Inflammatory myopathies

Review in Mayo Clinic Proceedings.  

What transfusion threshold for UGI bleeds?

Conservative was better in this study.

Writing as therapy and a tool for enhanced professional growth

Maybe this is why we blog.

Troubleshooting high ventilator pressures

Via Academic Life in Emergency Medicine.

Problems with EHR templates and other documentation tools

EHRs were touted early on as time savers while facilitating documentation in support of better reimbursement. The real world truth, as has since been discovered, is that it doesn't work that way if you want to be in compliance. And the regulatory compliance people are getting wise to that fact according to a recent article in Today's Hospitalist. If you want to be in compliance, say the authors, you either need to dictate, free text or spend a significant amount of time deleting and editing. Sorry, that's just the way it is.

From the article:

Hospitalists would never order an MRI scan unless it was medically necessary. Ditto for laboratory studies. But that can all change at the bedside where physicians may not think as much about medical necessity and instead go with their standard scripts for review of systems and physical exam.

Asking a patient with a femoral neck fracture about polydipsia? Probably a stretch. Cranial nerve examination on a patient with a diverticular abscess? Abuse, for sure, and potentially fraud.

That last one doesn't compute for most hospitalists. MRI scans cost thousands of dollars, but cranial nerve examination is just words on paper. What's the big deal?

My favorite is “pupils equal and reactive to light and accommodation.” I don't know about you but I have not checked accommodation in years.

What to do with troponin elevations when the clinical picture is uncertain

The ACCF 2012 Expert Consensus Document is helpful.

Points of interest:

MI type designations 1-5, respectively, denote unstable coronary artery obstruction, demand ischemia (supply/demand imbalance), sudden unexpected cardiac death, association with PCI and association with CABG. Though all are considered MI only type 1 is considered ACS.

In other situations troponin elevations signify myocardial involvement but not MI such as stroke, PE, sepsis, heart failure (see here) and chest trauma.

Some cases are non cardiac and due to lab artifacts or interfering substances (e.g. heterophile antibodies).

Consider the pretest probability and apply bayesian reasoning in unclear cases.

A CKMb is useful for confirmation in some cases.

Stroke after cardiac catheterization

It doesn't happen very often but it happens. Nowadays regional thrombolysis or clot retrieval may be options.

Octreotide for non-variceal UGI bleeds: state of the controversy

An update at the Emergency Medicine PharmD blog.

Mesenteric vein thrombosis

A free full text review is available from Mayo Clinic Proceedings.

Just a few points of interest:

Think of it when the patient's pain “seems real” and is out of proportion to physical findings.

Pain reaches maximum intensity relatively slowly whereas in acute mesenteric arterial occlusion maximum intensity occurs within minutes or even seconds.

Risk factors for arterial occlusion are cardiovascular---atrial fibrillation and atherosclerosis, whereas for MVT a structural or inflammatory abdominal process is often the underlying cause. Absent that, and in many cases, MVT is a disease of thrombophilia, We are taught to think thrombophilia when clots occur in unusual places. In MVT myeloproliferative disorders, with JAK2 mutation as a marker, stand out.

More about the JAK2 mutation can be found here.

Early anticoagulation improves outcomes. The degree of GI bleeding typically associated with MVT is seldom a contraindication.

Indications for surgical intervention are discussed.

Whither sedation interruption?

A lot of folks are no doubt rethinking the notion of daily sedation interruption in view of last November's JAMA paper which at first glance goes against the teaching of the past few years:

Intervention Continuous opioid and/or benzodiazepine infusions and random allocation to protocolized sedation (n = 209) (control) or to protocolized sedation plus daily sedation interruption (n = 214). Using validated scales, nurses titrated infusions to achieve light sedation...

Results Median time to successful extubation was 7 days in both the interruption and control groups...

Conclusion For mechanically ventilated adults managed with protocolized sedation, the addition of daily sedation interruption did not reduce the duration of mechanical ventilation or ICU stay.

So what does it mean and how might it change practice? To put the study in perspective it's helpful to listen to the interview with one of the authors available at the link above.

