Nurses doing housekeeping chores

---including cleaning and decontaminating patient care areas. Hard to believe but true according to a TV news report.

A particularly rich piece of the corporate spin concerning the measure is found at 1:06 into the video with the reference to Florence Nightingale.

HT to the blogger at ofcourseitsaboutyou who said:

Especially insulting is the implication that Florence Nightingale would have wanted nurses to return to doing housekeeping in the hospital. Nightingale wanted nursing to move forward, not backward.

Vandy is pretty resource heavy and the place I'd least expect this to happen.

When I first saw the report I thought somebody was joking. But as I thought more I realized that this is not the first time health care workers have been pushed outside their professional boundaries. Doctors, for example, were asked to become secretaries with the rollout of CPOE. Few dared to call it out as it was so cleverly disguised as technology for the enhancement of patient safety.

Chemistry and physics lectures

From Brian Swarthout.

Baroreceptor failure

Here is a case report and brief review.

It can present with syncope, orthostatic hypotension, labile blood pressure and heart rate. Blood pressure is difficult to control and requires a special approach. Risk factors include neck irratiation (carotid sinus damage) and possibly chest irradiation (aortic arch baroreceptor damage).

When to suspect the diagnosis: the profile above in the context of a history of neck or chest irradiation or brainstem stroke.

Testing to confirm or exclude the diagnosis: no fixed algorithm. Exclusion of other causes. Tilt table testing may be helpful.

Full text at the above link.

Roth spots and little black bags

Here's another delightful essay by Herbert Fred.

With the demise of the little black bags (which were provided as gifts from the drug companies) came the end of routine use of the ophthalmoscope.

Patterns of cardiac arrest due to aortic dissection or aneurysm

From a recent study:

Materials and Methods:

Patients who were transported to this department from January 2005 to December 2010 and subsequently diagnosed with AD were included in this study. Patients with asymptomatic AD or those with AD that did not develop CPA were excluded. The AD was classified into four categories: Stanford A (SA), Stanford B (SB), thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA)...

Results:

There were 24 cases of SA, 1 case of the SB, 8 cases of ruptured TAA and 9 cases of ruptured AAA. The frequency of males among all subjects was 69%, the average age was 72.3 years old and the frequency of hypertension was 47.6%. There was no ventricular fibrillation (VF) when the patients with AD collapsed. A loss of consciousness was the most common complaint. The outcome of the subjects was poor; however, three patients with SA achieved social rehabilitation. Two out of the three had cardiac tamponade and underwent open heart massage.

Conclusion:

The current study revealed that mortality of cardiac arrest caused by the AD remains very high, even when return of spontaneous circulation was obtained. VF was rare when the patients with AD collapsed. While some cases with CPA of SA may achieve a favorable outcome following immediate appropriate treatment.

Excessive CVP levels and microcirculatory impairment

From BMC Anesthesiology:

Methods

We performed a post-hoc analysis of a prospective study in septic patients who were resuscitated according a strict non-CVP guided treatment protocol. Simultaneous measurements of hemodynamics and sublingual Sidestream Dark Field imaging were obtained 0 and 30 minutes after fulfillment of resuscitation goals. Data were examined for differences in microcirculatory variables for CVP less than or equal to or greater than 12 mmHg and its evolution over time, as well as for predictors of a microvascular flow index (MFI) less than 2.6.

Results

In 70 patients with a mean APACHE II score of 21, 140 simultaneous measurements of CVP and sublingual microcirculation (vessels less than 20 µmeter) were obtained. (MFI) and the percentage of perfused small vessels (PPV) were significantly lower in the ‘high’ CVP (greater than 12 mmHg) group as compared to patients in the ‘low’ CVP (less than or equal to 12 mmHg) group (1.4 ± 0.9 vs. 1.9 ± 0.9, P = 0.006; and 88 ± 21% vs. 95 ± 8%, P = 0.006 respectively). Perfusion pressure (MAP–CVP) and cardiac output did not differ significantly between both CVP groups. From time point 0 to 30 minutes, a significant increase in MFI (from 1.6 ± 0.6 to 1.8 ± 0.9, P = 0.027) but not in PPV, was observed, while CVP and perfusion pressure significantly decreased in the same period. In a multivariate model CVP greater than 12 mmHg was the only significant predictor for a capillary MFI less than 2.6 (Odds ratio 2.5 (95% confidence interval 1.1-5.8), P = 0.026). 

