Thrombolytic therapy for patients with submassive PE: the controversy continues

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.

Protamine dosing

---with a focus on reversing LMWH. Via Emergency Medicine PharmD.

Acute aortic syndrome: dissection, intramural hematoma and penetrating atheromatous ulcer

Free full text review.

Post MI medication dosing

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.

The electrocardiographic P wave in emphysema

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.  

Glucocorticoid use and increased VTE risk

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!

Right ventricular infarction

Free full text review.

SIADH

Diagnosis and treatment with a focus on the new vaptan drugs. Via Medscape.

Toward a better understanding of Takotsubo cardiomyopathy

Case descriptions and a mini-review. 

What if TPA is indicated in a code

---for that strongly suspected massive PE or a STEMI that goes into PEA. Here's a quick reference.

Very early thrombolysis in ischemic stroke

Better outcomes were seen when treatment was given within 90 minutes of symptom onset.

Report in Stroke.

More from Medpage Today.

Will we use the electrocardiogram for all it's worth?

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.

Heart failure care: hospitalist model associated with improvement in performance but not outcomes

There was even a small borderline statistically significant increase in mortality associated with the hospitalist model. Article here.

When and if to restart warfarin after a GI bleed

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.

Unexplained failure to wean? Get to the heart of the matter.

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.

Intensive targeting of resources to high risk heart failure patients

---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.

Reflections on blogging

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.

Choosing wisely in hospital medicine

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.

Performance measures fail

----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.

Wide complex tachycardia: is it VT or not???

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.