. I've blogged about it extensively before. One of the most maligned Pharma campaigns in all of medicine resulted in improved outcomes, even reduced mortality, in septic patients.

Even mild hypophosphatemia may cause muscle weakness

Via Renal Fellow Network.

Accountable care organizations


P4P is unethical

---says Retired Doc. He's right.

The acceptance of P4P is so antithetical to the basic medical ethical tradition that I cannot believe professional organizations of physicians are supporting it...

Monday, October 25, 2010

Diagnosis of SIADH

---and differentiation from other forms of hyponatremia. This is often difficult because volume assessment can be tricky and there are nuances to the interpretation of urine chemistries. Here's a review article on the subject and a nice summary post at Renal Fellow Network.

Dialysis dysequilibrium

I used to hear about this back in med school, but it doesn't happen much anymore, in this era of earlier initiation of dialysis.

One of the mechanisms is the osmotic effect of urea. Ordinarily urea is an “ineffective osmole.” That changes when large amounts are cleared rapidly from the blood. Water can move into the brain faster than urea can move out.

There's an interesting post on this at Renal Fellow Network.

Renal Tubular Acidosis

A presentation from Slideshare.

Friday, October 22, 2010

Peter Orszag's novel idea for tort reform

Peter Orszag's solution to the malpractice problem seems plausible enough at first glance. His latest New York Times column opens:

The health care legislation that Congress enacted earlier this year, contrary to much of today’s overheated rhetoric, does many things right. But it does almost nothing to reform medical malpractice laws. Lawmakers missed an important opportunity to shield from malpractice liability any doctors who followed evidence-based guidelines in treating their patients.

Plausible enough until you think about it. True, the health care reform package did nothing to help ease the malpractice crisis. Orszag's solution? A little further on in the article he gets a little more specific:

The traditional way to reform medical malpractice law has been to impose caps on liability — for example, by limiting punitive damages to something like $500,000. A far better strategy would be to provide safe harbor for doctors who follow evidence-based guidelines. Anyone who could demonstrate that he has followed the recommended course for treating a specific illness or condition could not be held liable.

So, Orszag seems to be saying, (since his strategy is “far better”) forget the caps. Let the punitive damages remain, to leverage doctors into adherence to evidence-based guidelines. Malpractice crisis? Solved. Regional variations and inefficiencies? Gone. Quality chasm? Closed. Win-win situation. Unless you've got a clue about how health care really works.

There's no way this would solve anything. Even if it could, by Orszag's own admission, we'd have to wait a while for relief:

 ...this approach to reform will require larger investments in research into what works and what doesn’t. Fortunately, both the health care reform act and the 2009 economic stimulus act provided additional financing for such comparative effectiveness medical research, and the health care act provides for a Patient-Centered Outcomes Research Institute to coordinate the work. It’s a good start.


I'd like to thank Michael Kirsch, MD, who alerted me to this article in my comments.

Hospitals getting sued more often

The pace of malpractice claims against hospitals is picking up, according to a recent report from Aon Risk Solutions and the American Society for Healthcare Risk Management...
Erik Johnson, health care practice leader for Aon Risk Solutions’ Actuarial and Analytics Practice, tells the Health Blog it’s not clear why the frequency of claims against hospitals is edging up. ..

I've got an idea why, and a clue is found in the last paragraph of the WSJ Health Blog post:

A full 23% of hospital professional liability costs are associated with health-care acquired infections, health-care acquired injuries, medication errors, objects left in surgery and pressure ulcers, the report says.

Pressure ulcers, falls and infections have now been lumped in with objects left in surgery under the legal standard of res ipsa loquitur due in part to the efforts of the IOM and the popular media. Thanks, guys.

Wrong-site wrong-patient procedures

Via Archives of Surgery:

Design  Analysis of a prospective physician insurance database performed from January 1, 2002, to June 1, 2008...
Results  A total of 25 wrong-patient and 107 wrong-site procedures were identified during the study period. Significant harm was inflicted in 5 wrong-patient procedures (20.0%) and 38 wrong-site procedures (35.5%). One patient died secondary to a wrong-site procedure (0.9%). The main root causes leading to wrong-patient procedures were errors in diagnosis (56.0%) and errors in communication (100%), whereas wrong-site occurrences were related to errors in judgment (85.0%) and the lack of performing a "time-out" (72.0%). Nonsurgical specialties were involved in the cause of wrong-patient procedures and contributed equally with surgical disciplines to adverse outcome related to wrong-siteoccurrences.

