Medical reversal is the latest hype. What is it? Here's the simple version: 1) Doctors treated based on opinion and tradition, with a lack of strong evidence or weak evidence that was rushed into implementation. 2) Really good evidence finally came along to refute said treatment. 3) Reversal of thinking resulted.
Now I'm here to tell you that it just ain't that simple. Indulge me and let's be more nuanced for a moment.
What prompted me to write this was an article and accompanying editorial in this month's Mayo Clinic Proceedings on the subject. I figured I had better weigh in before popular media outlets catch hold of it and dumb it down.
Beyond the fact that science is tentative, medical reversal takes on many forms and occurs for multiple and complex reasons. Three examples I've lived through come immediately to mind. On the surface they are similar but when examined closely hardly warrant being placed in the same category.
The latest one making the rounds is perioperative beta blockers (see here and here). Yes, it's a reversal and a big one, but not a very good example because it's an anomaly. It's an anomaly because the publications that drove the initial enthusiasm are now beset with questions of research misconduct.
Another example from a few decades ago almost fits the formula above. In the 1970s and 1980s the practice of suppressing premature ventricular contractions (PVCs) with antiarrhythmic drugs was widespread but based on weak rationale and little evidence. Then, 24 years ago today, evidence based medicine (even though we didn't call it that back then) came to the rescue in the form of the CAST results. The reversal, which ensued virtually overnight, is perhaps to this day the most widely cited example of why we needed evidence based medicine.
An example from about a decade ago concerns strict glycemic control in the ICU. Bob Wachter offered an insightful analysis on how that one bit the dust. Reversal again, but for yet a different reason. By the time strict glycemic control in critical illness came into fashion EBM was going full tilt, so a lack of EBM was not to blame. Rather, as Wachter explains, it was a misuse of the principles of EBM by turning evidence into a performance metric. (Turning the evidence based approach into performance, by the way, trumps two of the three principles of EBM but that's a topic for another post).
The authors of the Proceedings article came up with 146 examples from the past decade of what they consider to be reversals. But many of the examples were not true reversal. Some were merely examples, common in medicine, of one RCT conflicting with the results of another. Prescient clinicians have long understood the tentative nature of a single RCT and that differences in design and study populations often lead to differing results. This is not medical reversal. Other examples represented the phenomenon known as the swinging pendulum, something long known and accepted throughout the history of modern medicine. Others merely reflected later studies modifying, though not contradicting, prior research. It's a stretch to imply that any research finding that changes practice is a reversal. And some of the examples cited did not even warrant change in practice.
Accompanying the article is a video segment in which the lead author suggests that patients should do their own critical analysis of treatments offered them and consider avoiding interventions not supported by RCTs lest they find themselves harmed by a treatment later to be reversed. But many treatments now in common use which are widely regarded as life saving remain unsupported by high level RCTs. Examples include antimicrobial therapy for bacterial meningitis, and ehrlichiosis and antcoagulation for venous thromboembolism. Would the authors hesitate to administer these treatments? (Well, don't laugh).
We've long known and accepted that new research often modifies the conclusions of prior research. But the author, throughout the video, is trying to turn this into something worse. This is illustrated at 05:52 where he cites the AFFIRM study as contradicting rhythm control as a strategy in the management of atrial fibrillation. Nonsense. AFFIRM showed similar outcomes in populations teated with rate control and rhythm control. Pre-AFFIRM, clinicians used clinical judgment to determine which strategy to use. Post-AFFIRM they're doing the same. AFFIRM refined our understanding of the treatment of atrial fibrillation but it was not a game changer and it was certainly not a reversal.
The phenomenon of reversal has been widely hyped and the Proceedings article is no exception. But there are lessons we can learn from the paper. Sometimes we just need to slow down. Bob Wachter said it well:
Although many, including me, have long lamented the glacial pace of adoption of evidence-based practices in American medicine (often 5-15 years after the emergence of truly robust evidence supporting a practice), this traditional time lag did have one virtue: it allowed the literature to mature.
Maybe we're relying too much on the latest tweet and should go back to the textbook every now and then.
Academic emergency medicine is doing an amazing job of reviving electrocardiography. The new generation of ECG masters (to fill the void left by Marriott and the rest of that dying breed among his contemporaries) is coming largely from emergency medicine. Why EM of all places? I think it's because they are discovering that the electrocardiogram, as opposed to other tests, provides highly specific and predictive information on many sick and crashing patients, and does it fast. And the ED is where you need it really fast.
So with that introduction here's a post on the electrocardiographic diagnosis of posterior MI from one of my favorite emergency medicine blogs.
Posterior MI has been the victim of confusing terminology. It often occurs along with inferior infarction and decades ago inferior and posterior MIs were lumped together such that all inferiors were termed “posterior” by many clinicians. Later, in an attempt to make the proper distinction, posterior MIs were designated “true posterior.” The traditional method for easy electrocardiographic diagnosis is the mirror test in which you flip the tracing over and upside down, hold it up to a light and “read through” the back side, premised on the idea that leads V1-3 provided a mirror image of the indicative changes.
The above referenced post goes through the diagnostic criteria as well as the placement for leads V7-9. By the way, V6 is right next door to V7. Don't go to the bank on it but on the standard 12 lead it may offer some clues.
Image: Mt. Moran, Grand Teton National Park, and its mirror image in Jackson Lake.
This entity has also been called septic encephalopathy. It has been talked about for years though not a whole lot is known about it.
Yes, with surprising accuracy. There's even a formula to estimate the EF. New findings validating the electrocardiographic criteria along with a review of previous studies are presented in this paper.
A review in the green journal:
Clinical Significance
• In acute stroke, first exclude intracranial hemorrhage, a contraindication to thrombolysis.
• Cervical and cerebral arteries can be evaluated with computed tomography (CT) or magnetic resonance (MR) angiography to look for clot, significant stenosis, dissection, arterial occlusion, and other vascular abnormalities.
• Perfusion studies can be performed with either CT or MR to assess for ischemic penumbra and core infarct.
• Conventional angiography is typically reserved for intra-arterial therapy.
I blogged some concerns on this topic the other day. Now we have this new paper in Heart. So what did they do? They excluded the discredited publications on the topic and did a meta-analysis on what was left:
Results Nine secure trials totalling 10 529 patients, 291 of whom died, met the criteria. Initiation of a course of β-blockers before surgery caused a 27% risk increase in 30-day all-cause mortality (p=0.04)...
Conclusions Guideline bodies should retract their recommendations based on fictitious data without further delay. This should not be blocked by dispute over allocation of blame. The well-conducted trials indicate a statistically significant 27% increase in mortality from the initiation of perioperative β-blockade that guidelines currently recommend. Any remaining enthusiasts might best channel their energy into a further randomised trial which should be designed carefully and conducted honestly.
