The Society of Hospital Medicine has published its top 5 list:
RESULTS:
The 5 recommendations that were subsequently approved by the SHM Board are: (1) Do not place, or leave in place, urinary catheters for incontinence or convenience or monitoring of output for non-critically ill patients (acceptable indications: critical illness, obstruction, hospice, perioperatively for less than 2 days for urologic procedures; use weights instead to monitor diuresis). (2) Do not prescribe medications for stress ulcer prophylaxis to medical inpatients unless at high risk for gastrointestinal complications. (3) Avoid transfusions of red blood cells for arbitrary hemoglobin or hematocrit thresholds and in the absence of symptoms or active coronary disease, heart failure, or stroke. (4) Do not order continuous telemetry monitoring outside of the intensive care unit without using a protocol that governs continuation. (5) Do not perform repetitive complete blood count and chemistry testing in the face of clinical and lab stability.
This is a good start. Recommendation (1) is helpful because it gives specifics to guide foley catheter use though I found the last phrase amusing: ..use weights instead to monitor diuresis. Is the panel implying that it's too much to ask the nursing staff to get an accurate I&O on a voiding patient?
Recommendation (2) concerning stress ulcer prophylaxis is vague but does address a major concern. Clearly stress ulcer prophylaxis is over utilized. The Surviving Sepsis Guidelines are even more restrictive, stating that even among critically ill septic patients GI prophylaxis should be reserved for those with increased bleeding risk. GI prophylaxis though not an official performance measure in terms of P4P or public reporting has become a de facto performance measure due to EMR driven pathways, institutional processes and various care bundles. The harmful effects have only recently been appreciated.
Right off the bat there's a problem with how recommendation (5) reads: Do not perform repetitive complete blood count and chemistry testing in the face of clinical and lab stability. Most patients with clinical and lab stability would not meet criteria for continued hospital stay! But putting that aside, do hospitalized patients need daily labs? Repeated blood testing is driven by the EMR which offers daily draws as a check list option on many order sets and pathways. My subjective impression is that we saw a lot less of this in the paper world. Given the virtual disappearance of arbitrary transfusion targets for most patients daily CBCs are not necessary in hematologically stable patients. With chemistries we have a different set of concerns. Awareness is rising concerning hyponatremia and hypokalemia as safety issues for hospitalized patients. Inpatients have elevated vasopressin levels (and thus SIADH physiology) just by virtue of being sick and in the hospital. They are at risk for hyponatremia even when isotonic fluids are administered. Hypokalemia is common due to multiple factors including the use of diuretics, straight normal saline as the EMR driven default IV fluid, the use of inhaled beta agonists and corticosteroids with mineralocorticoid activity. Its avoidance is particularly important given the multiple QT prolonging drugs used in the hospital. Finally, the daily assessment of renal function is important in many patients for the early detection of acute kidney injury and the adjustment of drug dosages. It's hard to make an evidential case either way but daily chemistries, in my view, are worthwhile in many hospitalized patients.
Here are two more I would add:
Do not order imaging studies for pulmonary embolism without first documenting a pre-test probability assessment.
Do not automatically employ CT angiography as the modality of choice to test for pulmonary embolism. Unless the patient has COPD or an abnormal chest xray V/Q scanning has better test characteristics.
----time and time again. That statement, which I've been making and backing up with evidence for years in these pages, is still at odds with popular belief. Just to make sure I'm not misunderstood I want to draw some distinctions. What I am criticizing is performance. I'm not talking about quality, evidence based medicine or guideline adherence. Performance is to be distinguished from all those.
Like guidelines, the processes targeted by performance metrics are, for the most part, supported by evidence. But that's where the similarity stops. Guidelines offer perspective and nuance on how to apply the best evidence. Performance takes an evidence based care process, isolates it from its appropriate clinical context and turns it into a game. The ensuing unintended consequences rule the day and the measures fail.
If there's one measure that's inherently more robust that the others it's got to be door-to-balloon time for STEMI. The evidence and physiologic rationale are so strong, how could it miss? But it does. The mortality rate for acute coronary syndrome has been declining for while. The advent of door-to-balloon performance did not impact the rate of decline. A new paper just out in NEJM takes a closer look. It starts out encouraging:
Methods
We analyzed annual trends in door-to-balloon times and in-hospital mortality using data from 96,738 admissions for patients undergoing primary PCI for ST-segment elevation myocardial infarction from July 2005 through June 2009 at 515 hospitals participating in the CathPCI Registry. In a subgroup analysis using a linked Medicare data set, we assessed 30-day mortality.
Results
Median door-to-balloon times declined significantly, from 83 minutes in the 12 months from July 2005 through June 2006 to 67 minutes in the 12 months from July 2008 through June 2009 (P less than 0.001). Similarly, the percentage of patients for whom the door-to-balloon time was 90 minutes or less increased from 59.7% in the first year to 83.1% in the last year (P less than 0.001).
So far so good, but there's more:
Despite improvements in door-to-balloon times, there was no significant overall change in unadjusted in-hospital mortality (4.8% in 2005–2006 and 4.7% in 2008–2009, P=0.43 for trend) or in risk-adjusted in-hospital mortality (5.0% in 2005–2006 and 4.7% in 2008–2009, P=0.34), nor was a significant difference observed in unadjusted 30-day mortality (P=0.64).
So this, arguably the strongest of all the core measures, fails as have so many of the others. A related article in Medpage Today offers speculation. Maybe some essentials of care are being overlooked as patients are rushed to the cath lab under pressure to “satisfy the measure.”
All would agree that time is muscle and that the shorter the time to reperfusion the better. Minimizing door-to-balloon time is a great endeavor. But, like so many other evidence based modalities, toxicity occurs when it becomes a performance metric.