These were in just one state, mind you.

What do these data say about Joint Commission's universal protocol? On the one hand, had it been adhered to fully a number of occurrences could have been averted (72% of instances were associated with failure to perform a time-out). On the other hand, looking in the body of the paper, there was no decrease in incidence over the years following the rollout of JC's protocol in 2004.

Skeptical Scalpel, who weighs in here, seems to share my annoyance about distorted reporting of medical issues by popular media. The example I found particularly amusing was this from the NYT:

In the worst case reported, a chest tube was inserted into the wrong lung — the healthy one — and it collapsed, killing the patient.

I'm just an internist but I didn't know there was a correct lung to insert a chest tube into. The pleural space is quite far enough, thanks.

I know I'm nitpicking but that's just sloppy.

Subtle ECG findings of acute LAD occlusion

---and a look back through the retrospectroscope at Grunt Doc's patient who went to the cath lab with a normal ECG.

A mini lecture by Dr. Smith over at his wonderful ECG blog points out some of the subtle changes of early acute LAD occlusion. These are often patients who present very early, before classic “STEMI” changes develop. A look back at the tracing of Grunt Doc's patient who went to the cath lab with a “normal” ECG and turned out to have acute proximal LAD occlusion may show some of the subtle changes, particularly the “fat” upright anterior precordial T waves, longish QT and poor R wave progression, findings which rule against benign early repolarization.

Sometimes in difficult cases such as this a repeat tracing only moments later may reveal diagnostic ST elevations. Grunt Doc's tracing was not diagnostic and no one would be criticized for not shouting “STEMI.”

Thursday, October 21, 2010

Dabigatran (Pradaxa) is approved

H/T to Dr. Wes.

You can get full prescribing info from the company's web site here.

It's a direct thrombin inhibitor and is approved for non-valvular a-fib only.

Resident work hours

Skeptical Scalpel to AMSA: Stop whining. (SS apparently hasn't heard that when you use the catch phrase “patient safety” you can justify nearly any position).

Anyhow it looks like further work hour restrictions are coming down the pike along with even more unintended consequences.

I don't know the answer to this debate. It's easy for someone my age to extol, decades later, the days of grueling house staff working conditions. But I certainly didn't appreciate it in real time and did my own share of whining. A program director back in the 70s once said “I run a punishing internship and if they'd let me I'd make it even more punishing.” That wasn't healthy, but now we're headed to the opposite extreme. A colleague once told me of the struggles his program went through to adapt to the restrictions. Residents who exceeded the work hour limits were told to fudge their time sheets so the program would be in compliance. Between sessions at SHM 2010 I overheard an attendee on his cell phone frantically telling his subordinate back home to send certain residents home NOW.

I'd like to see some work hour limits for us old farts but with public policy going the direction it seems to be headed now that probably won't happen soon.

STEMI alert---false alarm!

In this era of rapid mobilization of the cath lab crew I wonder how many false alarms we're going to be seeing. Here's an example from Dr. Smith's blog of someone who pulled the STEMI trigger on a Brugada pattern.

More on CPR-ACLS 2010

A podcast interview with blogger Tom Bouthillet and Dr. Monica Kleinman, incoming Chair of the Emergency Cardiovascular Care committee can be accessed here at MediCast and is well worth the listen if you're interested in the thinking behind the changes and how they'll affect your practice.

Here are a few points of interest mixed in with a few of my own observations:

Benchmarking. Measurement of outcomes got increased emphasis in the 2010 guidelines. The notion is that each community should know its own numbers and that these numbers should drive process improvement. We rate schools, water quality, crime rates and the like, so why not emergency cardiac care? We already have some data on community survival rates. The three regions of the US which departed from the AHA guidelines to implement Ewy's cardiocerebral resuscitation demonstrated a quantum leap in neurologically intact survival. Others, which stayed with the guidelines, showed much lower survival but with considerable variation among cities.

Post resuscitation care is another link added to the chain of survival.

The 2010 guidelines come short of adopting Ewy's cardiocerebral resuscitation protocols and therefore don't go far enough. Lay rescuers are to be taught compression only CPR but professional rescuers are stuck with the old 30:2 with only the initial sequence changed (compressions first then breathing). Thus, “best practice” falls five more years behind best evidence. In the spirit of transparency Dr. Kleinman noted that during guideline development there was considerable debate, and there was a “camp” of experts who wanted to eliminate ventilations altogether in adult cardiac arrest.

