Activated protein C for severe sepsis: what's the current status?

Activated protein C (Xigris) is given a soft recommendation for use in patients with severe sepsis at high risk of death in the latest version of the Surviving Sepsis guidelines.


In recent years it has fallen out of use due to various controversies, including allegations of undue Pharma influence, concern about bleeding risk and mixed evidence since the publication of PROWESS concerning optimal patient selection.


So what is its current status?


Two recent articles caught my attention, which I haven't blogged before. This large propensity matched retrospective cohort study showed a mortality benefit almost identical to that observed in PROWESS. This updated Cochrane review, on the other hand, found no evidence of benefit.


So for now the drug remains controversial. We'll have to wait for the results of Prowess-SHOCK, in which it is studied in the sickest of patients, to get better answers.


Meanwhile in a recent podcast at the EM Crit blog sepsis expert Emanuel Rivers, the originator of early goal directed therapy (EGDT) was asked about the controversy. He cited the increasing evidence that use of Xigris is time dependent, and blames some of the negative results on giving the drug inappropriately late, remarking that inappropriately late use in the course of sepsis has unfortunately “done this drug in.”

Upper extremity DVT

Here is a recent review in the American Journal of Medicine.


Some key points:


Deep veins are defined as brachial, acillary, brachiocephalic, IJ and subclavian veins. Basilic, cephalic and EJ are considered superficial.


Secondary UE DVT is the most common presentation, and is usually due to central IV catheters including peripherally inserted (PICCs). Other risk factors such as malignancy are included.


Primary UE DVT is less common and also known as Paget-Schroetter syndrome. It may be precipitated by vigorous arm activity and may be associated with thoracic outlet abnormalities.


The diagnostic approach is similar to that for LE DVT although supporting research data are relatively sparse.


There appears to be a lower incidence of concomitant PE although sequellae are otherwise similar to those of LE DVT.


Treatment, including duration, is similar to that for LE DVT.


Because cosmetic and comfort issues are more likely to surface with UE DVT than for LE DVT, thrombolysis (systemic or regional) or catheter extraction are often considered. However, data are limited and based on the evidence, at present, such techniques are recommended mainly for patients with massive clot burdens.

Could your patient's seizures be due to hyponatremia?

The answer may be more difficult than you think according to this post from Renal Fellow Network.

Electronic medical records disappoint

---according to this essay :

As with any system, an EHR produces the outcome for which it was designed. The most widely used EHRs are designed for auditing, compliance and billing. They are not designed for more efficient patient care in the office, better communication among providers, or the collection of group data for quality improvement efforts. As yet, there is no evidence that the use of an EHR provides less expensive care and/or better outcomes.

Indeed there is no evidence, only dogma, and it's dogma that's being forced down doctors' throats. Go to the link and read the rest. Not just anyone could speak such heterodoxy but this article was written by none other than the president of the American College of Physicians.


HT to Health Care Renewal.

Preoperative anemia associated with worse surgical outcomes

---in this much talked about study. Although the differences in outcomes between those with and without anemia held up to severity adjustment it's tempting to think that anemia was a marker of something else going on in the patient (infection, inflammation?) that may have impacted outcomes rather than a reduced oxygen carrying capacity. This will be studied further. We don't have an answer about whether a more aggressive transfusion strategy is warranted.


Via Hospital Medicine Quick Hits.

Subglottic secretion drainage

---decreased VAP in this meta-analysis.

Necrotizing soft tissue infections

Here is an excellent review of the topic.


A few key points---


Definitions and classifications:


The FDA classification is broken down into complicated and uncomplicated skin and soft tissue infections. Complicated soft tissue infection basically means any infection at deep enough levels to require surgical intervention. However, the FDA designations exclude necrotizing infections.


Necrotizing infections are designated types I, II, III and miscellaneous.


Type I infections are mixed infections, with both aerobic and anerobic organisms. Their pathogenicity is driven largely by host factors especially diabetes. Fournier's gangrene represents but one example and is defined by location in the perineal or genital area.


Type II infections are monomicrobial, involving certain necrotizing (popularly known as “flesh eating”) strains of either beta strep or Ca-MRSA. Host factors play a lesser role.


Type III infections are rare, very severe infections, with gas gangrene as the prototype.


Miscelaneous infections include water borne infections with Vibrio vulnificus as a prototype.


Ancillary diagnostic tools, including imaging and clinical scoring, as well as a table of antibiotic recommendations, are included in the article.

