Performance does not equal quality

DB in a recent rant explains why performance measures don’t translate into quality. He says the boosters have pulled a fast one on us by confusing performance with real quality. I have to agree. Let’s call the performance measures what they are---performance measures, not quality measures.

One of his commenters gently takes him to task:

The best we can do is to continually test the relationships between “quality measures” at all levels and the final results we desire. Waiting for perfect measures is unrealistic.

I have to ask: if you don’t think guidelines should be followed in the populations for whom they are designed (which is how we identify the denominator populations for Bernoulli-distributed process measures), with whom are you really arguing?

I suppose the alternative is to reject empiricism entirely and adopt the framework of Cartesian doubt.

I don’t read DB as knocking EBM, or even guidelines, although he has been critical of the way they are promoted. My take is that today’s performance measures have little to do with true EBM. Moreover the performance police, in an effort to get everyone on board with a minimum standard of guideline based care, have misappropriated and over simplified those same guidelines.

A six hour ER wait time

---is better than six months. That’s why many patients, even insured patients, are going to the ER for their primary care. Read about it in Kevin’s USA Today op-ed.

ALLHAT hype

It’s not the way science is supposed to work. You don’t go out and hype your results after they are published. A research publication should stand, in the arena of scientific discussion and critical examination, on its own merits. But that’s not the way the ALLHAT steering committee looked at things. From the moment of its publication the study was spun and promoted like the latest woo.

ALLHAT did change practice. Thiazide prescriptions increased following its publication, but apparently not enough, according to the New York Times, to suit the boosters:

“It should have more than doubled,” said Dr. Curt D. Furberg, a public health sciences professor at Wake Forest University who was the first chairman of the steering committee for the study, which was known by the acronym Allhat. “The impact was disappointing.”

What was the vested interest in hyping ALLHAT? Some of the lead investigators, together with the media, seeking to advance the premise that pharmaceutical industry marketing had set back the cause of science in the treatment of hypertension, saw the study as a gigantic “see we told you so.”

Sure there were lessons in ALLHAT for the treatment of hypertension but the hype surrounding the study distracted us from a reasoned critical analysis of the findings. The message of the promoters, that thiazide diuretics were, plainly and simply, the starting drugs of choice for hypertension, went way beyond the study findings. There were serious concerns about the design, execution and interpretation of ALLHAT which I won’t belabor here. DB dealt with them in his blog as I did in these pages.

Some time ago on I cited concerns about the metabolic hazards of thiazides and a documented risk of sudden cardiac death. A recent meta-analysis, showing a similar trend towards increased sudden death, added to the concern. The senior investigator, renowned hypertension expert John Oates, said:

“If it's true, it's probably the largest adverse effect in the history of modern pharmacology. The number of individuals affected over the last 50 years would be staggering.”

The trend, while coming short of statistical significance, would be enough for the media to blow a new proprietary drug out of the water. The New York Times was silent.

Although thiazides, as I explained here, do have a very important role in the treatment of hypertension, the notion that thiazide monotherapy is the unequivocal first step in hypertension treatment was not supported by ALLHAT and now, we know, is just plain wrong.

All that wheezes is not asthma

About a third of patients who carried a diagnosis of asthma turned out not to have asthma at all in this study. A related editorial makes the point that underdiagnosis as well as overdiagnosis of asthma is common, and the major error is failure to do spirometry.

I wish the paper had provided the real diagnoses of the patients who didn’t have asthma. An interview with one of the authors suggests that many of these patients had an acute viral illness with bronchospasm, were declared to have asthma and never formally tested or tapered off their medications.

If my patient gets an infection it’s somebody else’s fault

I found this ad in the ICU lounge:

It reflects our new culture. The patient safety movement purported to replace a culture of blame with one of transparency and constructive system change. But the movement’s obsession with “never events”, aided and abetted by popular media, has had the opposite effect. I’m afraid this is headed in the wrong direction.

Making sense of the guidelines: pneumonia

I am reposting my 11/03/08 pneumonia guideline summary because the categories need clarification. Updated comments are italicized.