Quantitative waveform capnography. This is now in the main cardiac arrest algorithm. The beauty of this technique is its multiple uses, starting with confirmation of ETT placement, to monitoring the maintenance of ETT placement, to monitoring the quality of compressions to alerting the provider of return of spontaneous circulation.

Atropine, which began to see a diminished role in 2005, is now gone from the cardiac arrest algorithm. It maintains a role in bradycardia.

Wednesday, October 20, 2010

Drug company influence and prescribing

PLOS Medicine has just published another systematic review on this topic. Although the review purports to be an update on prior reviews, it contains little in the way of new information. In fact it ignores the most significant new research findings in the field. More on that below. The conclusion reads:

With rare exceptions, studies of exposure to information provided directly by pharmaceutical companies have found associations with higher prescribing frequency, higher costs, or lower prescribing quality or have not found significant associations. We did not find evidence of net improvements in prescribing, but the available literature does not exclude the possibility that prescribing may sometimes be improved. Still, we recommend that practitioners follow the precautionary principle and thus avoid exposure to information from pharmaceutical companies.

Although no conflict of interest statement was included in the paper there are significant concerns about at least two of the authors, Peter Mansfield and Joel Lexchin. I have no doubts about the honesty of these authors but they are (like the rest of us) biased. In the case of these particular two authors the bias is heavily negative towards interactions between the medical profession and the pharmaceutical industry. Both, in one way or another, have campaigned over the last decade to drum up public opposition to physician-pharma interactions. Both were involved in the No Free Lunch initiative. Having participated in the No Free Lunch listserv with these authors I can imagine the presuppositions they must have brought to this analysis.

Despite this bias, the authors apparently felt the evidence was inconclusive and had to base their recommendations against interaction on the precautionary principle (assume the worst and play it safe).

In my Medscape Roundable piece a couple of years ago I explained what was wrong with the published literature on this subject (my emphasis):

Studies in support of this argument do not give a balanced view. Surveys of the effects of drug detailing on doctors' prescribing have focused selectively on areas of overuse, such as antibiotics in the ambulatory setting and new expensive drugs compared with equally effective generics. Although some promotions undermine evidence-based practice, others may enhance it. Because promotional literature is a mix of good and bad information, the net effect on patient care is not known. Many heavily promoted treatments are evidence-based and known to be underutilized by doctors. A good example is the inadequate use of low-molecular-weight heparin for thromboembolism prophylaxis.[11] The promotion of statin drugs[12-14] and angiotensin-converting enzyme inhibitors for appropriate patients[15-17] is another example. Such a promotion toward best practice has been ignored in published studies. Research in a broader range of clinical situations is needed before conclusions can be made about the overall effect on evidence-based practice.

Unfortunately opportunities for much of this research have been lost, because many evidence-based treatments have gone generic and are no longer promoted in the way they once were and the pipeline for truly innovative drugs is running pretty dry at the moment. In that same Medscape piece I also argued that none of the studies on the effects of promotion looked at outcomes. Since I wrote that piece there has been one very important study on industry supported promotion of evidence-based practice, and it looked at clinical outcomes. I am referring, of course, to the Surviving Sepsis Campaign, one of the most maligned industry campaigns in all of medicine. Suffice it to say, (for background see posts here, here and here) the campaign was associated with better adherence to evidence-based practice and reduced mortality. For Steve Novella's take at Science Based Medicine go here.

States' lawsuits against Obamacare

Here's an update from Wesley Smith.

Huge increases in health insurance premiums in Connecticut blamed on Obamacare

Via NBC Connecticut.

Wesley Smith opines:

Ta da!  Way to go President Obama and Democratic Congress.  Way to control health care costs.
But they knew this would happen.  I mean, how could they not?  But why? I believe the point of Obamacare is to destroy the private health insurance system, which would leave only the government there to pick up the pieces. Then, it will be ration, ration, ration, and centralized control, control, control over our lives–in the name of promoting “wellness” and “cutting costs.”
Repeal. Reform. Replace. Defund.

Democrats on Obamacare: Now that we know what's in the bill, let's fix it

Via Politico, via Secondhand Smoke.