Hip fracture comanagement

Here are some tips presented at a session at the SHM 2011 national meeting.

Pradaxa, bleeding and the kidney

Here's a recent review and related post at The Kidney Doctor. Background here.

Nephrotic syndrome

Nephrotic syndrome is a podocyte disorder and is discussed in this review.


Points of interest---


The podocyte provides structural support for the glomerular capillary tuft and is important in the secretion of the collagen network of the GBM:

Failure to secrete this network results in a range of hereditary nephropathies, the type IV collagenopathies.

Type IV collagenopathies include Alport syndrome, nail patella syndrome, and thin basement membrane disease; all can be considered podocyte disorders.

The pathophysiology of podocyte injury explains why patients do not generally have active urinary sediment, in contrast to the glomerulonephritides:

Subepithelial immune complexes (as in MN) or podocyte injury usually do not lead to leukocyte recruitment and inflammation, but rather disrupt the GFB.

Typically, urine sediment is devoid of leukocytes and erythrocytes.

Disruption of GFB leads to proteinuria.

In contrast, injury to mesangial or endothelial cells, which are in direct contact with blood (containing leukocytes, complement, and inflammatory proteins), typically leads to inflammatory kidney disease (nephritis) with active urine sediment.

All patients with nephrotic syndrome are at risk for renal vein thrombosis, but especially those with membranous nephropathy. RVT may be asymptomatic, present with pain, or as a sudden decline in renal function.




Minimal change disease (MCD)


Inflammatory mediators---> podocyte injury---> foot process effacement.


10%-15% of nephrotic syndrome (NS) in adults, 90% in kids.


Secondary causes of MCD: drugs, neoplasia, others.




Focal segmental glomerulosclerosis (FSGS)


Pathogenesis complex and varied, but involves podocyte injury and podocytopenia.


Most common cause of NS in adults overall.


Can progress to ESRD.


Can be idiopathic but many secondary causes.




Collapsing glomerulopathy


Controversial whether a type of FSGS or a distinct entity.


Disease association: HIV.




Membranous nephropathy (MN)


Subepithelial immune complex deposition.


Primary or secondary. Many secondary causes.


Primary: antibodies enter subepithelial space and bind to podocyte antigen.


Secondary: a) circulating immune complex dissociates then reforms in subepithelial space or b) antigen lodged in subepithelial space and subsequent immune response. Specific antigen (tumor antigen, infectious particle, etc.) depends on underlying disease.


Long list of secondary causes (drugs, infections, neoplasia, rheumatic diseases).


Most common cause of NS in elderly, caucasians.


Urine: no “active sediment” but microhematuria common.




Miscellaneous disorders


Collagenopathies, etc., see above.


Via Nephron Power.

Diagnostic skepticism---a victim of competing interests

When I first read this post by Dr. Robert Centor at DB's Medical Rants about diagnostic skepticism I wondered why anyone would need to write about such a no-brainer. After all, rigorous skepticism is ingrained in us as physicians, right? But as I thought about it I realized that skepticism is lacking from day to day practice. As a hospitalist (and I'm sure this is true for other physicians) I have observed many things that conspire against diagnostic skepticism. These include the pressures of time, the performance movement and other competing interests as well as even the electronic medical record.


Some of the performance measures, particularly those that are time dependent, may cause the clinician to rush to a diagnosis. How many patients in the ER, for example, have been inappropriately diagnosed as pneumonia because the physician was in a rush to satisfy the time-to-antibiotic performance metric? How many patients with chest pain and ST elevation have been inappropriately rushed to the cath lab with pericarditis or even benign early repolarization because of the pressure of door-to-balloon time? Diagnostic skepticism does take time. Time to think.


Time pressures may also be driven by a variety of other administrative agendas. With all the emphasis today on rapid ER throughput, for example, patients need a quick diagnostic label as their ticket to get them admitted in a timely manner. These labels are administratively important but may lead to incorrect diagnoses. Other competing interests are about money, such as “clinical documentation” and DRG coding.


The EMR itself may enable inappropriate diagnosis and undermine diagnostic skepticism in a number of ways. Electronically generated problem lists and note templates are tied to the decades-obsolete ICD-9 codes. You can always free text the patient's real diagnosis but it's more often the electronically generated garbage that will be forwarded from note to note over time thus perpetuating inappropriate diagnosis. So in order to employ diagnostic skepticism you have to sit down and think. Not only that but you may have to undo some of the electronic garbage generated by the EMR. It all takes time. Time that hospitalists all too often don't have.