The pneumonia guidelines are complicated. They consist of two sets of guidelines (community acquired pneumonia, CAP, and health care associated pneumonia, HCAP) which are distinct but have just enough overlap to be confusing. Both guidelines stratify patients into high and low resistance risk groups. The respective groups are similar in the two guidelines with distinctions that seem nit picking and at times don’t make sense. (Why, for example, is ceftazidime listed as an antipseudomonal drug in the HCAP guideline but not the CAP guideline?). Add to this the criteria for site of care (home vs ward vs ICU) and de-escalation (PO switch, discharge and stopping therapy). Who can remember it all? You can look it up each time---the guidelines are open access full text---but opening up and browsing those large pdf files is cumbersome.

Is it worth the trouble? Although guidelines are not a substitute for clinical judgment, you may ignore them at your patients’ peril. In the case of pneumonia it has been shown repeatedly (here, here, here, here, here, and here) that guideline adherence is associated with better outcomes.

Here is my attempt to remedy pneumonia guideline chaos by condensing the essentials in one post. The figures below summarize the information I find my self looking up most often. (The complete guidelines should be read in their entirety, once or twice. They contain a world of information on etiology, pathogenesis and diagnosis, not covered here).

Hospital acquired pneumonia (HAP), ventilator associated pneumonia (VAP) and health care associated pneumonia (HCAP) are listed in the guidelines as separate categorizations. Among these three categories, however, the antibiotic recommendations are based on microbiologic risk and are the same for a given level of risk. Therefore, for purposes of this guideline summary I have lumped the three categories together as HCAP.

A practical definition of HCAP which encompasses all three categories is pneumonia with any one of the following characteristics: onset 48 hours or more after admission; two or more days of acute care hospitalization in the past 90 days; nursing home residency; IV antibiotic therapy, chemotherapy or wound care within the past 30 days; hemodialysis. Other pneumonias would be considered community acquired pneumonia (CAP).

After adjudicating a patient as CAP or HCAP go to the appropriate section below to assign microbiologic risk. Note that conditions defining a patient as “HCAP” and “HCAP, high microbiologic risk” overlap greatly but are not interchangeable. Rigid application of some distinctions becomes nit picking. Clinical judgment and common sense are required.

The fourth line under the category HCAP, high microbiologic risk should read “two or more days of hospitalization in the last 90 days.”






Note: The above table classifies CAP and HCAP according to the risk of resistant organisms. CAP is also independently classified as to eligibility for ICU placement. Aside from the obvious indications of shock and mechanical ventilation, guideline recommendations for ICU placement include patients with any 3 of: RR 30 or above; PO2/FiO2 250 or below; multilobar infiltrates; acute alteration in mental status; BUN 20 or above; WBC below 4000; platelet count below 100,000; hypothermia (core below 36C); hypotension requiring fluid challenge.

Admission decisions can be based on the CURB-65 criteria or the pneumonia severity index.

Miscellaneous: No time rule for antibiotic admin; guidelines say give in ER. Legionella and pneumococcal urine antigen determinations are recommended for many, but not all, categories of patients. For CAP, blood cultures are considered optional in some of the lowest risk patients.

New evidence post guideline publication: Steroids for severe CAP? Maybe; stay tuned. Statins? Promising. CA-MRSA is a bad actor, and is emerging. Think of it.

Primary biliary cirrhosis review

From the Orphanet Journal or Rare Diseases.

Movement disorder emergencies

Life threatening, underappreciated. Via CCJM.

Check out Endotext

The main page reads We offer the only complete, authoritative, constantly updated, down-loadable source on clinical endocrinology, without registration or cost. Almost seems too good to be true, but what I’ve checked out so far is very good. (H/T to Robert J. Rushakoff speaking at Bob Wachters’ 12th Annual Hospital Medicine course).

Antiarrhythmic effects of statins

In this study they decreased atrial fib/flutter by 53% and inappropriate AICD discharges by 39%.