It's been tweeted around today that this represents a big reversal. Indeed it does, though not as abrupt as it might appear. Guideline writers began narrowing their recommendations for perioperative beta blockade back in 2009, since which time the only remaining class I recommendation regarding perioperative beta blockers is that they be continued perioperatively for those patients already taking them for a class I indication. Initiation in various high risk situations has since 2009 carried a IIa recommendation. The class I indication will likely stay. The IIa ones will likely go away in view of the new meta-analysis.
Health care in the U.S. is fragmented and disorganized. Policy experts for years have sought ways to remedy the problem through coordination and integration of care. On the national level results have been disappointing. Only an exceptional few local systems have been able to pull it off effectively. These are worth looking at. One example is Wisconsin-based Gundersen Health, recently profiled in Mayo Clinic Proceedings.
To get a visceral appreciation for the culture needed to have integrated health care read Atul Gawande's collection of anecdotes about other communities.
A recent review provided as free full text in Mayo Clinic Proceedings covered some underappreciated, though not really new, concepts about risk factors for atrial fibrillation.
Of note:
Evidence that caffeine increases risk is hard to come by. However, it is well known that alcohol does so in a dose related fashion.
Metabolic syndrome is a risk factor for atrial fibrillation as are some of its individual components including obesity. On the opposite end of the spectrum so is extreme exercise. This paradox suggests that atrial fibrillation represents two distinct diseases.
A recent post at Billy Rubin's Blog pointed me further down the trail of exercise and the heart. He cited a New York Times health blog piece concerning the paradox, which he thinks sends the wrong message to some. What concerned me more about the article was the implication that the paradox is new or controversial:
The Vasaloppet, a grueling 56-mile cross-country ski marathon held each March in northwestern Sweden, provides a convenient venue for studying the impacts of intense, prolonged aerobic exertion on the human body, and in recent years, several studies have reported on the generally enviable fitness and longevity of the racers.
But the newest Vasaloppet-related study, published in June in The European Heart Journal, is worrisome.
It's not all that controversial and certainly not new. Here are the findings of the European Heart Journal study:
Aims We aimed to investigate the association of number of completed races and finishing time with risk of arrhythmias among participants of Vasaloppet, a 90 km cross-country skiing event...
Methods and results..Primary outcome was hospitalization for any arrhythmia and secondary outcomes were atrial fibrillation/flutter (AF), bradyarrhythmias, other supraventricular tachycardias (SVT), and ventricular tachycardia/ventricular fibrillation/cardiac arrest (VT/VF/CA). Among 52 755 participants, 919 experienced arrhythmia during follow-up. Adjusting for age, education, and occupational status, those who completed the highest number of races during the period had higher risk of any arrhythmias [hazard ratio (HR)1.30; 95% CI 1.08–1.58; for greater than or equal to 5 vs. 1 completed race], AF (HR 1.29; 95% CI 1.04–1.61), and bradyarrhythmias (HR 2.10; 95% CI 1.28–3.47). Those who had the fastest relative finishing time also had higher risk of any arrhythmias (HR 1.30; 95% CI 1.04–1.62; for 100–160% vs. greater than 240% of winning time), AF (1.20; 95% CI 0.93–1.55), and bradyarrhythmias (HR 1.85; 95% CI 0.97–3.54). SVT or VT/VF/CA was not associated with finishing time or number of completed races.
The results were driven entirely by bradyarrhythmias and atrial fibrillation. The atrial fibrillation seen here was almost certainly vagally mediated atrial fibrillation, a long and well known clinical entity associated with extreme athletic conditioning. It and the vagally mediated bradyarrhythmias reported in the study can occasionally pose a clinical nuisance but for the most part are pretty benign.
But extreme vagotonia (and vagal tone is often considered a manifestation of a healthy cardiovascular system) is not the only consequence of ultra conditioning. The authors of the above review published an earlier paper in the Proceedings about structural damage that can occur:
Emerging data suggest that chronic training for and competing in extreme endurance events such as marathons, ultramarathons, ironman distance triathlons, and very long distance bicycle races, can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which return to normal within 1 week. Over months to years of repetitive injury, this process, in some individuals, may lead to patchy myocardial fibrosis, particularly in the atria, interventricular septum, and right ventricle, creating a substrate for atrial and ventricular arrhythmias. Additionally, long-term excessive sustained exercise may be associated with coronary artery calcification, diastolic dysfunction, and large-artery wall stiffening.
This of course refers to a healthy population. There are those occasional individuals who have sudden events related to acute exertion because of pre-existing disease. The clinical significance, if any, of the structural changes cited above is not known.
Like other things in nature, there seems to be some optimal dose of exercise beyond which diminishing return and maybe even harm occur. We're not sure what the magic number is but the authors of the Proceedings papers seem to think it is about an hour a day.
Here's a nice summary over at Academic Life in Emergency Medicine.
This is the most extensive review of the experience with these infections I’ve seen. Lots of good information here.
I'm not sure I believe it but this study showed it to be as good as an anticoagulant in the extended phase of prophylaxis after hip surgery:
Intervention: After an initial 10 days of dalteparin prophylaxis after elective THA, patients were randomly assigned to 28 days of dalteparin (n = 400) or aspirin (n = 386).
Measurements: Symptomatic VTE confirmed by objective testing (primary efficacy outcome) and bleeding.
Results: Five of 398 patients (1.3%) randomly assigned to dalteparin and 1 of 380 (0.3%) randomly assigned to aspirin had VTE (absolute difference, 1.0 percentage point [95% CI, −0.5 to 2.5 percentage points]). Aspirin was noninferior (P less than 0.001) but not superior (P = 0.22) to dalteparin. Clinically significant bleeding occurred in 5 patients (1.3%) receiving dalteparin and 2 (0.5%) receiving aspirin. The absolute between-group difference in a composite of all VTE and clinically significant bleeding events was 1.7 percentage points (CI, −0.3 to 3.8 percentage points; P = 0.091) in favor of aspirin.
Limitation: The study was halted prematurely because of difficulty with patient recruitment.
Conclusion: Extended prophylaxis for 28 days with aspirin was noninferior to and as safe as dalteparin for the prevention of VTE after THA in patients who initially received dalteparin for 10 days. Given its low cost and greater convenience, aspirin may be considered a reasonable alternative for extended thromboprophylaxis after THA.
I wonder whether either treatment did anything. Evidence favoring the extended phase (beyond 10 days) of prophylaxis must be somewhat weak, as the ACCP guidelines do not give it a definite recommendation (they only suggest it).
What are we to do now that much of the literature on this topic is beset with allegations of research fraud? A review last year in the green journal tried to make sense of things. Key points:
• The evidence regarding the cardiac benefit of perioperative beta blockade is in doubt owing to allegations of research fraud.
• Perioperative beta blockade must be administered appropriately and judiciously in a narrow spectrum of patients.