It's all made worse by the conflicting incentives. As a hospitalist, for example, what are some of the metrics you are held to? ER throughput, discharge time, patient satisfaction, coding and length of stay to name a few. These all take time away from diagnostic skepticism. Hospitalists are not incentivized for their diagnostic skills.


Our hospitalist leaders (except of course for Dr. Centor) are not helping matters. Take a look at the Society of Hospital Medicine website. There are some great resources there but almost all of them are about system and administrative issues in hospital medicine. There is no focus on diagnostic skills.


So the notion of diagnostic skepticism is very simple. All you have to do is stop and think. Take a moment to consider whether the diagnostic label perpetuated by the EMR is really true. Who knows, you may experience a Dr. House moment. You may even save a life.

Obamacare's CLASS program on hold

What does it mean for the rest of the law?

Does the Joint Commission improve the quality of hospitals?

Well, a study just published in the Journal of Hospital Medicine implies that maybe it does. Investigators looked at publicly reported performance data for accredited and non-accredited hospitals. Here are the findings:

RESULTS:

Hospitals accredited by The Joint Commission tended to have better baseline performance in 2004 than non-accredited hospitals. Accredited hospitals had larger gains over time, and were significantly more likely to have high performance in 2008 on 13 out of 16 standardized clinical performance measures and all summary scores.

CONCLUSIONS:

While Joint Commission-accredited hospitals already outperformed non-accredited hospitals on publicly reported quality measures in the early days of public reporting, these differences became significantly more pronounced over 5 years of observation. Future research should examine whether accreditation actually promotes improved performance or is a marker for other hospital characteristics associated with such performance.

So does this mean that the Joint Commission improves the quality in our hospitals? No. Does it even mean that Joint Commission accreditation is associated with better quality? No. We need to examine some questions.


First, what about these non-accredited hospitals? Well I was surprised to learn from the paper that as many as 18% of hospitals are not accredited. The study compared those hospitals that were never accredited for the entire study period with those that were accredited the whole time. Although the authors were not explicit about it, the strong sense I got from reading the paper is that these were all hospitals which chose not to seek accreditation rather than those which tried and flunked year after year. It seems to me that accreditation by the Joint is a lot like a hospital's report on performance measures. They share almost identical incentives. Both amount to public report cards. So if your hospital administrators are not interested in one they're not likely to be as interested in the other, compared to hospitals that seek accreditation. In my view the study demonstrated nothing more than that.


But the fundamental flaw in this paper, to me, is that the authors seem to confuse performance with quality. I've blogged extensively before on this fallacy. The authors are smart folks (Bob Wachter among them). Surely they are aware of the difference. I only wish that in their discussion they had made a clear distinction.


HT to Hospital Medicine Quick Hits.

When's the last time government made taking care of patients easier? More effective? More efficient?

Via Health Care BS.

A rapid test for tetanus immunity status

The Tetanus Quick Stick.

ACE inhibitor induced small bowel angioedema presenting as an acute abdomen---CT characteristics

From the American Journal of Roentgenology:

ACEI-induced small-bowel angioedema should be included in the differential diagnosis when patients receiving ACEI therapy present with abdominal complaints and the following combination of findings on CT examination: ascites, small-bowel wall thickening, dilatation without obstruction, and straightening.

Symptoms resolve within a few days of stopping the ACEI.


Via Hospital Medicine Quick Hits.

B natriuretic peptides in patients with chest pain

---are useful for risk stratification, and complementary to troponin assays, according to this paper.

The flaws of modern medicine

Anything coauthored by George Lundberg and Clifton Meador has to be interesting which is why I link it here.

Another chapter in the colloid-crystalloid debate: albumin as initial resuscitation fluid for sepsis?

Albumin had a slight edge, barely statistically significant, in this meta-analysis.

Approach to the patient with severely elevated blood pressure

So you're called by the ER doc, saying “I've got this previously healthy patient” (maybe he was seen for a minor injury) “and he had a blood pressure of 190/120, asymptomatic. I've given him a couple of doses of clonidine. He's been here for over four hours and I can't get it below 180/100, so I think he needs to come in to be observed and treated overnight.” We've all been there. That seems to be the knee jerk approach. But is it the best approach? How can the best evidence guide us?


It's all nicely outlined in a review published in American Family Physician, linked from a post at The Kidney Doctor. The review is concise, practical and evidence based, and one of those few full text articles from AFP freely available on line (BTW, AFP now has the most restrictive access policy of any journal I know. You normally can't even get the abstract unless you are a subscriber).


