From a recent study in Chest:
Results: Six observational studies (n = 149,856) and six RCTs (n = 41,375) were included for analysis. On pooling observational studies, there was an increased risk of AF (OR, 1.27; 95% CI, 1.16-1.39) among bisphosphonate users. Further, analysis of RCTs revealed a statistically significant increase in the risk of serious AF (OR, 1.40; 95% CI, 1.02-1.93) and no increase in the risk of stroke (OR, 1.07; 95% CI, 0.85-1.34) or cardiovascular mortality (OR, 0.92; 95% CI, 0.68-1.26) with the use of bisphosphonates.
Conclusions: Evidence from RCTs and observational studies suggests a significantly increased risk of AF requiring hospitalization, but no increase in risk of stroke or cardiovascular mortality, with the use of bisphosphonate.
Neuromuscular blocking agents, corticosteroids and nitric oxide, among other agents, are discussed in this review.
The use of neuromuscular blocking agents was systematically studied and found to be beneficial early in the course of ARDS, for 48 hours, in this trial. The study population consisted of patients with a pO2 to FiO2 ratio of below 150. Ventilator mechanics and oxygenation were improved. Mortality benefit was confined to patients with a ratio of below 120. Prolonged post treatment paresis was not observed more frequently in the treatment group. This result was supported in a meta-analysis. UpToDate considers neuromuscular blockade potentially beneficial in severe disease, probably safe when used within limitations as illustrated by recent clinical trials but not recommended for routine use and in need of further study.
Inhaled nitric oxide may buy some time as a rescue modality but has not been shown to improve clinical outcomes.
Corticosteroids have been considered in a variety of situations in both early and later stages of ARDS, and remain controversial. At present the only clearly established role is in specific steroid responsive conditions (e.g. acute eosinophilic pneumonia) causing ARDS.
Many biomarkers have been looked at. For adult hospitalized patients procalcitonin is the most promising. An evidence summary is contained in two companion articles, here and here.
Diets characterized by high Mediterranean diet score and low glycemic load were beneficial in this study.
There are a couple of good articles on this topic in a recent issue of CCJM (here and here).
CT calcium scoring has been widely misunderstood by both health professionals and the public for a number of reasons. My own confusion concerned the pathophysiologic rationale. After all we were taught that calcification of atherosclerotic plaques was characteristic of advanced coronary artery disease, right? Moreover it was all too often the young, soft (and presumably non-calcified) plaques, those little blisters on the endothelial lining, that ruptured and caused catastrophic events. How then could calcium imaging be an early detection tool let alone one to assess preclinical risk? Those questions bugged me for a while and had me digging in Big Robbins, Braunwald's Heart Disease and the Path Guy for better answers. I wanted to know exactly when in the pathogenic sequence of atherosclerosis calcification occurred.
It turns out my assumptions were simplistic. Although atherosclerosis may be well underway when calcification occurs, calcium incorporation is not confined to the late stages of the process. Evidently calcium is incorporated before significant stenosis is seen even though considerable plaque maturation may have occurred. This is due in part to the phenomenon of outward remodeling. Moreover, plaques that rupture may be mature plaques but whose fibrous caps have been eroded by inflammatory mediators.
That said, non-calcified plaques can still rupture, making the use of calcium scoring in symptomatic patients problematic, one of the discussion points in the first of the two CCJM articles. Those authors agree with the prevailing view which is that scoring is useful mainly for the screening of asymptomatic patients and has little role in symptom evaluation. Cardiac calcium scoring for symptomatic patients gets little mention in U.S. Guidelines. An older guideline focused on cardiac CT in general gives it no better than a IIb recommendation. The current unstable angina/NSTEMI guidelines, which include evaluation of undifferentiated patients with chest pain, do not recommend it at all.
The second CCJM paper, a companion editorial, takes a more positive view of this controversial use of calcium scoring:
Taken together, these data suggest that the absence of coronary calcification in people at low to intermediate risk indicates a very low likelihood of significant stenotic coronary artery disease and foretells an excellent prognosis.