• Whenever implemented, attention to hemodynamic parameters is critical to ensure the safety of perioperative beta blockade.
• Greater oversight and structural reform is necessary to prevent perioperative research misconduct.
The authors go through the rapidly swinging pendulum of the last few years concerning perioperative beta blockers and elaborate on the above points:
1 First, we must exercise clinical restraint and recognize the double-edged sword that is perioperative beta-blocker treatment. While beta-blockers blunt surgical hemodynamic stress to preserve myocardial oxygen supply, the price paid is failure to augment cardiac output in situations where blood loss, systemic vasodilation, and intravascular volume shifts are the norm. This scenario is more compelling in the elderly, who, owing to preexisting vascular stiffness and reductions in peak heart rates, have narrower volume “set-points” and are more at risk of systemic collapse. We must therefore limit beta blockade to patients with established coronary artery disease already on this therapy, or in those with documented ischemia and concerning cardiac symptoms facing high-risk surgery. Any generalizations beyond these subsets are not supported by current evidence and may be associated with significant harm.
2 Second, in a post-POISE era, we can no longer afford to overlook the risks associated with this treatment. Whenever considered, beta-blockade should be started weeks, not days, before surgery with slow and careful titration to individual heart rate and blood pressure. Correspondingly, unless concerns about hemodynamic instability surface, beta-blockers must not be discontinued abruptly in patients undergoing surgery in order to avoid precipitating a withdrawal state leading to sympathetic activation and cardiac events. However, even when administered for appropriate indications, careful monitoring for hypotension and bradycardia coupled with judicious withholding of medication must be planned. Without such supervision, perioperative beta blockade remains a dangerous and potentially lethal practice.
Who says there's no evidence based treatment for ADHF? A lot of people say so particularly in view of the disappointing results with nesiritide and other novel heart failure treatments. But here's a paper suggesting a method of administering loop diuretics which pays dividends in terms of an important clinical outcome: readmission. From the paper:
This analysis aimed to compare clinical outcomes of patients admitted with ADHF who received a diuretic dosing protocol with those who received the usual diuretic therapy. We performed an observational medical records review to compare the use of a nurse-driven diuretic dosing protocol with usual diuretic dosing for patients admitted with ADHF during a 1-year period. Using a propensity scoring model, comparisons were made between groups for total weight loss, length of stay (LOS), 30-day readmissions, in-hospital mortality, 30-day mortality, and acute kidney failure. Sixty-eight of the 596 patients admitted with ADHF during the study period received the diuretic protocol. Protocol use was associated with an additional 2.63-kg weight loss (P=.003) but a trend toward increased LOS compared with patients receiving usual care (P=.097). However, patients receiving the protocol had a significantly lower risk of 30-day readmission (odds ratio, 0.46, 95% confidence interval, 0.22–0.95). Protocol use was not associated with significant differences in kidney failure, inpatient mortality, or 30-day mortality. A diuretic dosing protocol for patients admitted with ADHF improves weight loss and may lower 30-day readmissions, at the cost of potentially increasing LOS.
More from Today's Hospitalist.
It doesn't happen often but when you need it you need it. Here are some tricks of the trade and cautions.
In today's culture doctors who speak up may find themselves walking on thin ice according to this Medscape piece which concludes:
"If someone feels morally obligated to speak out, they have to accept the fact that it may be an ugly fight along the way," Noone says. "That's why I advise doctors to think twice before blowing the whistle."
Via Academic Life in Emergency Medicine.
This is a great video. I would like to add some nuance and point to some features that deserve special emphasis.
Early goal directed therapy (EGDT) remains in the new (2012) Surviving Sepsis Guidelines where it is referred to as quantitative resuscitation and protocolized resuscitation.
The lecture starts off with some definitions. He is a little fuzzy on the distinction between severe sepsis and septic shock, but so are the guidelines. They term it sepsis induced tissue hypoperfusion. The concept of septic shock is of practical importance because it defines the patient as being eligible for EGDT and to meet criteria in the septic patient you need either hypotension following the initial fluid boluses or an elevated lactate. You need one or the other, not necessarily both.
Starting at 3:02 the speaker mentions multi-organ dysfunction syndrome (MODS). That's an old term that isn't mentioned much in today's definitions but remains clinically valid. It means just what it says and is the late result of a cascade of injurious mediators and hypoperfusion that starts earlier. The early cascade marks the window of opportunity for interventions. By the time MODS sets in therapeutic efforts are less likely to produce good outcomes. The cascade often presents in the ER whereas MODS more typically is seen hours or days later in the ICU. So concerning the effectiveness of treatment remember: location, location location! The E in EGDT stands not only for early but also for ER. The incentive may be to just get the patient up to the ICU but previous trials with goal directed therapy commencing in ICU showed no benefit. EGDT, in contrast, has been shown to reduce mortality. The objective is to start EGDT in the ER and stave off MODS in the ICU. That's the point he's making at 4:01 in the video.
At 4:23 he mentions the CRASH syndrome. I'd never heard this term though am well familiar with the concept. It is a useful construct and goes like this: although for most infections the initial inflammatory cascade in the ER sets the stage for MODS and death later in the ICU (so that the ultimate consequences of the cascade are not usually seen in the ER) a few exceptional infections are more likely rapidly fatal, or at least rapidly progressive to MODS, right there in the ER. These include meningococcemia, neutropenic sepsis, encapsulated bacterial infections in asplenia, infections in liver failure and necrotizing fasciitis. (MRSA pneumonia is also mentioned though I think that it can appear more indolent on occasion).
At 5:54 he says he would probably intubate most septic patients. I would take issue though I agree with the principle he is trying to invoke. That is, the diaphragm is a big oxygen consumer and lactate generator and it is sometimes helpful in the septic patient to off load it. Intubation may be an underutilized intervention in sepsis though many patients can be managed without it. In fact, the surviving sepsis guidelines mention mechanical ventilation ONLY in those patients in whom sepsis is complicated by ARDS.
Again at 6:47 he talks about the distinction between early goal directed therapy and goal directed therapy, and correctly points out that prior research showed that when goal directed therapy was delayed until arrival to ICU it was not helpful whereas EGDT started in the ER was associated with the NNT of 6.
The discussion of pressors begins at 7:55. Norepi is the front line drug. He lists vasopressin as second to be added as a NE sparing agent. The guidelines, however, list epinephrine as second in line and vasopressin as third.
Try not to be too distracted by the dog whining in the background. The poor pooch sounded starved for attention.