Companies that decrease health benefits in the wake of Obamacare: add Boeing to the list

From NPR:

Aerospace giant Boeing is joining the list of companies that say the new health care law could have a potential downside for their workers.
In a letter mailed to employees late last week, the company cited the overhaul as part of the reason it is asking some 90,000 nonunion workers to pay significantly more for their health plan next year.
Via Secondhand Smoke

Tuesday, October 19, 2010

Misreading of echocardiograms not uncommon

Medpage Today reports on an abstract presentation from the American Society of Echocardiography:

A review by sonographers of cardiologist-interpreted echocardiography findings at a Milwaukee medical center during a period of just over a year indicated major discrepancies in 29% of cases, leading to unnecessary further diagnostic testing or treatments for the wrong indication, according to a study presented here at the American Society of Echocardiography meeting.

Monday, October 18, 2010

The 2010 ACLS guidelines are here!

The entire document is available as free full text and can be found here.

For a quick overview of the changes you can read the executive summary. I may have more to say about the guidelines as I work through the entire document but some highlights are here (comments apply only to adult patients):

The time honored ABC sequence for basic life support is out. CAB is in.

Forget “look, listen and feel.” If someone collapses and isn't breathing (or is only gasping) call 911 and start pumping.

Compression only CPR moves from being an option to the preferred method for lay rescuers.

Depth of compression changes from 1.5-2 inches to 2 inches or greater.

Quantitative waveform capnography for confirmation and maintenance of ETT placement now has a Class I recommendation.

Routine use or cricoid pressure is out.

For monomorphic, regular, stable wide complex tachycardias of unknown etiology you can now use adenosine.

For unstable bradycardia after failure of atropine chronotrope infusion (by which I assume they mean a dopamine drip) is equal to transcutaneous pacing.

The post resuscitation bundle, including a hypothermia protocol and early PCI, even while the patient is comatose, is recommended.

Triage of stroke patients to a designated center is a Class I recommendation.

Admission to a dedicated stroke unit is a Class I recommendation.

The extended time window for TPA administration for ischemic stroke is recognized, with slightly different exclusion criteria for the extended window.

There's a lot to talk about here, and I'll probably be posting additional details later.

Basic clinical skills: not dead but in critical condition

The physical exam has devolved into a symbolic “laying on of hands” and a coding facilitator. If those are its only functions we may as well abandon it from medical practice, as its only real clinical consequence is the spread of germs. There are other ways to generate revenue and make emotional connection with the patient. Those who defend it for its diagnostic power risk ridicule for being anachronistic. Left to its natural course this situation will only get worse. There are some clinician warriors who are fighting to restore and preserve basic clinical skills. DB is one of them, and he recently linked to this New York Times article about another: Dr. Abraham Verghese.

How metabolic alkalosis perpetuates itself

---and why it is accompanied by hypokalemia. Concise summary post at Nephron Power.

Prescription drugs occasionally cause false positive urine drug screens

From AJHP:

A total of 25 reports of false-positive UDS results were identified. Categories of medications included antihistamines, antidepressants, antibiotics, analgesics, antipsychotics, and nonprescription agents. Reports of false-positive results were found for the following formulary and nonprescription medications: brompheniramine, bupropion, chlorpromazine, clomipramine, dextromethorphan, diphenhydramine, doxylamine, ibuprofen, naproxen, promethazine, quetiapine, quinolones (ofloxacin and gatifloxacin), ranitidine, sertraline, thioridazine, trazodone, venlafaxine, verapamil, and a nonprescription nasal inhaler. False-positive results for amphetamine and methamphetamine were the most commonly reported. False-positive results for methadone, opioids, phencyclidine, barbiturates, cannabinoids, and benzodiazepines were also reported in patients taking commonly used medications. The most commonly used tests to screen urine for drugs of abuse are immunoassays, even though false-positive results for drugs of abuse have been reported with a number of these rapid-screening products.

If you're a busy hospitalist this is bound to come up from time to time.

Classic papers: vasculitis

Every once in a while a paper comes out that’s so important it deserves a permanent place in the clinician’s library where it can be referred to and read in the original again and again. I’ve recently found two such classic papers in the field of rheumatology, published in Rheumatic Disease Clinics of North America. The two papers, published six years apart, have the same title, one being an update of the other: Vasculitis: a set of pearls and myths.

Here are a few from the two papers.

Pearl: Classic Polyarteritis Nodosa Spares the Lungs.

Pearl: Classic polyarteritis nodosa (PAN) is often a curable illness.

Myth: PAN is sometimes associated with ANCA.

Pearl: The Development of Mononeuritis Multiplex in the Absence of Diabetes Mellitus or Multiple Compression Injuries Strongly Suggests the Presence of Vasculitis.