Conclusion

We observed a significant association between a higher CVP and impairment of microcirculatory blood flow. Further research is needed to elaborate on our hypothesis generating findings that an elevated CVP may act as an outflow obstruction of organ perfusion.

Interobserver variations in the interpretation of ECGs concerning for STEMI

From a recent study:

A cross‐sectional survey was performed consisting of 36 deidentified ECGs that had previously resulted in putative STEMI diagnoses. Emergency physicians, cardiologists, and interventional cardiologists participated in the survey. For each ECG, physicians were asked, “based on the ECG above, is there a blocked coronary artery present causing a STEMI?” The reference standard for ascertaining the STEMI diagnosis was subsequent emergent coronary arteriography. Responses were analyzed with generalized estimating equations to account for nested and repeated measures. One hundred twenty‐four physicians interpreted a total of 4392 ECGs. Among all physicians, interreader agreement (kappa) for ECG interpretation was 0.33, reflecting poor agreement. The sensitivity to identify “true” STEMIs was 65% (95% CI: 63 to 67) and the specificity was 79% (95% CI: 77 to 81). There was a 6% increase in the odds of accurate ECG interpretation for every 5 years of experience since medical school graduation (OR 1.06, 95% CI: 1.02 to 1.10, P=0.01). After adjusting for experience, there was no significant difference in the odds of accurate interpretation by specialty—Emergency Medicine (reference), General Cardiology (AOR 0.97, 95% CI: 0.79 to 1.2, P=0.80), or Interventional Cardiology physicians (AOR 1.24, 95% CI: 0.93 to 1.7, P=0.15).

Conclusions

There is significant physician disagreement in interpreting ECGs with features concerning for STEMI. Such ECGs lack the necessary sensitivity and specificity to act as a suitable “stand‐alone” diagnostic test.

That last sentence may only be true when the popular formulaic approach to electrocardiographic interpretation is used. There are many well known STEMI mimics as well as examples of acute coronary occlusions that do not meet simplistic STEMI criteria (STEMI equivalents). Many such examples, recognizable by sophisticated observers, may have been ignored in this sample of physicians. The simplistic approach may be driven by todays STEMI performance incentives.

In the discussion section the authors correctly state:

However, the impetus for this study sprung largely from the notion that categorization of ECGs into dichotomous STEMI and not‐STEMI groups is often over‐simplified. This notion has importance particularly in respect to appropriateness criteria for STEMI team activation protocols. Many analyses of STEMI team activations categorize electrocardiographic ST segment elevations as a binary variable—present or not present. Such dichotomies fail to capture the graded nature of ST‐segment elevations and may grossly oversimplify the challenging task of diagnosing true STEMI patients from the much larger cohort of at‐risk patients presenting with chest pain or equivalent symptoms...

While these data speak to the difficult nature of discerning accurate from inaccurate STEMI diagnoses on the basis of ECGs alone, they also suggest that considering electrocardiographic ST elevations as a dichotomous variable for the purposes of catheterization activation protocols or appropriateness analyses may be insufficiently discerning.

The insufficiency of such a dichotomous approach is illustrated by outcomes and pathology data suggesting that the STEMI/NSTEMI distinction is baseless.

Clinical and electrocardiographic presentations of takotsubo cardiomyopathy

In this series physical stress was more often the trigger than emotional stress. All manner of electrocardiographic presentations were noted but anterior ST elevation and T wave inversion were most characteristic.