Hepatic encephalopathy

Ammonia is instrumental in the pathogenesis. It’s not just a marker.

Ammonia causes astrocyte swelling and alterations in neurotransmitter metabolism.

Cytokines cause astrocyte swelling, explaining the role of infection in precipitating HE.

Those are some of the interesting points in a review published in Seminars in Liver Disease, one of the better reviews I’ve seen on the subject.

T wave abnormality: cardiac or cerebral?

In 1954 George Burch described T wave abnormalities as myocardial ischemia mimics in patients with a variety of acute cerebral insults. His classic paper, which popularized the term cerebral T waves, is available as free full text here. (Note the nine lead electrocardiograms recorded from the string galvanometer on photographic paper).

Fifty four years later we’re just beginning to understand the neurocardiac mechanisms. Those mechanisms, along with a few ECG examples, were recently reviewed in the American Journal of Emergency Medicine. An algorithm to help differentiate cardiac from cerebral T wave abnormalities is presented. However, considerable overlap between the patterns exists.

Web based diabetes management tutorials

General management

Inpatient management

H/T to Robert J. Rushakoff, from his talk at Bob Wachter’s Hospital Medicine course.

Von Hippel-Lindau Disease

Review in JAMA.

Hospitalists and the economy

I can already hear the buzz at SHM 2009. How will the recession affect the hospitalist movement? How should hospitalists be compensated in tough economic times? And, one more time, How can we measure and demonstrate our value?

The past few weeks have seen some interesting and provocative posts on this subject. Adam Singer, author of The Hospitalist Blog, thinks the economic woes of hospitals will trickle down to hospitalists. His solution? If I read him correctly, he thinks hospitalist programs should become “self sufficient” and subsist entirely (or almost entirely) from their billing revenues:

Herein lays the opportunity for hospitalist groups of all types to seize this moment and reevaluate their business models with the goal of reducing their dependency on hospital subsidy dollars to sustain their practices. There are some situations where obtaining hospital stipends are totally appropriate, such as providing on-site night coverage or caring for a disproportionate share of indigent patients, but these situations are more the exception than the rule. Focus on finding opportunities and staffing models for your practice that will generate enough profit so that your practice is self-sustaining. Better to view your hospital subsidy as a luxury that your practice could live without if you had to, rather than as a necessity that you need in order to survive. It can be done.

I’m skeptical as to how that can be done. I think he plans to explain in installment three.

Bob Wachter’s prognosis, though not quite so pessimistic, is guarded:

My own feeling is that we should accept our share of any shared pain. If budgets are being cut across our institution, we should participate in reasonable belt tightening.

(Do ya think hospital CEOs should participate too, Bob?) ;)

What disturbs me just a wee bit in both posts is the characterization of hospitalist compensation. Referring to the difference between what programs are paid and the fees they produce, Adam uses the term “subsidy” and Bob talks about “support payments.” It implies most programs don’t really “earn their keep.” The usual workaround for that uncomfortable notion invokes all the mental gymnastics about hospitalists’ “value.”

Sure, hospitalist programs bring a great deal more to health care systems than the fees they generate. Much of that value, though, is intangible. It can’t be measured. Here’s the value test: imagine waking up some morning to find that your hospital’s hospitalist program has imploded.

Another new clinical blog

Well, not so new---it’s been up and running since April---but I just found out about it from the Clinical Cases and Images blog. The masthead for Renal Fellow Network reads: A website written for renal fellows by renal fellows with one new "Nephrology Teaching Point" posted on a daily basis. Hard core clinical content. No fluff. I like it.

AHA 2008 roundup

I’m late with this and it’s all been posted elsewhere, so why here and now?

Very seldom do medical research findings warrant coverage as breaking news. Rare findings which are really earth shattering are often not appreciated as such until months or years later. Many media reports from the AHA sessions were little more than sound bites and many were over hyped. When those reports came out I was too busy and tired to blog. Now, after an opportunity to check primary sources and think about the findings, I offer my own take on some of the ones that interested me.

