Coordination and integration of health care

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.

Epidemiology of atrial fibrillation: emerging concepts

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.

Brugada syndrome: glance at an ECG, save a life

Here's a nice summary over at Academic Life in Emergency Medicine.

Infections due to Klebsiella Pneumoniae Carbapenemase (KPC) producing bacteria: a systematic review

This is the most extensive review of the experience with these infections I’ve seen. Lots of good information here.

Aspirin for VTE prophylaxis???

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).

Whither perioperative beta blockade?

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.

Protocol driven diuretic dosing in acute decompensated heart failure (ADHF)

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.

IV epinephrine when the patient has a pulse

It doesn't happen often but when you need it you need it. Here are some tricks of the trade and cautions.

Patient advocate or disruptive physician?

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."

Early goal directed therapy: Patwari Academy video

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. 

Converting from an IV diltiazem drip to PO

Here's a handy conversion. Via Emergency Medicine PharmD.

The Arora Internal Medicine Board Review controversy revisited

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.

Mitral regurgitation as a risk factor in non cardiac surgery

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).

Carotid artery stenting

An update.

COPD and heart failure

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.

Pulmonary embolectomy

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.

Pulmonary mucormycosis

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.

Pacemaker mediated angina

This purports to be the first published description which is surprising. I think I've seen this.

Prophylactic platelet transfusion in patients with hematologic malignancy

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.

Lower doses of IV diltiazem for rate control of atrial fibrillation

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.

LV outflow tract tachycardias

Here's a brief overview.

Glucagon for asthma exacerbation?

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.

Hemodialysis for dabigatran removal

---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.  

Four factor PCC now available in the U.S.

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.