Certification and maintenance of certification: a critical look

Among the many assumptions that underlie the board certification (BC) and maintenance of certification (MOC) processes most are based on weak evidence or no evidence at all and others address the wrong questions. Here are a few:

A physician's knowledge wanes over time after training

That's generally accepted. There is a cerebral half life for many of the facts learned during training. The principle may not apply so much to knowledge in the physician's content area, which is reinforced by experience.

The process leads to better patient outcomes

There is weak evidence around this claim but it doesn't address cause and effect.

The public wants it

The statement is well supported by survey data but is it enough to justify the onerous and expensive process if evidence for real quality and outcome improvement is lacking?

An outsider (eg the specialty board) knows best the learning needs of the individual physician

A philosophical more than an evidential assumption, it's held up to ridicule by physicians “on the ground” while apparently holding sway with policy makers.


What does the evidence really say? Two reviews which address the question are noteworthy. This one from a couple of years ago was authored by officials of the ABIM and tends to be promotional although it cites much the same evidence noted in this recent and somewhat more objective review (related editorial here).

Here's the short version:

Patient outcomes

BC: Data on the correlation between BC status and patient outcomes are mixed. While some show a positive association the causality is unknown. It is equally likely that BC status and patient outcomes are linked by common factors inherent in the caliber of the physicians or their training programs.

MOC: The relationship to patient outcomes has not been specifically examined for MOC.


Processes of care

Both BC and MOC have been shown to correlate with performance metrics, but such metrics have not been validated as surrogates for quality or outcomes.


The more recent review has some interesting tidbits about participation in MOC. Participation among the leadership of internal medicine, even officials of the ABIM, was low! From the review:

We also calculated the recertification rate of the internal medicine leadership in various organizations using information collected from various websites in July 2009, which was approximately 20 years after the change in certification to a time-limited process. The initial ABIM task force on recertification has a recertification rate of 18% (3/17). The ABIM Board has a recertification rate of 20% (6/20). The editorial board for the Annals of Internal Medicine has a recertification rate of 9% (2/22). The ACP Governors have a recertification rate of 4% (2/54). The ACP Board of Regents has a recertification rate of 8% (2/26). The ACGME-RRC Internal Medicine Committee has a recertification rate of 0% (0/12). These are the statistics for internal medicine recertification only; the rates for recertification in subspecialty areas are slightly higher (Table 2). We repeated part of this analysis in June 2012. Twenty-six members of the ABIM board had lifetime certification, and six (23%) have voluntarily recertified. Thus, the participation by senior leadership in internal medicine has been unusually low; this seems surprising since many of these individuals promoted the initial process.

The editorial elaborates on this finding.

Novel oral anticoagulants for atrial fibrillation

A set of resources from the European Society of Cardiology.

New cholesterol guidelines: a brave and wise departure from current practice?

Well, that's the claim made in a recent BMJ editorial on the new guidelines (HT to DB's Medical Rants). To recap, the emphasis of the new guidelines was to treat with fixed doses of statins based on patients' risk rather than titrating to goal. While this represents a shift from the old recommendations it is not a radical departure from current practice. The “set it and forget it” approach offered by the new guidelines was, I suspect, already common in clinical practice. Moreover, based on accumulating research evidence it is more common nowadays for patients suffering acute vascular events to be discharged from the hospital on high statin doses, without much attention to their baseline lipids, similar to those recommended in the new guidelines. What the document did, though, was codify this practice which, one would hope, will cause it to be more uniformly and systematically applied. So this will not result in the “tectonic shift” that the BMJ author has claimed.

Then he goes on to say this:

A spate of studies over the past few years contributed to an insight that had previously eluded the field. Cholesterol plays a key role in atherosclerosis, but its modification by drugs does not always produce the expected result. Drugs have thousands of effects and their influence on cholesterol concentrations does not convey their net effect on patient risk. Trials showed that lowering LDL-C and raising high density lipoprotein cholesterol did not necessarily lower risk.8 9 10 11

Those trials did not ask the simple question of whether pharmacologic alteration in lipid levels would reduce events. With the exception of one study which may be an outlier because it involved a novel class of drugs these trials essentially addressed whether adding a second drug would address residual risk after statin therapy. Older studies which did ask the simple question supported the lipid hypothesis and provided evidence that altering LDL and HDL cholesterol levels leads to a reduction in important clinical events. I reviewed those studies in yesterday's post.