The American Board of Internal Medicine and the new ethos of academic honesty
I blogged several times in 2010 concerning this controversy and ended the series with a summary post here. Recently Mayo Clinic Proceedings published two articles on the topic. Among the authors of the first paper is the immediate past president and CEO of ABIM Christine K. Cassel, MD. Both papers deal with intellectual property rights of the ABIM and larger issues of academic honesty. Both papers attempt to delineate the boundaries of propriety. The Cassel piece makes it clear:
There is no ambiguity in what we ask physicians to agree to:
•Each physician who registers to take an ABIM examination is directed not to communicate examination content.
•Before admission to the examination, at the start of each examination, and immediately following the examination, physicians agree to a pledge of honesty to “not disclose, copy, or reproduce any portion of the material contained in this examination,” and they are warned that “ABIM will impose severe penalties on any candidate involved in efforts to provide specific examination question content to others.”
Not to disclose..any portion of the material.. OK. Reasonable people might disagree on exactly what that means. But it purports to be unambiguous and the sentence about not disclosing any portion has no qualifiers. As such it forces a certain interpretation. After taking the exam it's OK to say “Boy that was hard!” But statements like “I couldn't believe all the lupus questions on the test” speak to content. If you want to play it safe consider yourself gagged. ABIM means business.
The other paper, by Ruhnke and Doukas, suggests there are reasonable boundaries that can be drawn as to what is appropriate in exam discussions but ultimately fails to make a clear distinction. More below about that.
What happened---here's a brief summary for those new to the controversy:
About three years ago ABIM accused an internal medicine board review company, Arora, of harvesting board exam content from recent attendees and using such content, alleged to consist of actual exam questions, to teach subsequent courses. A suit filed against Arora was settled in ABIM's favor. It was not pleasant for ABIM diplomats who took the Arora course:
Over two thousand diplomats of the ABIM who had attended an Arora course (approved for 42 AMA category 1 CME hours) got a letter from ABIM expressing disappointment in their ethics for not blowing the whistle. A copy of this letter is to be maintained in those diplomats' ABIM files...
..emails between course attendees and Dr. Arora were examined, and a smaller number of physicians, 135 or so, were targeted for more severe sanctions (more than just the letter). In addition, a few of that latter group were sued by ABIM.
Meanwhile ABIM got into a tiff with another board review company, Frontrunners, over similar accusations of teaching from the test. There was a long and tortuous legal trail which I have not been able to follow with clarity. (As far as I can tell neither side is the clear winner yet). One of the issues is whether ABIM in partnering with the American College of Physicians (ACP) is trying to monopolize the board prep industry.
In the discussion that follows I will cover five aspects of the controversy: 1) general observations about board review resources; 2) conflicts of interest, real or perceived, driving ABIM's actions against board review companies; 3) ABIM's proprietary interest and violations of its intellectual property rights; 4) broader issues pertaining to academic honesty; and 5) where do you draw the boundaries?
General observations about board prep:
Though there are differences in degree all board review courses, to one extent or another, are guilty of what ABIM has accused Frontrunners and Arora of. This includes those that are unabashedly commercial like Frontrunners and those that are affiliated with academic institutions like Mayo, Hopkins, etc. Having attended several in the latter category I have heard speakers who have written board questions, recently taken the exam themselves and gotten feedback from residents. Without question they use the information thus gained in their teaching points. I am left wondering which courses ABIM will target next.
Conflicts of interest, real or perceived, on the part of the ABIM:
ABIM has partnered with ACP in the board prep and recertification process. Is that a conflict of interest that motivated ABIM to go after competing board review companies? I would find it difficult to believe. I really don't know. But if the conflict isn't real it is widely perceived. And perceived conflicts are important as well as real ones in the minds of many ethicists. Public perception, they might argue, impacts public trust. If the public doesn't care practicing internists do. Internists in the rank-and-file need to feel that the ABIM is working for them and not against them. But confidence in the Board among practicing internists seems low these days.
ABIM's proprietary interest and copyright infringement:
I must say I was new to the idea of exam content as intellectual property when this controversy first erupted. It's clear, nevertheless, that the Board deems it so. ABIM has every right to defend its intellectual property. Candidates who took the exam signed a pledge and were bound by it. Those who disclosed exam content were wrong for violating the pledge. If it stopped there it would be easy enough to understand, but the Board didn't drop the matter there, choosing instead to elevate the discussion to the subject of academic honesty. That's where things get a little fuzzy.
Broader issues of academic honesty:
Let's be clear again: if a candidate for certification signed a non-disclosure pledge and then violated it they were wrong. But the ABIM goes a step further and calls it cheating. That warrants further discussion.
During the long educational journey we travel to become physicians we gradually learn the rules and values of academic honesty. These values are internalized to form an ethos that is agreed upon and shared among peers. We all know you can't copy from someone else's exam paper, bring unauthorized notes to the exam or plagiarize. Those activities constitute cheating. But what about studying from past exam content? Is that cheating as the Board claims? Apart from any consideration of stealing content (which is a legitimate concern of the Board) if studying from old exams is inherently wrong that's a new ethos. It's not part of the one we learned during our higher education. Using old exams as study material is common in graduate and post-graduate education. This is not the “it's OK because everybody's doing it” argument because professors have long recognized the process and even encourage it by posting their old exams on the web. Here is just one example from MIT. So look at what is going on. The Board is pointing to a practice long accepted by institutions of higher learning and suddenly calling it cheating. One could argue that it is or it isn't but if it is it's just been redefined. (It's a bit of a stretch so if you think I'm building a straw man read here). Why did the Board shift the discussion? They conflated two issues (copyright and academic honesty) that should be discussed separately. (Note that the Ruhnke paper, as I have quoted below, acknowledges and implicitly legitimizes the practice in higher education of studying from old exam materials).
Fuzzy boundaries:
If, as the Board claims, this is really about professionalism and academic honesty then any meaningful (not just verbatim) conveyance of exam content for teaching purposes would be a violation. Any form of teaching to or from the test would be a violation. That means every board prep resource out there, whether private or academically affiliated, is suspect. Indeed the very designation “board review” is suspect. It's simply what board review courses do. They teach the test. All of them.
The Ruhnke article makes that very point (even implicating ACP's board prep resources!), suggests there are boundaries we can draw to address the issue, but then fails to delineate them:
The distinction between cheating and guided study is crucial. Historical test questions are routinely used throughout higher education,9 and recent examination experience is commonly used to create focused study materials. The American College of Physicians produces the Medical Knowledge Self-Assessment Program, which includes a summary of high-yield information likely to appear on the examination.10 The introduction states, “The content was turned over to 11 carefully selected chief residents and fellows who had recently passed the certification exam. These physicians strained the essential testable points.” The editor continues, “As a frequent lecturer on Board preparation, I rely on input from hundreds of post-examination residents. With their ideas in mind, I refined the outline of Board Basics to target important topics and eliminate nonessential information.”10 Used by medical students for over 2 decades, the First Aid series is updated annually based on examinee reports. Using a focused study guide and sample questions created with examinees' input bears some similarity to using practice questions that may have been on a recent examination as a vehicle for targeted learning. The difference lies in the detail and specificity of the information conveyed to future examinees. Nevertheless, from the public's perspective, both practices represent shortcuts for examination success.