Myth: Temporal Artery Biopsies Are Not Necessary in Some Cases, Because They Do Not Change Treatment. Starting corticosteroids without making every effort to confirm the diagnosis by biopsy is a sin that often comes home to roost only months later when the patient suffers side effects of corticosteroids and the next physician to evaluate him or her is left to wonder whether or not he or she ever really had GCA at all.

What does one do if the biopsy is negative but GCA still seems likely? In such cases, we recommend reviewing the biopsy with the pathologist to confirm the adequacy of the specimen and the negative reading. It is also important to ensure that a Congo red stain of the tissues was performed to exclude amyloid deposition, because amyloidosis may mimic GCA closely. One may also consider having a temporal artery biopsy performed on the contralateral side if both sides were not biopsied initially. Finally, if the biopsies are unequivocally not diagnostic of GCA but there is still a strong case for the disease on clinical grounds, treat the patient for GCA, fully assured that everything possible to confirm the diagnosis has been done.

Pearl: Aspirin is an important adjunct to glucocorticoids in the therapy of GCA. Two retrospective cohort studies demonstrated that a baby aspirin along with prednisone is more effective at preventing visual loss and cerebral ischemic events than is prednisone alone.

Pearl: Immunosuppressive Therapy Is Not Required for Most Cases of Henoch-Schonlein Purpura. Treatment with corticosteroids is recommended in the setting of critical organ involvement that does not seem to be self-limited.

Pearl: Henoch-Schonlein Purpura in the Adult May Present in the Same Fashion As Microscopic Polyangiitis. Although HSP is less common in adults than in children, it should always be considered in the differential diagnosis of vasculitis. HSP in adults may be initially misdiagnosed as MPA.

Pearl: The Churg-Strauss Syndrome Tends to Unfold in Three Stages. A prodromal phase characterized by allergic disease (typically asthma or allergic rhinitis), which may last from months to many years; an eosinophilia/tissue infiltration phase in which remarkably high peripheral eosinophilia may occur and tissue infiltration by eosinophils is observed in the lung, gastrointestinal tract, and other tissues; a vasculitic phase in which systemic vasculitis afflicts a wide range of organs, ranging from the heart and lungs to the peripheral nerves and skin.

Pearl: Churg-Strauss Syndrome Has a Striking Predilection for the Peripheral Nerves and Myocardium.

Myth: CSS is an ANCA-associated vasculitis. A substantial percentage of patients who have CSS—more than 50% in some studies—are ANCA-negative.

Myth: CSS is caused by the use of leukotriene inhibitors. This myth, approximately as old as leukotriene inhibitors themselves, is a classic case of confounding... The tapering of prednisone permitted by a leukotriene inhibitor eventually unmasks the underlying CSS.

Pearl: Scurvy can mimic ANCA-associated vasculitis, particularly MPA. Scurvy can cause perifollicular petechiae that mimic purpura, extensive gum inflammation, and alveolar hemorrhage, all of which could be confused with MPA. Think of scurvy when a severely malnourished patient is suspected of having an ANCA-associated vasculitis.

Pearl: Takayasu's Arteritis Is Included in the Differential Diagnosis of a Young Woman Presenting with Cardiomyopathy. The myocardium may also be involved in TA with histologic features of an inflammatory myocarditis.

Pearl: Headaches in Takayasu arteritis are bad news. Takayasu arteritis tends to cause bilateral subclavian artery stenoses and stenosis of the infrarenal aorta or narrowing of the large vessels to both lower extremities. Unfortunately, it can also cause renal artery stenosis , leading to renin-mediated hypertension.. .blood pressure measurements in the arms and even the legs do not provide accurate reflections of the central aortic pressure, which may become dangerously elevated. The patient who has Takayasu arteritis and intractable headaches requires a serum renin measurement, a thorough investigation of the circulation to all extremities, precise imaging of the renal arteries, and an accurate determination of the central aortic pressure.

Myth: Buerger's Disease Is a Disorder of Men. Although the classic Buerger's disease patient is a young male smoker in the fourth or fifth decade of life, … Women now comprise between 11% and 23% of all Buerger's disease cases.

Myth: Buerger disease is a systemic vasculitis. Buerger disease is characterized pathologically by a highly cellular thrombus with relative sparing of the blood vessel walls. Multinucleated giant cells can even be observed within the clot in Buerger disease. The architecture of the vascular wall is preserved, and there is no fibrinoid necrosis. The histopathologic findings in this disease provide significant insights into why systemic immunosuppressive therapy is relatively useless in Buerger disease.