Can we say now that sedation interruption is of dubious benefit? No. Can we say that the evidence in support of sedation interruption is mixed? No. Prior research has established the benefits of sedation interruption. What is important to understand about this study is the comparison group which was treated with a protocol designed to sedate as lightly as possible. This is in contrast to conventional sedation in which patients definitely benefit from daily interruption.

If there is a practice changing message form this study it is that sedation, protocol driven to be as light as possible is better than conventional continuous sedation and so is sedation interruption and you need to do one or the other but not necessarily both. The study is not a license to ignore the need to use protocols to limit sedation and it is my suspicion that both approaches are about equally onerous to the ICU staff.

Don't forget procainamide---it's still around

Though all but forgotten among emergency medicine and hospitalist types it has a prominent place in several guideline recommendations. These are summarized in a recent post at Emergency Medicine PharmD. The relevant guideline documents are linked in the post. Of note:

The Canadian guidelines give it a class I recommendation for conversion of acute onset a fib to sinus rhythm. The a fib duration needs to be known with certainty to be less than 48 hours. (And by the way, enough of this nonsense about diltiazem converting patients to sinus rhythm. This misconception seems to be pervasive. It is driven by the fact that many patients with acute a fib convert spontaneously while on dilt for rate control. True, true and unrelated. Dilt's mechanism is in the AF node and there's nothing there that drives a fib).

The ACCF/AHA/HRS guidelines give it a class I recommendation for pre-excited a fib (WPW) provided the patient is hemodynamically stable.

The ACLS 2010 guidelines give it a class IIa recommendation for hemodynamically stable monomorphic VT (favored over amiodarone).

Keep in mind that procainamide can cause Torsades so watch the QT and be mindful of the K+ and Mg++.

Post-marketing experience with dabigatran

---is reassuring according to a recent JACC paper:

Conclusions In this ‘everyday clinical practice’ post-approval nationwide clinical cohort, there were similar stroke/systemic embolism, and major bleeding rates with dabigatran (both doses) compared to warfarin. Mortality, intracranial bleeding, pulmonary embolism, and myocardial infarction were lower with dabigatran, compared to warfarin. We found no evidence of an excess of bleeding events or myocardial infarction amongst dabigatran treated patients in this propensity-matched comparison against warfarin..

Mayo Clinic review of new oral anticoagulants

I've blogged a lot on the novel anticoagulants already but this review is important to bookmark because it's free full text and brings everything together including hard to find information on questions such as use in HIT (theoretically appealing but not yet verified) and the treatment of VTE in cancer.

Your patient on Plavix breaks a hip. Now what?

According to this small study from Mayo you don't have to wait to get it fixed.

Opioid deaths

I ranted so much about this I got tired of it a couple of years ago. But then I noticed, via the Emergency Medicine PharmD blog, this little item in JAMA. It seems 2011 marked the eleventh consecutive year of increase in drug overdose deaths, and this was driven primarily by opiates. Do the math and it dates back to when the “pain as the fifth vital sign” campaign was getting into high gear. As concern for patient perceptions continues to trump clinical judgment don't expect the trend to reverse anytime soon, warns the blogger.

Critical care drug doses at a glance

I have a few quibbles and might consider a couple of these to be suggested doses. Useful overall nevertheless. Via Emergency Medicine PharmD.

Calcium contraindication in dig mediated hyperkalemia: fact or myth?

That question is examined in a recent post at the Emergency Medicine PharmD blog, with no pat answer.

Palliative care

Here's a review containing another one of those top ten lists specialists wished others knew about their specialty. Palliative care is widely misunderstood by health care workers, patients and their families. The review makes several points to dispel misconceptions:

Palliative care is not hospice care. It's not even necessarily end of life care. In fact, it is better applied early in the course of a long illness than toward the end. Contrary to intuition, it may prolong rather than shorten survival. Its application is not confined to cancer but extends across a wide spectrum of severe and complex illnesses. Its focus is not just disease management but also detailed communication with patients and their families, aligning care with the patient's goals and unique attributes and coordination of complex care across the continuum. And, according to the authors, specialty level expertise applied to all the above.