So what are the appropriate boundaries? It all depends on whether this about copyright or the larger issue of academic honesty. If it's about academic integrity as the Board claims, then all existing board review courses should come under scrutiny because they teach from past exam content.
From a recent paper in the American Journal of Medicine:
Methods
Patients with significant mitral regurgitation (moderate-severe or severe) undergoing noncardiac surgery were identified using surgical and echocardiographic databases at the Cleveland Clinic. The mechanism of mitral regurgitation was identified and classified as ischemic or nonischemic. By using propensity score analysis, we obtained 4 matched controls (patients undergoing noncardiac surgery without mitral regurgitation) for each case. The primary outcome was defined as a composite of 30-day mortality, myocardial infarction, heart failure, and stroke...
Results
A total of 298 cases and 1172 controls were included in the study. The incidence of primary outcome was significantly higher among patients with mitral regurgitation (22.2%) compared with controls (16.4%, P=.02). Analysis of the secondary outcomes revealed significant differences in perioperative heart failure (odds ratio, 1.4; 95% confidence interval, 1.02-2.0) and perioperative myocardial infarction (odds ratio, 2.9; 95% confidence interval, 1.2-7.3). Of patients with mitral regurgitation, those with ischemic mitral regurgitation had significantly more events than those with nonischemic mitral regurgitation (39.2% vs 13.3%, P less than .001).
The strong association between these two conditions is too often overlooked. The association has implications for diagnosis and management and is covered in this free full text review.
Once nearly extinct, the victim of a self-fulfilling prophecy, it is making a comeback and has a role in the care of selected patients with PE.
It appears to be an emerging infection according to this review. Think of it in cases of recurrent or non resolving pneumonias especially in the immunocompromised.
Recently published in NEJM:
Conclusions
The results of our study support the need for the continued use of prophylaxis with platelet transfusion and show the benefit of such prophylaxis for reducing bleeding, as compared with no prophylaxis. A significant number of patients had bleeding despite prophylaxis.
I was tipped off about this paper by a post at the Emergency Medicind PharmD blog. Apparently the dose of dilt for a fib rate control had not been well studied. In this study lower doses ( 0.2 mg/kg or less as an initial bolus) worked as well as the labeled doses and caused less hypotension.
The topic was reviewed at the Emergency Medicine PharmD blog. Glucagon somehow bypasses the beta receptor to stimulate adenyl cyclase so it makes physiologic sense, but the clinical evidence is scant. Apparently it's pretty benign but is thought of as a last resort measure.
---is questioned in this post at emergency Medicine PharmD. Well, I guess we don't know enough yet about how well HD really works, but the stuff is dialyzable and there's no evidence based alternative in terms of an antidote.
A nice summary post on the use of the product is up at Emergency Medicine PharmD. Full prescribing info on the product (Kcentra) is here.
Another post at the same blog has some background information. According to that post high level data are lacking about what's really the best agent for warfarin reversal though four factor PCC has at least theoretical advantages. Don't forget, too, that the ACCP guidelines now recommend it over other agents for reversal. My guess is that it is expensive and will be the topic of P&T committee discussions across the country in the coming weeks.
No, but a casual glance at this paper might give that impression. It deserves a more careful read. From the article:
Importance Federal efforts about public reporting and quality improvement programs for hospitals have focused primarily on a small number of medical conditions. Whether performance on these conditions accurately predicts the quality of broader hospital care is unknown...
Methods Using national Medicare data, we compared hospital performance at 2322 US acute care hospitals on 30-day risk-adjusted mortality, aggregated across the 3 publicly reported conditions (acute myocardial infarction, congestive heart failure, and pneumonia), with performance on a composite risk-adjusted mortality rate across 9 other common medical conditions, a composite mortality rate across 10 surgical conditions, and both composites combined...
Results..Hospitals in the top quartile of performance on publicly reported conditions had a 3.6% lower absolute risk-adjusted mortality rate on the combined medical-surgical composite than those in the bottom quartile (9.4% vs 13.0%; P less than .001). These top performers on publicly reported conditions had 5 times greater odds of being in the top quartile on the overall combined composite risk-adjusted mortality rate (odds ratio [OR], 5.3; 95% CI, 4.3-6.5)...
Conclusions and Relevance Hospital performance on publicly reported conditions can potentially be used as a signal of overall hospital mortality rates.
You can read more here from Medpage Today.
What is important to understand is that the mortality composites were for conditions OTHER than the three publicly reported ones. The connection between performance measures, real quality and outcomes is intangible and there is no warrant from the findings of this study for a direct cause and effect relationship.
What might the intangible factors be? For one thing, hospitals that score high on performance measures may be more resource rich and better staffed. After all it takes considerable time and effort to dot the i's and cross the t's in the medical record in order to score well. Performance is in large part a labor intensive medical record game. Other factors might be that a high scoring hospital has more hospitalists, more robust systems in place or a stronger culture of excellence. We really don't know, do we?
So, my final take...
What we knew before this study:
Performance does not equal quality.
Although performance measures were implemented to incent adherence to evidence based treatments they led to unintended consequences and have, for the most part, not been proven to benefit patients.
What we know in light of this study:
While there is no direct cause and effect relationship between performance and quality, both may be influenced in like manner by poorly understood external factors.
This recently came out in NEJM and everyone's talking about it:
In a randomized, double-blind, placebo-controlled trial conducted at 114 centers in China, we randomly assigned 5170 patients within 24 hours after the onset of minor ischemic stroke or high-risk TIA to combination therapy with clopidogrel and aspirin (clopidogrel at an initial dose of 300 mg, followed by 75 mg per day for 90 days, plus aspirin at a dose of 75 mg per day for the first 21 days) or to placebo plus aspirin (75 mg per day for 90 days). All participants received open-label aspirin at a clinician-determined dose of 75 to 300 mg on day 1...
Results
Stroke occurred in 8.2% of patients in the clopidogrel–aspirin group, as compared with 11.7% of those in the aspirin group (hazard ratio, 0.68; 95% confidence interval, 0.57 to 0.81; P less than 0.001). Moderate or severe hemorrhage occurred in seven patients (0.3%) in the clopidogrel–aspirin group and in eight (0.3%) in the aspirin group (P=0.73); the rate of hemorrhagic stroke was 0.3% in each group.
Conclusions
Among patients with TIA or minor stroke who can be treated within 24 hours after the onset of symptoms, the combination of clopidogrel and aspirin is superior to aspirin alone for reducing the risk of stroke in the first 90 days and does not increase the risk of hemorrhage.
Here's more from Medpage Today.