Pearl: Buerger disease does not occur in only one limb. If called to see a patient who has intense ischemia in only one limb and no angiographic evidence of disease in other extremities, Buerger disease is not the diagnosis.

Myth: Buerger disease may present with Raynaud phenomenon. Buerger disease causes digital ischemia equaled by few other disorders, but it is not because of Raynaud phenomenon.

The two articles combined comprise about 100 pages of text. They are worth reading in their entirety. Study them and know vasculitis. Access the papers via MD Consult or ask your hospital librarian to get copies.

Thursday, October 14, 2010

STEMI, NSTEMI or STEMI equivalent?

It doesn't matter much what you call this pattern so long as you know it indicates acute LAD occlusion. The author of the post calls it a STEMI. But it's a STEMI only in a sense—-in the sense that it represents acute LAD occlusion and should therefore be treated like a STEMI. But I would prefer to call this a STEMI equivalent because from a pure morphology standpoint it's a NSTEMI, there being no ST segment elevation, at least not in two contiguous leads (the minimal ST elevation in V1 could pass as normal variant ST elevation in that lead).

This is a good example of why, in the recent literature review published by Dr. Brendan Phibbs, the STEMI/NSTEMI distinction was meaningless in terms of pathologic correlation.

In the case under discussion here, the indicative STEMI equivalent changes are found mainly in V2 and V3. Note the high amplitude, broad based T waves (spread-eagle T waves as Barney Marriott affectionately called them). The pattern is typically seen in the very early “hyperacute” phase, so a repeat tracing minutes later often shows the typical ST segment elevations.

The blog author makes some important teaching points about this fascinating case:

Never trust the computer. Computerized ECG interpretation was introduced into clinical use in the early 80s. Although several generations of new machines have come out since then, almost three decades later they remain notoriously inaccurate. Most of the time you can trust them with the numeric data, which saves you some work with the calipers, but for analysis of rhythm, ischemia and infarction patterns all bets are off.

Be cautious in the interpretation of ST depressions. Contrary to what the computer may try to tell you, ST segment depressions do not localize ischemia (T wave inversions and ST elevations do, but ST depressions don't). However, ST depressions may indicate that ischemia is present and they may constitute reciprocal changes which sometimes offer the most important clues in the entire tracing. In this case, the author makes the point that when ST depressions are in the inferior leads only they likely represent reciprocal changes of anterior or high lateral STEMI equivalent and should be considered such in appropriate clinical circumstances, until proven otherwise.

The post also has some pearls on differentiating benign early repolarization from pathologic ST elevations, and is worth reading in its entirety.

Corticosteroids for CAP?

There's been some interest in this over the past couple of years, but not enough evidence to change practice. This recent paper showed no benefit.

Wednesday, October 13, 2010

Medical show and tell: scurvy

Via Emergency Physicians Monthly.

Don't forget the new milk alkali syndrome

Which might now be better named the calcium alkali syndrome. TUMS is the new culprit and, according to this post from Nephron Power, it's the third most common cause of hypercalcemia resulting in hospital admission.

Epilepsy or syncope?

Is it in your head or your heart? If the EEG is normal, think heart.

Extended duration VTE prophylaxis in medical patients

Extended duration (post hospital) VTE prophylax in medical patients is is controversial and difficult to implement. This RCT suggests that it is beneficial only in selected patients:

Results: Extended-duration enoxaparin reduced VTE incidence compared with placebo (2.5% vs. 4%; absolute risk difference favoring enoxaparin, −1.53% [95.8% CI, −2.54% to −0.52%]). Enoxaparin increased major bleeding events (0.8% vs. 0.3%; absolute risk difference favoring placebo, 0.51% [95% CI, 0.12% to 0.89%]). The benefits of extended-duration enoxaparin seemed to be restricted to women, patients older than 75 years, and those with level 1 immobility.

Conclusion: Use of extended-duration enoxaparin reduces VTE more than it increases major bleeding events in acutely ill medical patients with level 1 immobility, those older than 75 years, and women.

Concordant and discordant ST changes, and what looks like torsades usually isn't

Lots of lessons in “advanced” electrocardiography in this case posted by Dr. Smith.

The EKG club

A discussion group on all aspects of electrocardiography and related topics.