I did find some good points in the editorial. For example the author makes this point which is fundamental in the application of clinical trials to the principles of evidence based medicine:

Also, the risk thresholds for treatment should be understood as recommendations and not dictums. For any individual, the decision about the worth of a drug treatment depends on how that person feels about potential benefits, burdens, and harms—something that no writing group can determine. Ultimately, the decision depends on our ability to provide patients with the knowledge and guidance needed to make high quality decisions about their treatment.

Then he makes this point about performance measures:

The new guidelines are also a cautionary tale about the premature translation of medical guidelines into performance measures. They highlight that the push to chase targets was based on speculation, not on direct trial evidence, and opened the door to the use of drugs that had not been fully tested.

Performance measures, while they appeal to guidelines and research evidence, do so without appropriate critical analysis and expertise which is one reason they ultimately fail.

The new cholesterol guideline: is it really a paradigm shift?

There's a lot of misinformation flying around about the 2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults. Some of the popular distortions include the idea that the guideline authors threw away the LDL targets and sent a message that lipid lowering doesn't matter. That's not what the document says at all. Over and over in the guideline the authors acknowledge that cholesterol reduction is the goal of statin therapy. Heck the title of the guideline, as linked above, makes that pretty explicit! And while they de-emphasized specific targets they didn't throw them out altogether. What the panel did was recognize that major lipid lowering trials were not designed to test titrated dosing of drugs to particular targets. Accordingly the major recommendations of the document are based on patients' overall risk more than their lab values. In the nine years since the ATP update on lipid management we've learned a great deal about the pleiotropic effect of statins. But LDL reduction remains an important part of the story and the guideline writers acknowledge that. There's no new paradigm here. They are merely making the recommendations more respectful of historic clinical trial design. I think it's a mistake to extend the interpretation beyond that.

Last month Dr. Robert Centor, blogging ad DB's Medical Rants, expressed his approval of the new guidelines. I agree with him that we needed a more evidence based approach. But then DB makes this statement:

The brilliance of the new guidelines comes from the writing group understanding that lowering the cholesterol level does not improve important outcomes, but statins (discovered and popularized because they lower cholesterol) improve outcomes regardless of ones initial cholesterol. Other drugs that lower cholesterol or raise HDL do not improve important outcomes!

But wait a minute. There's a substantial body of research showing that lipid lowering reduces clinical events no matter how you do it. Though some of the studies have confounders, as a whole they point to the importance of LDL reduction. The Oslo study, though confounded by more smoking cessation in the intervention group, suggested a reduction in coronary events attributable to dietary reduction of cholesterol. The LRC trial showed a reduction in events attributable to LDL lowering by means of cholestyramine resin. Clinical trials of other non statin drugs also showed reduction events attributable to lipid lowering though confounded by the ability of those particular drugs to raise HDL cholesterol: the Coronary Drug Project (niacin), the WHO study (clofibrate); and the Helsinki study (gemfibrozil).

Sidebar: the Coronary Drug Project also serves as a reminder that we had comparative effectiveness research back in the 1960s. The concept is not new, only the name designed to serve political ends and give authors catchy options for their titles.

The importance of LDL in the pathogenesis of atherosclerosis has been established for a long time. Our understanding of how that works is more nuanced than it was decades ago. In our more complex understanding of atherosclerosis and new appreciation of the pleiotropic effects of statin drugs we realize more than before that the LDL concentration is not the whole story. But it remains an important part of the story.

Background: This review, though out of date for treatment recommendations, is a careful analysis of early trials establishing the lipid hypothesis and demonstrating improvement in meaningful clinical outcomes with diet and non statin drug treatments to lower cholesterol.