These data have already been incorporated into the British National Institute for Health and Clinical Excellence (NICE) guidelines, in which calcification scoring is an integral part of the management algorithm in patients with chest pain who are at low risk.
I was initially surprised that the NICE guidelines would embrace it. It's not so surprising on further consideration given that it is cheaper than invasive or noninvasive angiography or stress imaging.
For the more widely accepted indication of asymptomatic screening it is important to keep in mind that the test is considered optional at best. That is, no clinical scenario is given a class I recommendation. Its main advantage in asymptomatic patients is that it will reclassify a fair number of asymptomatic patients who are clinically determined to be at intermediate risk.
Dr. Smith discusses such a case in his ECG blog. He makes some teaching points on various aspects of the case. Concerning the anterior precordial ST depression frequently seen in inferior STEMI we were formerly taught that it signifies “ischemia at a distance,” that is, in the distribution of the left coronary system. That was a myth. We now know that it's the mirror image of posterior STEMI. In fact, as a rule, true ST segment depression does not localize an ischemic process. ST elevation does, T wave inversion does but ST depression does not. It can signify ischemia somewhere but doesn't tell you specifically where.
It's easy enough to do but how helpful is it? Results in the literature are mixed. The number needed to screen, depending on the population studied, varies from 45 to over 300. There's an interesting literature review and comment thread at Academic Life in Emergency Medicine.
Braunwald and Morrow ask this question in a recent review in Circulation. It seems we’ve gone full circle:
It appears that we have now come full circle in our definition of symptomatic ischemic heart disease. Before the 1930s, 2 manifestations, stable angina and AMI, were recognized. Patients in the gray zone between stable angina and AMI that we now call UA were described 75 years ago and at first appeared to be quite rare. Over the next half-century, they were recognized with increasing frequency, and by 25 years ago, about one half of all patients with NSTE-ACS were considered to have UA. However, use of ever more sensitive biomarkers of myocardial necrosis, especially cTn, has steadily chipped away at the fraction of patients with NSTE-ACS without MI who therefore are still considered to have UA.
In the 70s terms such as “intermediate coronary syndrome” and “pre-infarction angina” were commonplace and conveyed a sense of urgency. The increasing sensitivity of cardiac biomarkers has gradually chipped away at those designations. They have all but vanished now with the advent of the more sensitive troponin assays.
This issue was reviewed recently in Cirulation. The HDL story is not over. Some of the points of the review:
The epidemiologic association between low HDL levels and cardiovascular disease is very strong.
The risks associated with low HDL can be moderated by nonpharmacologic means.
The main controversy regarding HDL concerns pharmacologic management. Early studies with niacin (e.g. the Coronary Drug Project) and fibrates (Helsinki I) showed reduction in cardiovascular events. However, several more recently conducted trials failed to show improvement attributable to pharmacologic treatment directed toward HDL. This is in part attributed to confounders such as concomitant statin treatment.
Questions for future and ongoing research include patient selection for treatment and new approaches in the pipeline.
Recent review in Circulation, free full text.
Three RCTs had failed to show benefit, so a meta-analysis was done and recently published:
Results
Three RCTs met inclusion criteria. The pooled data provided 2,303 patients, of which 1,150 were in the PFO closure group and 1,153 in the medical therapy group. In the ITT analysis, there were 43 events (3.7%) of the composite end point in the closure group compared with 61 events (5.3%) in the medical therapy group, with a trend in favor of the PFO closure (OR = 0.70; 95% CI, 0.47–1.05, P = 0.08). The incidences of TIA, ischemic CVA, and bleeding were not statistically different between the groups. There was a trend for the more frequent occurrence of atrial fibrillation in the PFO closure group (OR = 3.29; 95% CI, 0.86–12.60, P = 0.08). In the AT analysis, the composite end point was significantly less frequent in the PFO closure group (OR = 0.62; 95% CI, 0.41–0.94, P = 0.02).