Monday, October 11, 2010


The NNT is a web based tool that uses concise evidence summaries and neat little symbols to help users (doctors and patients) appraise evidence at a glance. The site was profiled recently in the WSJ Health Blog where Graham Walker, one of the site authors, was interviewed, and early on the article gets pretty confusing:

One of the site’s creators, Graham Walker, chief emergency resident at St. Luke’s-Roosevelt Hospital Center in New York City, tells the Health Blog he was surprised that data on the effectiveness of treatments “was out there, but not easily accessible.” 

Well that's odd sounding. Graham Walker's a pretty smart guy and I suspect EBM's nothing new to him. Did he really not know the data were out there? Or if he did, has he just decided it's not easily accessible? (It's been easily accessible for some time, of course).

If the NNT is critically appraising evidence who's critically appraising The NNT? Certainly not the WSJ Health Blog. There are some very concerning questions about the content that need to be asked. I'll attempt to address some of them here, but first a general comment. The basic idea of the project is sound. The process of EBM, which involves formulating the clinical question, hunting for evidence, critically appraising the evidence, assessing the magnitude of treatment effect and then applying all that to your patient's unique attributes is time consuming as I once blogged here and here. There are some secondary evidence sources on the web that perform some of those steps for you so you can take short cuts. The NNT does this in a very direct and simple way.

But maybe it's too simple. There are serious problems with the site's content. Let's look at a few examples. The section on TPA for ischemic stroke concludes “no benefits have been found for this intervention” and states that 1 in 20 patients will be harmed and none will benefit. A casual reader might wonder why the FDA hasn't yanked its approval, but those readers familiar with the long running controversy about TPA for ischemic stroke know where this is coming from. It becomes even more clear when you realize an important source of bias: all the site authors are emergency medicine physicians. It's well known that emergency medicine has been pushing back against TPA for ischemic stroke for years---almost ever since its approval for the indication. A balanced discussion of the controversy would have been welcome. Instead the authors seem to have spun the literature to the negative side in every conceivable way. I have blogged extensively about the nuances of this issue before and my take has been that while I am concerned about the consequences of declaring it as standard of care for ischemic stroke, I believe that, when applied with careful observance of the protocol and exclusion criteria, with appropriate systems of care in place and with meaningful informed consent, it is a useful intervention.

So how did they spin the evidence? First, in their evidence synthesis they included trials (9 out of the 11 they looked at) with a longer time window than that for which the drug is used. They justify that with this weak argument:

It has been argued that the difference between studies suggesting benefit and all other studies is the timing of the intervention. The Cochrane findings do not support this view, nor does one extensive post-hoc analysis.13 More importantly, the most recent study (ECASS-3) suggested benefits when thrombolytics were administered between 3 and 4.5 hours. This is outside the window that purportedly distinguished the NINDS trials, and effectively neutralizes time as the defining factor that separates trials concluding benefit from those that do not.

That issue is best addressed by this Lancet meta-analysis from May of this year:

Treatment was started within 360 min of stroke onset in 3670 patients randomly allocated to alteplase (n=1850) or to placebo (n=1820). Odds of a favourable 3-month outcome increased as OTT decreased (p=0·0269) and no benefit of alteplase treatment was seen after around 270 min. Adjusted odds of a favourable 3-month outcome were 2·55 (95% CI 1·44–4·52) for 0–90 min, 1·64 (1·12–2·40) for 91–180 min, 1·34 (1·06–1·68) for 181–270 min, and 1·22 (0·92–1·61) for 271–360 min in favour of the alteplase group. Large parenchymal haemorrhage was seen in 96 (5·2%) of 1850 patients assigned to alteplase and 18 (1·0%) of 1820 controls, with no clear relation to OTT (p=0·4140). Adjusted odds of mortality increased with OTT (p=0·0444) and were 0·78 (0·41–1·48) for 0–90 min, 1·13 (0·70–1·82) for 91–180 min, 1·22 (0·87–1·71) for 181–270 min, and 1·49 (1·00–2·21) for 271–360 min.

Patients with ischaemic stroke selected by clinical symptoms and CT benefit from intravenous alteplase when treated up to 4·5 h. To increase benefit to a maximum, every effort should be taken to shorten delay in initiation of treatment. Beyond 4·5 h, risk might outweigh benefit.

Although the NNT site updated the section on TPA in August of 2010 it contains no mention of the May meta-analysis.

In addition, the authors claimed that NINDS 1 showed no benefit from TPA. That conclusion is distorted. Although NINDS 1 did not show benefit at 24 hours NINDS 1, like NINDS 2, showed benefit at three months.