Extracorporeal life support (ECLS)

This refers to either extracorporeal membrane oxygenation (ECMO) or extracorporeal CO2 removal (ECCO2R), for a variety of indications but mainly ARDS. Here is a recent review.

The status of ECLS is evolving. In the 70s, following an early wave of enthusiasm for ECMO as treatment for ARDS, research evidence was disappointing. By the time of my early interest in critical care the idea was almost rejected out of hand. Subsequently it began to emerge as a rescue modality for ARDS in cases of therapeutic desperation. Technology improved and offered variations of the technique as additional options. Out of necessity considerable positive experience was gained during the 2009 pandemic. Also, as quoted from the review:

Also that same year, the conventional ventilatory support versus ECMO for severe adult respiratory failure (CESAR) study was published. The investigators used a “pragmatic” study design and were criticized for the inability to standardize mechanical ventilation management in the conventional care group.[30] Importantly, the CESAR trial demonstrated that protocolized care that included ECMO in an expert center for ARDS care yielded higher survival than the best standard care in tertiary intensive care units in the UK.[30]

Here is the CESAR study. It concluded:

We recommend transferring of adult patients with severe but potentially reversible respiratory failure, whose Murray score exceeds 3.0 or who have a pH of less than 7.20 on optimum conventional management, to a centre with an ECMO-based management protocol to significantly improve survival without severe disability.

So ECLS is making its way into clinical practice. The Extracorporeal Life Support Organization has published guidelines. The indications section reads:

A.

Indications

Acute severe heart or lung failure with high mortality risk despite optimal conventional therapy. ECLS is considered at 50% mortality risk, ECLS is indicated in most circumstances at 80% mortality risk. Severity of illness and mortality risk is measured as precisely as possible using measurements for the appropriate age group and organ failure. See patient- specific protocols for details. 

B.

Contraindications

Most contraindications are relative, balancing the risks of the procedure (including the risk of using valuable resources which could be used for others) vs. the potential benefits. The relative contraindications are: 1) conditions incompatible with normal life if the patient recovers; 2) preexisting conditions which affect the quality of life (CNS status, end stage malignancy, risk of systemic bleeding with anticoagulation); 3) age and size of patient; 4) futility: patients who are too sick, have been on conventional therapy too long, or have a fatal diagnosis. See patient-specific protocols for details.

Adipose tissue: metabolically active, proinflammatory

This review from the Archives of Medical Science helps explain the cardiovascular consequences of the metabolic syndrome.

Strengthened FDA warnings for Lexiscan and Adenoscan

New from the FDA:

The U.S. Food and Drug Administration (FDA) is warning health care professionals of the rare but serious risk of heart attack and death with use of the cardiac nuclear stress test agents Lexiscan (regadenoson) and Adenoscan (adenosine). We have approved changes to the drug labels to reflect these serious events and updated our recommendations for use of these agents. Health care professionals should avoid using these drugs in patients with signs or symptoms of unstable angina or cardiovascular instability, as these patients may be at greater risk for serious cardiovascular adverse reactions.

This was already reflected in the labeling but the warning has been strengthened. The risk is believed to be low, though the denominator is unknown. The last sentence in the quoted text is of concern, given a general perception that these agents should be safer in potentially unstable patients as opposed to dobutamine or treadmill exercise.

Therapeutic hypothermia after cardiac arrest: what’s optimum?

Results of two trials were presented at AHA.

In this one 33 C was no better as a therapeutic target than 36 C in terms of survival or neurologic outcome.

In the other study initiation of cooling pre-hospital was associated with greater incidence or re-arrest and need for diuretics but produced no survival or neurologic benefit.

Based on a related discussion at Medpage Today therapeutic hypothermia remains an important intervention. However we have yet to find the sweet spot in terms of optimal timing and “dose” of the intervention.