Here is a discussion of the article at Medpage Today.
This will be spun various ways. My summation is that while the evidence is inconclusive and no one can make a high level claim for closure over medical therapy the as treated analysis suggests that patients who successfully completed device therapy did better. The true practice of evidence based medicine in this situation will require a nuanced conversation with the patient. Statements like “we need to fix this hole in your heart to keep you from having another stroke” are unfounded. Dismissive statements like “PFO closure doesn't work” only reflect one's misunderstanding of the proper application of EBM.
The prevention of stroke in patients with PFO is, to say the least, controversial. It would seem plausible for device therapy to be superior to medical treatment and for systemic anticoagulation over antiplatelet therapy though neither has been proven convincingly. The UptoDate authors “suggest” medical over device therapy and “suggest” antiplatelet therapy over anticoagulation unless there is a specific reason to favor anticoagulation in the individual patient.
Evolving concepts and controversies are addressed in a recent review published in the Cleveland Clinic Journal of Medicine. The article is available as free full text. A few take home points will be mentioned here.
The optimal timing of CT scanning is based on the fact that the yield for detecting necrosis is relatively poor until 72 hours or so after presentation. Earlier scanning may be indicated in certain clinical circumstances suggestive of complications. Scanning at the time of presentation is justified if the diagnosis is unclear. That is to say that CT scanning provides just one of the three diagnostic criteria, the other two being clinical and laboratory. If those two are present CT is not necessary to make the diagnosis.
There has been a gradual shift in thinking about severity assessment. While prognostic assessment may be helpful in anticipating complications, advising patients and assembling resources it may not be as useful in an algorithmic approach to management as once thought. For example, a clinical determination of severe pancreatitis defines the patient as having pancreatic necrosis. In the traditional view that would be an indication for antibiotic therapy. But that thinking is not supported by evidence and no longer holds sway. In addition, the role of severity assessment as a target for fluid resuscitation is unclear. Traditional thinking held that assessment of pancreatitis as severe targeted patients for more aggressive initial fluid administration. A study form 2011 by Warndorf and colleagues, however, found the opposite: it was the patients with milder (so called “interstitial”) pancreatitis who benefited most, suggesting that the window of opportunity is lost once pancreatitis progresses to severe.
There are many clinical tools available for severity assessment. Traditional tools (e.g. Ranson) are falling out of favor because they require observation over time and cannot classify patients within the first 24 hours. Some more recently validated methods, particularly the SIRS determination, are simpler to use and enable severity assessment on the front end.
Current concepts in fluid resuscitation have become more nuanced. The traditional view of “more is better” was based mainly on theory, animal data and low level human studies. Despite those limitations it held sway until challenged a couple of years ago by a study I cited here. According to that study fluids in excess of 4.1L in the first 24 hours were associated with harm. The thinking is shifting from “the more the better” to “shoot for the optimum.” Under resuscitation may lead to pancreatic ischemia at the microcirculatory level triggering necrosis, mediator release, SIRS, vascular collapse and distant organ failure. Too much fluid on the other hand may lead to organ congestion and compartment syndrome.
In addition, fluid resuscitation should be front loaded. The Warndorf paper reported that patients given greater than one third the 72 hour total volume in the first 24 hours had better outcomes. Of note, that group also had lower total 72 hour volumes.
As to the actual amount to give, the CCJM review says:
Optimum resuscitation is controlled fluid expansion averaging 5 to 10 mL/kg per hour, with 2,500 to 4,000 mL given in the first 24 hours.
The way to accomplish this in an average sized individual is to front load in the first several hours. Such a protocol was described in a 2011 paper by Wu and colleagues. It is based on an aggressive initial bolus followed by high volume maintenance fluid rates for the first few hours but then calls for a sharp reduction in IV rate if the BUN comes down a bit at either of two lab checkpoints starting around 8 hours following presentation. Patients treated according to that protocol received less total fluid than those who were not and the total amount received came fairly close to the upper range recommended in the CCJM review. Outcomes were not improved with use of the protocol but the patient numbers were small. What was found was that patients treated with lactated Ringer's did better than those treated with saline whether on or off protocol. Again the numbers were small and the outcomes were soft: SIRS and CRP.