Also concerning is their analysis of anticoagulation for VTE. They conclude that while a few will be harmed by bleeding, 100% of patients will derive no benefit. It's hard to know where they're coming from here. There's no reason I can think of that they'd be biased against anticoagulation. Maybe they worship at the throne of the Cochrane database. The Cochrane review they cite indicates that there have been only two trials in recent history that address this issue, both of which were underpowered to detect a difference in outcomes. The lead author of that review, by the way, has a remarkable conflict of interest. Maybe they are approaching the topic from an extreme EBM purist view. From that point of view one could say, very technically speaking, that anticoagulation for VTE is not “evidence based.” I dealt with that issue in posts here and here. (BMJ's parachute study comes to mind).  It's an issue that deserves a more balanced approach than the NNT authors gave it. For a properly nuanced analysis, that makes the case that even though anticoagulation for VTE is not technically “evidence based” the evidence favoring treatment is overwhelming, the full text of this paper is a must read. (Also see my aforementioned posts for a description of the remarkable COI of the lead author of the Cochrane review). I don't want my next patient presenting with VTE to refuse anticoagulation. I hope they haven't read that section of NNT.

I have some concerns about other sections of the site, which I may address in a future post.

Colony collapse disorder---mystery solved?


Via Instapundit.

More on the Standard of Care Project

Grunt Doc weighs in.

Since I blogged about it here it looks like they've changed it from an on line petition to an actual vote by adding the option to disagree. Note the difference in font size, though.

More discussion on humanities, basic science and medical education

Anesthesioboist T guest blogs at Kevin MD on this subject. The post is titled Should humanities be the focus of prospective medical students? The question should not be whether humanities ought to be the focus. That implies a false dichotomy. Students can and should be well schooled in both humanities and basic science.

I agree wholeheartedly with the Anesthesioboist's points about the importance of a solid background in the humanities. But what concerns me about her post is what appears to be a straw man:

Most physicians who were science majors have of course come out in passionate defense of tradition, with some showing embarrassingly arrogant contempt for their counterparts in the humanities. They have called the Mount Sinai program an example of the “dumbing down” of American education, which I find patently offensive as a former English major who chose one of the most science-oriented specialties in medicine (but also, to my mind, one of the most artful).

And this---

I find the habit of many physicians of looking down at the humanities and humanities students completely obnoxious, but of course, I am biased.

I along with a few others who have expressed skepticism feel the jury's still out concerning the Mount Sinai program. We have expressed concern about the de-emphasis on basic science, which doesn't devalue humanities education in the least. There's plenty of room, even the traditional curriculum, for both.

Saturday, October 09, 2010

30 companies get exemptions from Obamacare provisions

USA Today story here.

Wesley Smith's take:

What a joke.  Last week there were reports that McDonald’s was going to drop its employees from health insurance coverage because Obamacare would increase the company’s costs.  This was roundly denied at the time, but now, guess what?  The bureaucrats have exempted McDonald’s and other companies–not to mention a big teacher’s union–from the rules that were supposed to protect us all. 

Doctors don't work on weekends?

That seems to be what Peter Orszag thinks. From his New York Times piece:

Doctors, like most people, don’t love to work weekends, and they probably don’t enjoy being evaluated against their peers. But their industry can no longer afford to protect them from the inevitable. 

Via Gateway Pundit.

Now that people are finding out what's in the health care bill

---they want it repealed according to another poll.

Friday, October 08, 2010

Republican agenda a recipe for a failed republic! NEJM

According to an NEJM perspective piece prospects for the upcoming midterm elections should terrify everyone!

Such an outcome would trouble ACA opponents: their goal is repeal. It would trouble ACA supporters: they want the law to work. But it should terrify everyone. The strategy of consciously undermining a law that has been enacted by Congress and signed by the president might conceivably be politically fruitful in the short term, but as a style of government it is a recipe for a dysfunctional and failed republic.

The outcome he's talking about is based on the fact that the Republicans would have a tough time repealing health care reform over an Obama veto. A more likely scenario is that they could defund or otherwise cripple it.

More from Wesley Smith.

Another performance system that doesn't work: SCIP

Being an Internal Medicine type I don't know a whole lot about SCIP so I'll leave the deconstruction to Skeptical Scalpel, guest blogging at Kevin MD. What's apparent from his analysis, though, is that the problems with SCIP mirror the problems of many other performance measures. It's not that they're not evidence based (they are) but when you turn then into a publicly reportable game the unintended consequences and the shortcomings of oversimplification come strongly into play.