Some key points:
Prior studies failed to show benefits of dual antiplatelet therapy but they looked at different patient populations (denser and more catastrophic strokes) and had different designs (later treatment).
This study (CHANCE) looked at a more narrowly defined population. It also treated patients earlier (within 24 hours with nearly half within 12 hours). That is important because the event rate was higher early on, particularly in the first two days.
Patient selection was based on the NIH stroke scale for stroke patients (had to be 3 or less) and the ABCD score for TIA patients (had to be 4 or above). Other important exclusions are described in the body of the paper which is available as free full text at the link above.
It is uncertain how well the conclusions of this study, based on a Chinese population (with different risk factors and possibly different genetically programmed responses to Plavix), apply to patients in the US, where a similar trial is getting underway.
From a recently published cohort study:
Patients: Veterans who initiated metformin or sulfonylurea therapy for diabetes. Patients with chronic kidney disease or serious medical illness were excluded.
Measurements: Composite outcome of hospitalization for acute myocardial infarction or stroke, or death...
...crude rates of the composite outcome were 18.2 per 1000 person-years in sulfonylurea users and 10.4 per 1000 person-years in metformin users (adjusted incidence rate difference, 2.2 [95% CI, 1.4 to 3.0] more CVD events with sulfonylureas per 1000 person-years; adjusted hazard ratio [aHR], 1.21 [CI, 1.13 to 1.30]). Results were consistent for both glyburide (aHR, 1.26 [CI, 1.16 to 1.37]) and glipizide (aHR, 1.15 [CI, 1.06 to 1.26]) in subgroups by CVD history, age, body mass index, and albuminuria; in a propensity score–matched cohort analysis; and in sensitivity analyses.
According to the authors and the editors it cannot be said whether metformin confers macrovascular benefit, sulfonylureas cause macrovascular harm or both. In the 1970s the University Group Diabetes Program (UGDP) study showed macrovascular harm attributable to sulfonylurea therapy and the class of agents has since carried a black box warning. The UKPDS also suggested superior outcomes with metformin including specifically the macrovascular outcome of stroke.
The authors of the cohort study cite other prior research suggesting superiority of metformin, particularly for macrovascular outcomes, despite similarity in glycemic control compared to other agents.
The emerging picture is that for microvascular disease the more you lower blood sugar the better, no matter how. For macrovascular disease this does not hold true in simple fashion. If lowering blood sugar does matter, it matters how and with what.
There is more and more coming out about this. Recently the green journal published Pneumonia: An Arrhythmogenic Disease?
Background
Recent studies suggest that there is an increase in cardiovascular disease after pneumonia; however, there is little information on cardiac arrhythmias after pneumonia. The aims of this study were to assess the incidence of, and examine risk factors for, cardiac arrhythmias after hospitalization for pneumonia.
Methods
We conducted a national cohort study using Department of Veterans Affairs administrative data including patients aged greater than or equal to 65 years hospitalized with pneumonia in fiscal years 2002-2007, receiving antibiotics within 48 hours of admission, having no prior diagnosis of a cardiac arrhythmia, and having at least 1 year of Veterans Affairs care...
Results
We identified 32,689 patients who met the inclusion criteria. Of these, 3919 (12%) had a new diagnosis of cardiac arrhythmia within 90 days of admission. Variables significantly associated with increased risk of cardiac arrhythmia included increasing age, history of congestive heart failure, and a need for mechanical ventilation or vasopressors. Beta-blocker use was associated with a decreased incidence of events.
Conclusion
An important number of patients have new cardiac arrhythmia during and after hospitalization for pneumonia. Additional research is needed to determine whether use of cardioprotective medications will improve outcomes for patients hospitalized with pneumonia. At-risk patients hospitalized with pneumonia should be monitored for cardiac arrhythmias during the hospitalization.
(My italics above).
Additional reading:
Aspirin to decrease adverse cardiac events in pneumonia patients.
Sudden cardiac death in pneumonia and other infections.
Review in American Family Physician.
This study found a 1 year increase in mortality in discharged elders, attributable mainly to high dose PPI use. PPIs are great drugs but they must be used discriminately. Overuse may be driven by the belief that these drugs are benign, consumer demand and poorly conceived care bundles resulting in inappropriate prescribing for “GI prophylaxis.” The mechanisms of harm are gradually being discovered. See here.
Though hospitalist programs have long relied heavily on locums and continue to do so, increasing controversy surrounds the practice according to this article in Today's Hospitalist. Staffing company and hospitalist program leaders interviewed for the article say the difficult issues are the high cost of hiring locum doctors, instability of group culture and perceived quality problems. Quality issues are not necessarily inherent in the locum doctor, as many excellent hospitalists see locum work as an opportunity for flexibility and better compensation. But even great locum docs may look inferior on various metrics (artificial quality surrogates) because they lack a sense of group ownership and are not under institutional performance incentives. Part of the appeal of locum tenens work may be a sense of freedom from performance pressure.
If hospitalist groups intend to rely less on staffing companies as some leaders claim the trade off is to look to other sources of temporary help such as within-the-group moonlighting. No matter how you slice it staffing shortages remain critical and there's no sign of relief, making me wonder if last year's downtick in hospitalist compensation was an anomaly.
Good on prevention, not so good if you get sick. The authors of this NEJM piece seem to like it but don't romanticize it, they say. OK. From the article:
The system is not designed for consumer choice or individual initiatives. There is no alternative, private-payer health system. Physicians get government benefits such as housing and food subsidies, but they are paid only about $20 per month. Their education is free, and they are respected, but they are unlikely to attain personal wealth. Cuba is a country where 80% of the citizens work for the government, and the government manages the budgets...
A nephrologist in Cienfuegos, 160 miles south of Havana, lists 77 patients on dialysis in the province, which on a population basis is about 40% of the current U.S. rate — similar to what the U.S. rate was in 1985. A neurologist reports that his hospital got a CT scanner only 12 years ago. U.S. students who are enrolled in a Cuban medical school say that operating rooms run quickly and efficiently but with very little technology. Access to information through the Internet is minimal. One medical student reports being limited to 30 minutes per week of dial-up access.
The authors suggest that's the result of the U.S. Economic embargo.
----think beyond the valve. It's really a disease of the entire aorta. From the review:
A more recent study has looked at the incidence of aortic complications in 416 BAV patients (mean and median age 35 years, range less than 1–89) [32]. Incidence of aortic dissection was found to be 1.5% in all patients regardless of the progression of BAV; however this increased markedly in patients aged 50 or older at baseline to 17.4% and even more in those found to have aneurysm formation at baseline to (44.9%). 25-year rate for aortic surgery was 25% and there was a significant burden of progression of disease to cause aortic dissection with 49 of the 384 patients without baseline aneurysms developing them during followup, giving an age-adjusted relative risk of 86.2 and an incidence of 84.9 cases per 10000 patient-years.