Though based only on physiologic rationale (lower microcirculatory pH in the pancreas is believed to activate enzymes and promote inflammation) and the one small study with soft endpoints the CCJM review recommends LR over saline.
Additional discussions in the review focus on nutrition (enteral is better than parenteral, NG is as good as jejunal, and enteral nutrition reduces infection), compartment syndrome (an emerging concern in pancreatitis) and the management of walled off necrosis and fluid collections.
4 factor PCC was associated with faster INR reversal, a lower red cell transfusion requirement and a better safety profile in this study.
Note that PCC is favored over FFP in the latest ACCP guidelines.
Some take home points from a recent review:
The CAST study changed our thinking about drug treatment of ventricular arrhythmias but it did not eliminate the practice altogether.
Drug treatment of ventricular arrhythmias is not indicated for prevention of sudden cardiac death but two indications remain: symptom control and prevention or treatment of tachycardia induced cardiomyopathy.
PVC burdens of more than 15% of heart beats as well as frequent runs of VT, even if asymptomatic, have been associated with the development of tachycardia induced cardiomyopathy.
There has been a shift toward safer drugs (e.g. beta blockers).
Some of the outflow tract and fasicular ectopic rhythms are amenable to ablation.
Outflow tract and fasicular tachycardias have characteristic morphology and their sites of origin can often be identified on the surface electrocardiogram.
This is gaining enthusiasm, devices are proliferating and research is ongoing. Free full text review here via Medscape. More data are needed to answer concerns about renal function decline related to the procedure and the durability of antihypertensive effect.
This CCJM review covers many of the same points I recently blogged here.
Atrial fibrillation is increasingly being recognized as a disease of obesity and the metabolic syndrome. A nice review (free full text) on the topic was recently published. Background here.
This review, available in free full text from Mayo Clinic Proceedings, is the best I've seen on this topic. Points I found interesting:
The traditional classification of SS into diffuse and limited (aka scleroderma vs CREST) is simplistic. Finer gradations based on the extent of skin involvement or rate of progression of skin disease may be more meaningful. Also, specific disease profiles based on auto antibody associations are emerging. Antibody-phenotype associations are shown in one of the tables in the article. Although the associations are not absolute (and there is a certain amount of overlap) the specific antibodies are fairly predictive such that antibody profiling early in the course of the disease is beneficial.
There are four pathophysiologic dimensions to SS: vasospasm, obliterative vasculopathy, tissue fibrosis and autoimmunity.
There is no “treatment for SS” per se. Treatment is directed at disease manifestations. Immunosuppression directed against autoimmune processes that drive certain clinical manifestations is recommended in selected circumstances but none of it is supported by high level data.
Corticosteroids, in disfavor because they increase the risk of renal crisis, should be used sparingly if at all.
A systemic review in the Annals of Internal Medicine:
Data Synthesis: Six good-quality systematic reviews compared NOACs with low-molecular-weight heparin (LMWH) for thromboprophylaxis after THR or TKR. Risk for symptomatic deep venous thrombosis, but not risk for death or nonfatal pulmonary embolism, was reduced with factor Xa inhibitors compared with LMWH (4 fewer events per 1000 patients). Conversely, the risk for major bleeding increased (2 more events per 1000 patients). Outcomes of dabigatran did not significantly differ from those of LMWH. Indirect evaluation of NOACs by common comparison with LMWH showed nonsignificantly reduced risks for venous thromboembolism with rivaroxaban compared with dabigatran (risk ratio [RR], 0.68 [95% CI, 0.21 to 2.23]) and apixaban (RR, 0.59 [CI, 0.26 to 1.33]) but increased major bleeding. New oral anticoagulants have not been compared with warfarin, aspirin, or unfractionated heparin.