JUPITER The NEJM abstract concludes with:

In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events.

So---statin treatment works for primary prevention in patients with “normal” cholesterol levels. Earthshaking? Hardly. We knew this a decade ago. Remember AFCAPS/TexCAPS?

This study helps confirm the findings of AFCAPS/TexCAPS and (I think) extends them to even healthier patients. The study was hyped and probably won’t (or shouldn’t) change practice much. For a thoughtful and nuanced view of JUPITER see the accompanying NEJM editorial.

When considering the use of statins for primary prevention in low risk patients one must weigh in absolute risk reduction (the NNT in JUPITER was 120 patients treated for 1.9 years), cost effectiveness (Dr. Wes does the math for Crestor here) and the risks of years and years of statin use.

What’s the significance of the hs-CRP test? Although statins (at least some) lower CRP levels, the main significance is that CRP, like diabetes, smoking and hypertension, is a risk factor and the higher the patient’s risk the bigger the bang for the buck with LDL reduction. This was shown several years ago for hs-CRP in a subgroup analysis of AFCAPS/TexCAPS. The statin used in that study, lovastatin (Mevacor) is now on Walmart’s $4 generic list. Do the math again and it looks a good deal better from a cost effectiveness standpoint.




Negative Thinking Predicts Depression in Heart-Failure Patients. Did we really need a study to figure that out?




LDL particle concentration versus LDL cholesterol concentration Via Reuters Health:

Risk of cardiovascular disease can remain high even after low-density lipoprotein (LDL) cholesterol target levels have been reached in patients with the metabolic syndrome.

We’ve known this for years. Although the guidelines have not emphasized it enough the concept of residual risk after statin therapy (RRAST) is emerging. LDL reduction is important and, in the aggregate, the lower the better. In many individual patients, though, it’s not enough. The fact that statin trials show RRR’s of 25-30% begs the question “why not 80%, why not 100%?” (Bob Superko addressed this in his classic paper here, and, along with Spencer King, provided an update here).

From the Reuters piece:

Risk may be better gauged with low-density lipoprotein particle concentration, investigators announced here at the American Heart Association's Scientific Sessions 2008.

High LDL particle concentration relative to LDLC concentration reflects the atherogenic lipoprotein profile (ALP) characterized by abnormally small LDL particle diameter. This is a phenotypic expression of the metabolic syndrome and for practical purposes many regard it as synonymous (this is not invariably so---the ALP is nicely explained in the Superko papers linked above). The ALP and the associated metabolic syndrome represent the most common genetic causes of CAD and are certainly the most important contributors to RRAST.

Perhaps most concerning from the AHA presentation was this:

"Lipoprotein particle concentration may go up as LDL cholesterol levels are lowered with treatment," Dr. Robert Rosenson of the University of Michigan at Ann Arbor told Reuters Health after he presented his team's findings regarding 401 patients with metabolic syndrome and a 10-year risk of coronary heart disease greater than10%.

This is a finding that needs better understanding. Do statins somehow turn on genes that cause metabolic syndrome? What’s the solution? When the patient is at goal with statin therapy the RRAST must be assessed. The determination of triglycerides, HDLC and the total/HDL ratio are helpful. If the metabolic syndrome is evident diet and exercise are the best treatments, and drug therapy options include niacins and fibrates.

It has been suggested that lowering LDLC to extremely low concentrations with statins may offset this residual---lower the cholesterol concentration enough with statins and eventually the particle concentration will go down, perhaps. In that connection note a little mentioned aspect of JUPITER---LDLC was lowered to a median of 55 and RRR’s were on the order of an unprecedented 50% in contrast to the 25-30% reductions cited for other statin trials. Maybe there’s something to it.




Vitamins C and E Here we go again. No benefit. Vitamin E may even be harmful. There’s never been any favorable evidence for vitamin C and vitamin E was blown out of the water years ago. That hasn’t stopped some from promoting it, though.