This quick reference from Academic Life in Emergency Medicine combines the Brugada criteria with some others. In the comments is a link to the more recently developed aVR criteria.
Read the report here.
The cases were associated with a newer formulation containing inactive ingredients designed to discourage crushing and dissolving.
And you can refer to this review as a reality check against all the non-evidence based prescribing and thyroid quackery out there.
It is available as free full text but here are a few take home points:
Start full dose replacement in younger and otherwise well patients.
Start low and go slow in older folks.
Start even lower in those with known CAD and those who might be suspected to have silent CAD based on risk factors, including the severity of the hypothyroidism itself.
Although subclinical hypothyroidism has an association with some adverse cardiovascular outcomes, whether treatment of same is beneficial is controversial. Treatment can often be withheld provided there is careful follow up, as many patients spontaneously revert to normal laboratory status.
Although the use of triiodothyronine and dessicated pig thyroid extract are employed by many practitioners they are unsupported by high level evidence. Further research is needed to define whether there are populations that will benefit from the adjunctive use of triiodothyronine.
This is all pretty much in line with an older review I blogged several years ago.
Guidelines from the ACP. It's really just good common sense.
From the AABB published free in the Annals of Internal Medicine:
Recommendation 1: The AABB recommends adhering to a restrictive transfusion strategy (7 to 8 g/dL) in hospitalized, stable patients (Grade: strong recommendation; high-quality evidence).
Recommendation 2: The AABB suggests adhering to a restrictive strategy in hospitalized patients with preexisting cardiovascular disease and considering transfusion for patients with symptoms or a hemoglobin level of 8 g/dL or less (Grade: weak recommendation; moderate-quality evidence).
Recommendation 3: The AABB cannot recommend for or against a liberal or restrictive transfusion threshold for hospitalized, hemodynamically stable patients with the acute coronary syndrome (Grade: uncertain recommendation; very low-quality evidence).
Recommendation 4: The AABB suggests that transfusion decisions be influenced by symptoms as well as hemoglobin concentration (Grade: weak recommendation; low-quality evidence).
Some insights on this topic from Emergency Medicine PharmD.
Mayo Clinic published an institution wide study here. Of note, patients with long QT intervals had a much higher all cause mortality (mean follow up 224 days). Only 10% had known congenital LQTS. Beyond the usual suspects (drugs, electrolyte disturbances) other less well appreciated conditions were cited as contributory to QT prolongation (DM, ACS, ESRD and others). The threshold for identifying patients as having long QT was generous----500 ms.
Related article in the same issue here.
High frequency oscillation (HFOV) has been recognized as a rescue modality for patients with ARDS refractory to conventional ventilation. Two papers in NEJM recently addressed HFOV as an initial modality of ventilation.
High-Frequency Oscillation in Early Acute Respiratory Distress Syndrome:
Methods
In a multicenter, randomized, controlled trial conducted at 39 intensive care units in five countries, we randomly assigned adults with new-onset, moderate-to-severe ARDS to HFOV targeting lung recruitment or to a control ventilation strategy targeting lung recruitment with the use of low tidal volumes and high positive end-expiratory pressure...
Results
On the recommendation of the data monitoring committee, we stopped the trial after 548 of a planned 1200 patients had undergone randomization. The two study groups were well matched at baseline. The HFOV group underwent HFOV for a median of 3 days (interquartile range, 2 to 8); in addition, 34 of 273 patients (12%) in the control group received HFOV for refractory hypoxemia. In-hospital mortality was 47% in the HFOV group, as compared with 35% in the control group (relative risk of death with HFOV, 1.33; 95% confidence interval, 1.09 to 1.64; P=0.005). This finding was independent of baseline abnormalities in oxygenation or respiratory compliance. Patients in the HFOV group received higher doses of midazolam than did patients in the control group (199 mg per day [interquartile range, 100 to 382] vs. 141 mg per day [interquartile range, 68 to 240], P less than 0.001), and more patients in the HFOV group than in the control group received neuromuscular blockers (83% vs. 68%, P less than 0.001). In addition, more patients in the HFOV group received vasoactive drugs (91% vs. 84%, P=0.01) and received them for a longer period than did patients in the control group (5 days vs. 3 days, P=0.01).
High-Frequency Oscillation for Acute Respiratory Distress Syndrome:
Methods
In a multicenter study, we randomly assigned adults requiring mechanical ventilation for ARDS to undergo either HFOV with a Novalung R100 ventilator (Metran) or usual ventilatory care. All the patients had a ratio of the partial pressure of arterial oxygen (PaO2) to the fraction of inspired oxygen (FiO2) of 200 mm Hg (26.7 kPa) or less and an expected duration of ventilation of at least 2 days...
Results
There was no significant between-group difference in the primary outcome, which occurred in 166 of 398 patients (41.7%) in the HFOV group and 163 of 397 patients (41.1%) in the conventional-ventilation group (P=0.85 by the chi-square test).
Related editorial here.
It may have a niche for patients who fail conventional mechanical ventilation but is not recommended for initial treatment.
Review in Mayo Clinic Proceedings.
Maybe this is why we blog.
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.
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.
It doesn't happen very often but it happens. Nowadays regional thrombolysis or clot retrieval may be options.
An update at the Emergency Medicine PharmD blog.
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.
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.
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++.
---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..
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.
According to this small study from Mayo you don't have to wait to get it fixed.
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.
I have a few quibbles and might consider a couple of these to be suggested doses. Useful overall nevertheless. Via Emergency Medicine PharmD.
That question is examined in a recent post at the Emergency Medicine PharmD blog, with no pat answer.
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.
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.
A review and a report of it presenting with electrical storm.
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 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.