I should know because I was involved in the movement nearly from the beginning. Back then the distinctive was that hospitalists were doctors who, having ascended a steep learning curve from practicing exclusively inpatient medicine, had a special degree of expertise and skill to meet the challenges of caring for the incredibly ill and complex patients who populate the hospital. In short, we were (once) valued for our clinical skills.
Right in line with this was the understanding that effective use of such skills would require enough time to spend with each patient. After all being a good clinician takes time. Practicing evidence based medicine takes time. This led early programs to define who and what they were clinically and to carefully structure coverage arrangements with appropriate restrictions. No one in their wildest imagination had any notion of taking over the hospital or admitting for everyone. At least not in the beginning. But hospitalist leaders started planting the seeds of that idea a few years ago.
I saw trouble brewing then and have blogged my concern many times since. I once made fun of the trend I observed as the hospitalist role was devalued and transitioned from expert clinician to utility player:
Hospitalist skill set, year 2000:
Management of CAP and HCAP
Management of sepsis
Management of venous thromboembolism
Management of DKA, adrenal crisis and other endocrine-metabolic emergencies
Management of COPD, asthma and ARDS, including ventilator management
Management of renal, fluid and electrolyte problems
Management of acute decompensated heart failure
Management of toxicologic emergencies
Providing consultation for complex and difficult diagnostic problems
Providing consultation for medical complications in surgical, subspecialty and general medical patients
Hospitalist skill set, year 2010:
Tweaking Press Ganey
Tweaking clinical documentation (DRGs)
Creative coding
Bed control
Admitology, roundology and dischargology for surgical and subspecialty patients
Cosmetic charting (performance measures)
Secretarial (CPOE)
So I recently found another published example of the trend in a recent issue of Today's Hospitalist: Universal admitters: hospitalists' new identity? The article cites the growing trend of hospitalists admitting nearly all comers regardless of the clinical need. This according to the article off-loads the specialists, expands the hospitalist's niche and serves the business needs of the institution. Several program leaders were interviewed. To their credit they paid lip service to the concerns about hospitalists becoming overburdened or taking on duties outside the scope of their training. Ultimately, though, to my disappointment, they seemed to one degree or another complicit with the new agenda.
For example:
"The greatest difficulty for hospitalist groups is not recognizing the value in being on the front lines of caring for the majority of patients," Dr. Bossard says. "Going into meetings with the idea that we're going to try to protect our turf and reduce the number of patients we carry by establishing rules to protect us won't work."
I have a little different view of protecting turf. If only the specialty services would protect their own turf! But they seem eager to give it up while hospitalists at the organizational level seem all to willing to capitulate and take it on.
Clinical skill has all but vanished as the raison d'etre for hospitalists. And in the article it's missing from the discussion of all the things the hospitalist “brings to the table,” for example computer skills:
Another factor driving hospitalists toward more admissions: Subspecialists are frustrated with electronic medical records. It makes sense to hand off the computer work associated with being the admitting physician to hospitalists, who log in much more screen time.
Though mentioned as an aside that paragraph says a lot about the changing agenda: the move toward hospitalist as secretary, H&P provider and off-loader.
Once an open access journal, American Family Physician for the past few years has been behind heavy access controls. Every once in a while a really good review shows up there. Recently they published this article on Guillain-Barré syndrome. It is worth reading in the full text if you can get it.
Some points of interest:
Though the varied spectrum of GBS has enough important features in common to discuss for practical purposes as a single entity it is probably best thought of as a group of diseases reflecting the different immune responses, different targets of immune injury (myelin vs axon), differences in epidemiology and the clinical variants.
Pain and autonomic instability are very common features, I think more than generally appreciated. So maybe you've got a patient presenting with funny unexplained pains and vital signs all over the map. Maybe with multiple preceding ER visits. Think of it!
Symptoms are bilateral and tend to be symmetric but may not be perfectly so at all points in the clinical course.
Reflexes have to be decreased but not necessarily absent at all points in the clinical course.
The epidemiology is complex. While often discussed in the context of Campylobacter jejuni, that infection is associated with a variant of GBS (axonal) not typical in the U.S. A variety of illnesses may precede GBS.
There are two arms of treatment: supportive and disease specific.
Supportive care addresses DVT prophylaxis, pain control, skin care, bowel and bladder issues, physical therapy, cardiac and vital sign monitoring and respiratory care. Multiple respiratory parameters can be monitored. The article lists, among other signs, forced vital capacity less than 20 mL/kg, maximum inspiratory pressure less than 30 cmH2O, and maximum expiratory pressure less than 40 cmH2O as risk factors for respiratory failure. The presence of any of the three signs, according to Up to Date, is an indication for urgent intubation and mechanical ventilation.
Disease specific modalities are plasma exchange and IVIG. One or the other is used, not both. Is one preferred over the other? The review article says plasma exchange is “first line.” The Up to Date section on treatment of GBS says the treatments are equivalent, and that IVIG tends to be favored due to availability and ease of use.
A recent paper reports a survey of state medical boards as to how they would respond to hypothetical scenarios:
High consensus was defined as more than 75% of respondents indicating that investigation was “likely” or “very likely,” moderate consensus as 50% to 75% indicating this, and low consensus as fewer than 50% indicating this.
Four online vignettes demonstrated high consensus: Citing misleading information about clinical outcomes (81%; 39/48), using patient images without consent (79%; 38/48), misrepresenting credentials (77%; 37/48), and inappropriately contacting patients (77%; 37/48). Three demonstrated moderate consensus for investigation: depicting alcohol intoxication (73%; 35/48), violating patient confidentiality (65%; 31/48), and using discriminatory speech (60%; 29/48). Three demonstrated low consensus: using derogatory speech toward patients (46%; 22/48), showing alcohol use without intoxication (40%; 19/48), and providing clinical narratives without violation of confidentiality (16%; 7/48).
In this study transient ECG abnormalities were seen around the time of the episode of pneumonia. Some resembled those seen in PE.
---after two more trials published in NEJM here and here.
There were problems with the data, leaving open the possibility of benefit. But it remains unproven. Perspective here via Medpage Today.
---was formerly known as diastolic heart failure. A recent paper was published in the American Journal of Medicine: Contemporary Prevalence and Correlates of Incident Heart Failure with Preserved Ejection Fraction:
Background
We assessed the prevalence of preserved left ventricular ejection fraction in patients with incident heart failure and differences in the demographic and clinical characteristics that may differentiate patients presenting with heart failure with preserved versus reduced left ventricular ejection fraction.
Methods
We identified all patients with newly diagnosed heart failure between 2005 and 2008 from 4 sites in the Cardiovascular Research Network on the basis of hospital discharge and ambulatory visit diagnoses, and assigned a category of preserved, borderline, or reduced left ventricular ejection fraction using data from electronic databases and chart review.