Irbesartan and heart failure with preserved EF

During a mean follow-up of 49.5 months, the primary outcome occurred in 742 patients in the irbesartan group and 763 in the placebo group. Primary event rates in the irbesartan and placebo groups were 100.4 and 105.4 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% confidence interval [CI], 0.86 to 1.05; P=0.35). Overall rates of death were 52.6 and 52.3 per 1000 patient-years, respectively (hazard ratio, 1.00; 95% CI, 0.88 to 1.14; P=0.98). Rates of hospitalization for cardiovascular causes that contributed to the primary outcome were 70.6 and 74.3 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% CI, 0.85 to 1.08; P=0.44). There were no significant differences in the other prespecified outcomes.

Again, this result for irbesartan (Avapro) is not new regarding ARB’s and heart failure with preserved ejection fraction (HFPEF). The CHARM-preserved study reached a similar conclusion years ago with candesartan (Atacand). There is little in the way of evidence from clinical trials to guide clinicians in the long term treatment of HFPEF. The best we can do now is to do a better job of treating their co-morbidities, of which they have many. If those co-morbidities include hypertension irbesartan as well as other antihypertensive agents might be reasonable choices. To say that irbesartan is of no value in the treatment of patients with HFPEF is simplistic. (Patients to be included in the irbesartan study could not have uncontrolled hypertension).




Perioperative beta blockers---another negative meta-analysis. From the Lancet paper:

The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available.

Well, they already have, quite some time ago. Now, the only strong guideline recommendation, for practical purposes, is that if the patient is already on a beta blocker for cardiovascular indications it should be continued perioperatively.




Statin dose-response relationships: Search Me This one’s a little complicated. Simvastatin (Zocor) was only marginally better at 80 mg in comparison to 20 mg daily in terms of reducing events in a secondary prevention study. But when this study is taken into account with multiple other statin trials the notion that lower LDLC is better still holds. Most disturbing was the markedly increased incidence of myopathy at the 80 mg dose. According to expert commentary about this study, if it’s desirable to seek very low LDLC targets in your patient it may be better to switch to a safer statin as opposed to increasing simvastatin to 80 mg. Simvastatin is safe when used according to the product safety labeling. This labeling, however, particularly the section on drug interactions, has become so complicated that simvastatin is getting a little tricky to prescribe. One has to review the patient’s entire med list and, unless one has a photographic memory, look up the labeling each time.

Classic paper: An unusual electrocardiographic pattern predicts dilated cardiomypoathy

Uncomplicated left bundle branch block is associated with a normal axis. Left bundle branch block with right axis deviation is a rare electrocardiographic pattern. In a classic paper Nicolic and Marriott described this pattern and noted a high predictive value for dilated cardiomypoathy. Subsequent observations have confirmed the association.

Point of care lactate levels for early identification of sepsis patients at high risk of death

It’s widely accepted that sepsis treatment should be regarded with the same urgency as trauma or acute STEMI. However early recognition of sepsis is notoriously poor. Is there a solution? How about a fingerstick lactate in the triage area? Better yet, in the ambulance? Here’s a study examining the issue.

Idiopathic pulmonary fibrosis

---was recently reviewed in the Orphanet Journal of Rare Diseases.

Key points:

While idiopathic pulmonary fibrosis (IPF) is often a wastebasket term for many patients with lung fibrosis it is actually a rare disease with specific diagnostic criteria. Because of its rarity and dismal prognosis (survival and quality of life worse than many forms of cancer) patients should not be given this label unless specific diagnostic criteria are met.

Terminology has been confusing, as the term IPF has been used interchangeably with usual interstitial pneumonia (UIP) and cryptogenic fibrosing alveolitis (CFA). UIP refers to the histologic pattern characteristic of IPF, not a particular disease. CFA is the former European term for IPF.

IPF is one of a large family of diseases popularly referred to as interstitial lung disease (ILD). ILD is an inaccurate choice of terms because these diseases usually have a phase or component of alveolitis. The preferred term is diffuse parenchymal lung disease (DPLD).

Pharmacologic options, covered in the review, are poor. Transplantation is appropriate in a select group of patients.