Immediate blood pressure lowering in ischemic stroke

In patients with acute ischemic stroke not receiving thrombolytics, the guidelines for years recommend avoidance of antihypertensive therapy up to levels of 220/120 (permissive hypertension). High level evidence to guide clinicians in one direction or the other, however, was lacking. The recently published CATIS trial (presented at AHA and published in JAMA) addressed the question:

Objective To evaluate whether immediate blood pressure reduction in patients with acute ischemic stroke would reduce death and major disability at 14 days or hospital discharge.

Design, Setting, and Participants The China Antihypertensive Trial in Acute Ischemic Stroke, a single-blind, blinded end-points randomized clinical trial, conducted among 4071 patients with nonthrombolysed ischemic stroke within 48 hours of onset and elevated systolic blood pressure. Patients were recruited from 26 hospitals across China between August 2009 and May 2013.

Interventions Patients (n = 2038) were randomly assigned to receive antihypertensive treatment (aimed at lowering systolic blood pressure by 10% to 25% within the first 24 hours after randomization, achieving blood pressure less than 140/90 mm Hg within 7 days, and maintaining this level during hospitalization) or to discontinue all antihypertensive medications (control) during hospitalization (n = 2033)…

Results Mean systolic blood pressure was reduced from 166.7 mm Hg to 144.7 mm Hg (−12.7%) within 24 hours in the antihypertensive treatment group and from 165.6 mm Hg to 152.9 mm Hg (−7.2%) in the control group within 24 hours after randomization (difference, −5.5% [95% CI, −4.9 to −6.1%]; absolute difference, −9.1 mm Hg [95% CI, −10.2 to −8.1]; P less than  .001). Mean systolic blood pressure was 137.3 mm Hg in the antihypertensive treatment group and 146.5 mm Hg in the control group at day 7 after randomization (difference, −9.3 mm Hg [95% CI, −10.1 to −8.4]; P less than  .001). The primary outcome did not differ between treatment groups (683 events [antihypertensive treatment] vs 681 events [control]; odds ratio, 1.00 [95% CI, 0.88 to 1.14]; P = .98) at 14 days or hospital discharge. The secondary composite outcome of death and major disability at 3-month posttreatment follow-up did not differ between treatment groups (500 events [antihypertensive treatment] vs 502 events [control]; odds ratio, 0.99 [95% CI, 0.86 to 1.15]; P = .93).

Conclusion and Relevance Among patients with acute ischemic stroke, blood pressure reduction with antihypertensive medications, compared with the absence of hypertensive medication, did not reduce the likelihood of death and major disability at 14 days or hospital discharge.

There are no findings from this new trial to indicate change from current guideline based practice.

Another novel anticoagulant scores against warfarin

ENGAGE AF was presented at AHA and published in NEJM:

Methods

We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding…

Conclusions

Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes.

The interpretation of the results is complex. Here is a related discussion in Medpage Today.

Pitfalls in the evaluation of patients for B12 deficiency

From a recent study:

Methods This retrospective study reviewed the electronic medical records of 192 patients initiated on intramuscular vitamin B12 injections.

Results Only 12 patients had objectively documented hematologic responses: decrease of mean corpuscular volume by greater than or equal to 5 fL with stable or improved hemoglobin. Another 5 patients had equivocal hematologic responses. There was one plausible neurologic response. Thus, only 18 (9.4%) of 192 patients had data supportive of a clinical response. In these 18 patients, the baseline serum B12 level was less than or equal to 107 pg/mL; only 3 patients also had a baseline serum methylmalonic acid level, which was greater than or equal to 1.29 μmol/L in all 3 patients.

Conclusions Currently, only a small minority of patients initiated on intramuscular vitamin B12 supplementation derive any meaningful clinical benefit. Furthermore, current testing recommendations for vitamin B12 deficiency are usually not followed.

The authors make several suggestions to improve diagnostic accuracy:

Reserve B12 testing for patients with a clear clinical indication.

Avoid reliance on a single test.

Laboratories should perform reflex testing of MMA levels and IF antibodies when low B12 levels are detected.

Hematologic responses should be followed during treatment and if the expected response does not occur evaluation for other conditions should be carried out.

Biochemistry free and easy

A free on line text form OSU.