Results
We identified 11,994 patients with incident heart failure; of these, 6210 (51.8%) had preserved left ventricular ejection fraction, 1870 (15.6%) had borderline systolic dysfunction, and 3914 (32.6%) had reduced left ventricular ejection fraction.
The authors list these key points:
•Heart failure with preserved left ventricular ejection fraction is the most common form of the heart failure syndrome among patients newly presenting with this condition.
•Women and older adults are especially affected.
•Patients with ejection fractions less than 40% comprise less than one third of those with incident heart failure.
•Evidence-based treatment strategies apply to only a minority of patients with newly diagnosed heart failure.
What does that last statement mean? Treatments have been validated by high level evidence for long term clinical outcomes (for the most part treatments with life prolonging neurohumoral antagonists) only for patients with clearly reduced ejection fractions. But those patients made up less than one third of the incident heart failure cases in this database. There's a commonly held maxim that “there is no evidence-based treatment available for HFPEF.” That's not exactly true. While there's no generalized treatment for the disease per se there are treatments for its manifestations (diuretics for pulmonary edema, rate controlling medications for atrial fibrillation) as well as its associated risk factors and comorbidities. These are, indeed, evidence-based and they treat the patient more than the disease.
According to this review it is emerging as a core skill for critical care docs. Will it be such for hospitalists??
From the review:
In recent years, several focused echocardiography protocols have been introduced [12]. These studies can usually be carried out by novice operators after a modest amount of training.
There's hope!
A case report and brief review of glucagonoma is presented here along with a discussion of a few other entities that can produce the same dermatosis. Free full text.
A concise review centering around a case report.
Misconceptions about Lyme disease abound and have fueled politicized debates and a good deal of quackery. A recent piece in the green journal (free full text) provides some clarity and includes a list of bullet points about the misconceptions. Here are a few:
Myth:
“'Blood tests are unreliable with many negatives in patients who really have Lyme disease'”
Fact:
“Just as with all antibody-based testing, these are often negative very early before the antibody response develops (less than 4-6 weeks). They are rarely if ever negative in later disease.”
Myth:
“'Antibiotics make blood tests negative during treatment'”
Fact:
“There is no evidence that this happens and no biologic reason it would.”
Myth:
“'Lyme disease is a clinical diagnosis that should be made based on a list of symptoms'”
Fact:
“No clinical features, except erythema migrans or possibly bilateral facial nerve palsy—in the appropriate context—provide sufficient specificity or positive predictive value. Laboratory confirmation is essential except with erythema migrans.”
Myth:
“'B. burgdorferi infection is potentially lethal'”
Fact:
“Although Lyme disease can cause heart or brain abnormalities, there have been remarkably few—if any—deaths attributable to this infection”
Myth:
“'If, following treatment, symptoms persist, or serologic testing remains positive, additional treatment is required'”
Fact:
“Multiple well-performed studies demonstrate that recommended treatment courses cure this infection. Retreatment is necessary occasionally, but not frequently.”
Now as readers know I'm not a fan of the Institute of Medicine (IOM) but they are quoted in the article and I happen to agree with what they said:
...strong emotions, mistrust, and a game of blaming others who are not aligned with one's views” have resulted in a heated and politicized debate. A number of factors have contributed to this “debate”—perhaps not the least of which is a tension between the concept of evidence-based medicine and medicine's historical inductive approach from anecdotal observation. This tension is reflected in 2 frequently repeated, interrelated assertions—that laboratory testing for Lyme disease is unreliable and that the disease should be defined “clinically”—meaning syndromically.
Much of this review is applicable to the EP lab although it contains some updated information on the surface ECG and how it can help in differentiating AVNRT from other SVTs.
From an article in the American Journal of Emergency Medicine:
A total of 1947 ED patients were enrolled; 192 (10%) were taking metformin; 305 (16%) died within 28 days. Metformin users had higher median lactate levels than nonusers (2.2 mmol/L [interquartile range, 1.6-3.2] vs 1.9 mmol/L [interquartile range, 1.3-2.8]) and a higher, although nonsignificant, prevalence of hyperlactatemia (lactate greater than or equal to 4.0 mmol/L) (17% vs 13%) (P = .17). In multivariate analysis (reference group nonmetformin users, lactate less than 2.0 mmol/L), hyperlactatemia was associated with an increased adjusted 28-day mortality risk among nonmetformin users (odds ratio [OR], 3.18; P less than .01) but not among metformin users (OR, 0.54; P = .33). In addition, nonmetformin users had a higher adjusted mortality risk than metformin users (OR, 2.49; P less than .01). These differences remained significant when only diabetic patients were analyzed.
Conclusions
In this study of adult ED patients with suspected sepsis, metformin users had slightly higher median lactate levels and prevalence of hyperlactatemia. However, hyperlactatemia did not predict an increased mortality risk in patients taking metformin.
According to a recent systematic review:
Results
Thirty reports describing 58 cases (41 preparations containing sorbitol and 17 preparations without sorbitol) of adverse events were identified. The colon was the most common site of injury (n=44; 76%), and transmural necrosis (n=36; 62%) was the most common histopathologic lesion reported. Mortality was reported in 33% of these cases due to gastrointestinal injury.
Conclusions
Sodium polystyrene sulfonate use, both with and without sorbitol, may be associated with fatal gastrointestinal injury. Physicians must be cognizant of the risk of these adverse events when prescribing this therapy for the management of hyperkalemia.
The only proven indication for PEEP is hypoxemia that is refractory to reasonable fractions of inspired oxygen. Yet, “five of PEEP” has become a default setting in mechanical ventilation no matter what the indication due to physiologic rationale and tradition. If cardiac decompensation (cardiogenic pulmonary edema) is in the loop of respiratory failure the physiologic rationale becomes even stronger because positive pressure applied anytime during the breathing cycle decreases afterload and has other hemodynamic benefits. That was the subject of this recent paper. The evidence is scant but PEEP appears to be safe and may offer clinical benefit when cardiac decompensation causes or complicates respiratory failure.
Here is an update in the American Journal of Emergency Medicine. Both the congenital and acquired forms are discussed. For congenital LQTS beta blockers are mentioned as first line therapy. The general principle guiding this recommendation is based on two different types of triggers for Torsades in patients with long QT: sympathetic surge (generally seen in the congenital form) and increased cardiac cycle length in the form of pause or bradycardia (the usual trigger in acquired cases). Overlap exists, however. Some acquired cases represent a mutation with weak expression, the phenotype manifesting for the first time in the face of an external factor such as an electrolyte disturbance or drug effect. And while the majority of genotypes respond to beta blockers some may not. The usual role of the hospitalist is to recognize abnormal repolarization in its various forms and address external triggers such as drugs and electrolyte disturbances, and know when to call the electrophysiologist.