Limitations: Head-to-head comparisons among NOACs were not available. Efficacy is uncertain in routine clinical practice.
Conclusion: New oral anticoagulants are effective for thromboprophylaxis after THR and TKR. Their clinical benefits over LMWH are marginal and offset by increased risk for major bleeding.
There's a point-counterpoint in a recent issue of Chest.
The bottom line is still that a general recommendation for lytic therapy in submassive PE is not supported by evidence based on hard clinical outcomes.
---with a focus on reversing LMWH. Via Emergency Medicine PharmD.
This is one of the reasons performance measures fail:
Background Current performance measures for AMI are designed to improve quality by quantifying the use of evidence-based treatments. However, these measures only assess medication prescription. Whether patients receive optimal dosing of secondary prevention medications at the time of and following discharge after AMI is unknown.
Methods We assessed treatment doses of beta-blockers, statins, and ACE/ARBs at discharge and 12 months after AMI among 6748 patients from 31 hospitals enrolled in 2 US registries (2003-08)...
Results Most eligible patients (greater than 87%) were prescribed some dose of each medication at discharge, although only 1 in 3 patients were prescribed these medications at goal doses. Of patients not discharged on goal doses, up-titration during follow-up occurred infrequently (∼25% of patients for each medication). At 12 months, goal doses of beta-blockers, statins, and ACE/ARBs were achieved in only 12%, 26%, and 32% of eligible patients, respectively.
So among patients who passed the core measures with flying colors few were actually treated according to guidelines.
More from Medpage Today.
For those interested in such things here's a paper. It says that a vertical frontal plane P wave axis is characteristic. In such patients a prominent negative P wave component in V1 often reflects anatomic displacement of the right atrium in emphysema rather than coexisting left atrial enlargement.
Here's another one to add to the list of risk factors. From the JAMA Internal Medicine paper:
Design Population-based case-control study using nationwide databases.
Setting Denmark (population 5.6 million).
Participants We identified 38 765 VTE cases diagnosed from January 1, 2005, through December 31, 2011, and 387 650 population controls included through risk-set sampling and matched by birth year and sex...
Results Systemic glucocorticoids increased VTE risk among present (adjusted IRR, 2.31; 95% CI, 2.18-2.45), new (3.06; 2.77-3.38), continuing (2.02; 1.88-2.17), and recent (1.18; 1.10-1.26) users but not among former users (0.94; 0.90-0.99). The adjusted IRR increased from 1.00 (95% CI, 0.93-1.07) for a prednisolone-equivalent cumulative dose of 10 mg or less to 1.98 (1.78-2.20) for more than 1000 to 2000 mg, and to 1.60 (1.49-1.71) for doses higher than 2000 mg. New use of inhaled (adjusted IRR, 2.21; 95% CI, 1.72-2.86) and intestinal-acting (2.17; 1.27-3.71) glucocorticoids also increased VTE risk.
It roughly doubles the risk. Even inhaled steroids!
Diagnosis and treatment with a focus on the new vaptan drugs. Via Medscape.
---for that strongly suspected massive PE or a STEMI that goes into PEA. Here's a quick reference.
Better outcomes were seen when treatment was given within 90 minutes of symptom onset.
Report in Stroke.
More from Medpage Today.
The authors of a Special Report in Circulation are concerned about the field of electrocardiography. The beginning of the paper is inflammatory:
The ECG is at a crossroads as to its future integration into modern medical practice. Those most interested in electrocardiography remain the old guard, whose careers evolved with this technology. They remain as enamored by the experiential mythology as by the experimental science of the ECG.
That not only sets an unfortunate tone for the rest of the paper (which makes some good points) but it's also inaccurate. I have pointed out before (e.g. here and here) the emergence of the new generation of leaders in the field. Striving to think beyond the old rigid rules and make electrocardiography more evidence based, they are anything but old guard.
With that aside on to the main points of the paper. (I don't think these were meant to be all inclusive. They are merely a list of examples of how the test has been misunderstood and misapplied).