So lots of helpful information there. But the authors fail in one aspect. They fail to define palliative care. They talk around it but don't define it. As I've become comfortable with the idea of palliative care in recent years I've come to know what it is. Despite that, no one has precisely articulated a definition that I know of.

If palliative care is a specialty as the authors claim, what are the distinctives? Again, we need a definition. A definition has two steps. First it places the thing under discussion in a general category. Then it lists attributes that distinguish that particular thing from other members of the same category. For example, step 1: Palliative care is a medical discipline.. Step 2: characterized by ?????. There's the hard part. What are the distinguishing characteristics of palliative care? The authors list quite a few characteristics. The problem is those characteristics don't distinguish palliative care from other disciplines of medicine: Palliative care focuses on severe illness in patients with multiple and complex problems. It applies expertise to the management of a variety of symptoms. It educates patients and their families on diagnosis, prognosis and the goals of treatment. It coordinates complex care across multiple disciplines and settings.

Do you begin to see the problem here? Palliative care is nothing more than good primary care. Or what an excellent internist or hospitalist should be doing. So yes, there is a definition for palliative care but it goes unspoken because the profession is, or should be, embarrassed by the fact that we need a “specialty” whose focus is to offload the rest of us from doing all those things that make for excellence in comprehensive care because we don't have the time.

Carbapenem-resistant gram negative infections: treatment update

Here's another review, available as free full text via Medscape.

High level data are lacking but what studies we have suggest the following take home points:

Candidate antibiotics include aminoglycosides, tygecycline, colistin and, yes, carbapenems.

Two or three drug combination therapy is advised over monotherapy.

Despite the fact that these are carbapenemase producing infections outcomes are better when a carbapenem (meropenem is the best studied) is included in the regimen.

Some promising gram negative agents are in the pipeline. Finally.

Cardiac sarcoidosis

A review and a report of it presenting with electrical storm.

Cardiorenal anemia syndrome?

Apparently so:

Anemia and chronic kidney disease are common in patients with heart failure (HF) and are associated with adverse outcomes. We analyzed the effect of cardiorenal anemia (CRA) syndrome, defined as anemia (hemoglobin less than 130 g/L for men, less than120 g/L for women) and stage 3 or greater chronic kidney disease (estimated glomerular filtration rate less than 60 ml/min/1.73 m2), in outpatients with HF. Consecutive patients with HF were prospectively enrolled from 2000 to 2005 (n = 748)...

CRA syndrome was present in 224 patients (30%). These patients had greater all-cause mortality (51% vs 26%, p less than 0.001), older age (mean 77 ± 8 vs 67 ± 14 years, p less than 0.001), and greater rates of diabetes mellitus (35% vs 23%, p less than 0.001) and ischemic heart disease (50% vs 35%, p less than 0.001). The independent predictors of mortality were CRA syndrome (hazard ratio 2.0, 95% confidence interval 1.4 to 2.8, p less than 0.001), left ventricular systolic dysfunction per grade (hazard ratio 1.5, 95% confidence interval 1.3 to 1.8, p less than 0.001), the absence of a β blocker (hazard ratio 1.6, 95% confidence interval 1.1 to 2.2, p = 0.005), New York Heart Association class per class (hazard ratio 1.5, 95% confidence interval 1.2 to 1.9, p less than 0.01), and age per decade (hazard ratio 1.6, 95% confidence interval 1.4 to 2.0, p less than 0.001). In conclusion, CRA syndrome was common in patients with HF and was an independent predictor of all-cause mortality.

Medical reversal

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.

Diagnosis of posterior MI

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.

Sepsis-induced brain dysfunction

This entity has also been called septic encephalopathy. It has been talked about for years though not a whole lot is known about it.

Can you predict LV function from a simple EKG?

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.

Acute stroke imaging: what hospitalists need to know

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.

Advice for sleep apnea patients traveling to altitude

From the JAMA patient information series. 

EM Cape Town

Emergency medicine procedure videos.

HT to Academic Life in Emergency Medicine.

The reversal on perioperative beta blockade: there's more

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.