Students and house staff are inadequately trained in electrocardiography.
As a result many practitioners lack the skills to utilize the electrocardiogram effectively. The authors give the following example:
Their understanding of ST elevation myocardial infarction criteria could be easily exposed by asking them to name the contiguous pairs of standard ECG leads. A disappointing number would refer to pairs of leads that are contiguous on the ECG display such as II and III or V1 and V4, rather than the leads separated by 30° going around the surface of the heart as specified in the guidelines.
That’s a reminder that the array of limb leads on the electrocardiograph tracing is not contiguous!
Traditional rules about contiguous leads are not evidence based and may be obsolete.
For example:
Examples of the experiential mythology that continue to haunt electrocardiography include the requirement for contiguous or adjacent leads instead of a single lead for fulfilling diagnostic criteria. The contiguous or adjacent lead constraint is a residual from the thick, noisy tracings from the early days of electrocardiography before high-impedance amplifiers, DC coupling, and digital processing produced the high-resolution tracings of today (Figure 1). Applying the criteria to a single digitally processed ECG lead would avoid the confusion previously discussed without affecting the diagnostic characteristics of the ECG.
The referenced figure is here. Today's leaders in electrocardiography, particularly those in emergency medicine, are well aware of the various types of “STEMI equivalent”---electrocardiographic patterns that signify acute coronary occlusion but do not meet the STEMI criteria of ST elevation in two or more contiguous leads. Unfortunately the door-to-balloon performance incentive may have encouraged rigid use of simplistic criteria as a substitute for thought and nuanced analysis of the electrocardiogram.
Use of the TP segment as the baseline is open to question.
According to the authors:
The T-P baseline remains from vectorcardiography, whereas the PR segment has many reasons to be set as the baseline, as explained in the Common Standards for Quantitative Electrocardiography statement.
The PR segment as baseline is problematic, however, as it is displaced in pericarditis and sometimes by the wave of atrial repolarization (Ta wave).
The electrocardiographic criteria for left ventricular hypertrophy are of questionable value.
It has long been known that the test characteristics for LVH are less than ideal. On the other hand we have more recently learned the potential value of the electrocardiogram for the assessment of left ventricular systolic function.
The dynamic nature of electrocardiographic patterns complicates the diagnosis of channelopathies.
The electrocardiogram can be very useful in the diagnosis of channelopathies such as Brugada syndrome and the long QT provided this limitation is kept in mind. In the case of the QT interval misunderstanding is widespread. Assessment of repolarization is complex and goes beyond a simple measurement of the corrected QT interval.
Computer interpretations are unreliable.
This remains true despite the fact that we've gone through several generations of machines since the technology was introduced decades ago.
New insights about J waves and early repolarization complicate electrocardiographic interpretation.
Specifically, we now know that there is benign and not so benign early repolarization. Background here, here, here and here.
The question is not whether electrocardiography remains clinically useful. Indeed the power of the electrocardiogram is evident as never before. The real question is whether we will use it for all it's worth.
There was even a small borderline statistically significant increase in mortality associated with the hospitalist model. Article here.
From a study in JAMA Internal Medicine:
Background Patients who not only survive a warfarin-associated gastrointestinal tract bleeding (GIB) event but also have an ongoing risk for thromboembolism present 2 clinical dilemmas: whether and when to resume anticoagulation. The objective of this study was to determine the incidence of thrombosis, recurrent GIB, and death, as well as the time to resumption of anticoagulant therapy, during the 90 days following a GIB event.
Methods In this retrospective, cohort study using administrative and clinical databases, patients experiencing GIB during warfarin therapy were categorized according to whether they resumed warfarin therapy after GIB and followed up for 90 days...
Results..Warfarin therapy resumption after the index GIB was associated with a lower adjusted risk for thrombosis (hazard ratio [HR], 0.05; 95% CI, 0.01-0.58) and death (HR, 0.31; 95% CI, 0.15-0.62), without significantly increasing the risk for recurrent GIB (HR, 1.32; 95% CI, 0.50-3.57).
Conclusions The decision to not resume warfarin therapy in the 90 days following a GIB event is associated with increased risk for thrombosis and death.
The median time to resumption of warfarin was 4 days.
I've blogged before (here, here and here) that occult cardiac ischemia or decompensation can be the cause of failure to liberate from mechanical ventilation. More recently another review has been published on the topic. It states that a rising BNP during a spontaneous breathing trial is predictive of cardiac decompensation leading to weaning failure and makes these additional points:
Ischemic heart disease, valvular heart disease, systolic or diastolic dysfunction contributes to increase in cardiac load and weaning failure.
Extra demand on cardiac working load imposed by SBT may become apparent when transferring patient from positive to spontaneous ventilation.
Diuretic therapy may be considered for excessive preload.
Noninvasive positive pressure ventilation is beneficial for weaning-induced pulmonary edema.
Further cardiac evaluation is necessary if changes in natriuretic peptide levels are detected during SBT.
---reduced readmissions in this study.
Medpage Today reports the study as showing that EMRs Lower Odds of Heart Failure Readmission. But that's not what the study showed at all. The EMR helped target patients for intervention, but it was not the intervention. The intervention included:
...(1) detailed inpatient clinical assessment, patient education and discharge planning by a HF nurse practitioner, pharmacist, nutritionist and case manager starting early in the hospital course; (2) a follow-up telephone call from a nurse within 48 h of discharge to assess whether the patient had obtained their medication and was aware of their outpatient follow-up appointments; (3) outpatient case management (consisting of individualised care management services based on specific post-discharge needs) for 30 days; (4) a cardiology appointment with a HF specialist within 7 days of discharge and subsequent cardiology follow-up for at least 1 month; and (5) a primary care appointment scheduled according to the urgency of non-cardiac problems.
The same EMR was in place during the control period.
The EMR can be leveraged in many effective ways but there is no evidence to support the popular belief that just having an EMR improves patient outcomes.
I missed my 8th blogiversary a few months ago. In fact I slept right through it. But recently in a reflective and expansive moment I dug from the archives an old pod cast interview from back when I started this blog. In it Kent Bottles asked me questions about why I blog and what I get out of it. I listened to it for the first time in years and was surprised to learn how little my attitudes have changed. So it's time to reflect. Here are my current ideas on blogging. Save for some nuance here and there they're pretty much the same as when I started:
1) I maintain a clinical focus. In 2005 there were a few hundred medical blogs but most were personal diaries or soapboxes. Very few featured hard core clinical topics. I found I had a niche. Not many other bloggers were doing what I planned to do. Since that time the number and quality of clinically focused blogs has increased (this seems mainly to have come from nephrology and emergency medicine) but I find there's still plenty of room for what I do.
2) Many of the so called clinical blogs back then were little more than news aggregators. I knew then as I do now that very little meaningful learning comes in the form of breaking news. Medical progress plods along incrementally. It builds on what was known before and needs to be explained in terms of what was known before. And now we have Twitter. How can you microblog complex medical issues with the nuance they need? I'll dump in a link post now and again but for the most part I try to provide perspective.
3) Beyond the fact that I was doing this in large part for myself I started out with clear objectives about my audience. I would direct my posts to health care workers, mainly physicians and physicians in training. Satisfying the learning needs of two vastly different audiences at the same time, clinicians and consumers, is extremely difficult and I know of only rare instances when it has been done effectively. Nevertheless many bloggers seem to be trying. Either that or they haven't bothered to address how they want to define their audiences. I believe it's best to define my audience even if I pay a price in traffic.
4) Finally, blogging helps me. It motivates me to read and maintain an edge in the content area of my work in hospital medicine. I have a long list of journals and other sources I scan regularly. When I run across an item of professional interest I blog it. This has produced an organized set of on line bookmarks I can access anywhere, anytime, when I'm looking for this or that article either for personal reference or to share with a colleague.
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.