According to the review the first thing you need to do is to classify the patient's elevated blood pressure. That can be confusing. Although JNC 7 (JNC 8 is supposed to come out next year) gives the traditional hypertension classification of prehypertension and stages 1 and 2 hypertension it does not define the terms for patients who present with severely elevated blood pressure. To make matters worse the terms out there right now are widely misused. Terms like “hypertensive crisis” are applied to so many different clinical circumstances they have become meaningless. “Malignant hypertension” used to mean something specific but has suffered the same fate in recent years. Even worse is the clinically inappropriate terminology in the ICD 9 codes we're forced to use (those are, what, 40 years out of date now?).


The terms are defined and the classification is succinctly presented in the review. Severely elevated blood pressure of any classification is defined as being greater than 180/100. If it is entirely uncomplicated without historical risk factors (heart disease, renal disease) or acute organ damage it's called severe asymptomatic hypertension or severe uncontrolled hypertension. If it is associated with historic cardiovascular risk factors or renal disease it is called hypertensive urgency. Finally, the term hypertensive emergency is reserved for individuals with evidence of acute organ damage. (Now when the latter are present they may trump the absolute level of blood pressure in defining a hypertensive emergency, e.g. aortic dissection, acute decompensated heart failure).


So that's step 1. Classify the patient using current terminology. How often is that done?


The article goes a little into pathophysiology. For our purposes I'll just mention the most important core concept: autoregulation. A graphic of the autoregulation curve is provided in the article. It's a familiar concept to most of you. If not, get it emblazoned in your hippocampus. Raise BP above the autoregulatory zone and you've got hypertensive encephalopathy. Go below, and perfusion of vital organs is proportional to blood pressure and may drop below critical levels. Acute “normalization” of blood pressure in the ER may take the patient into that zone.


As far as treatment is concerned go to the article, but here is the Cliff Notes version. In general the recommendations for starting patients on meds or admitting them to the hospital are a lot more conservative than what is commonly done. If it is really a HT emergency they go to the ICU. In HT emergency the BP target, the specific agent and route are specific to the underlying condition and are beyond the scope of this post as they are for the article.


For HT urgency or severe asymptomatic HT there appears to be no specific evidence that you should treat them in the ER or send them out with a prescription. Of course then the approach may be dictated by the patient's social situation. If non compliance, poor social connections or lack of a PCP complicate the situation it may be wise to have the patient spend the night in the hospital. But if the patient is better situated, according to the best evidence s/he could be sent home without meds with plans for very early PCP follow up (24-48 hrs if HT urgency, a week if severe asymptomatic HT) at which time the PCP would further evaluate the patient and initiate oral medication.

Fake doctor notes in Wisconsin: civil disobedience or something else?

The other day physician and journalist Ford Vox wrote a piece on the ethics and consequences of the fake medical excuses written by doctors in the Department of Family Medicine at the University of Wisconsin. In saying that the docs failed to understand the impact of their action on public perception of the profession, he was right. In crediting them with an act of civil disobedience he missed the boat:

Members of the University of Wisconsin's Department of Family Medicine, including both residents and attendings, felt compassion for the educators' cause, and wanted to participate in the display, but rather than symbolically protest in the streets alongside the teachers, they decided to perform an act of civil disobedience: The doctors wrote out fake sick notes for the teachers, many of whom were falsely using illness as an excuse to attend the protests..

Wrong. Civil disobedience is open. Say you wanted to protest U.S. military spending. An act of civil disobedience might be to openly refuse to pay income tax. It would not be an act of civil disobedience to cheat on your income tax even if you rationalized that the morality of your use of the money would exceed that of Uncle Sam. If that's too rude an analogy it illustrates the point. The doctors in Wisconsin may have thought they were demonstrating for social change but they were being, to use not so rude a term, disingenuous.


Also consider that those who commit true civil disobedience are open in facing the consequences of their actions. The Wisconsin doctors were not. When approached by reporters and videographers the docs offered lame (and unintentionally hilarious) defenses or told the reporters to get lost. One wonders if any of them, especially the residents involved, counted the cost in advance.


This little stunt may have been the use of the profession as a vehicle for social change but it wasn't true civil disobedience.

Fake notes by real docs in Wisconsin---anything new?

It's been over six months since faculty members of the University of Wisconsin department of Family Medicine made a stir when they decided social activism should trump evidence based medicine in the treatment of individual patients, and made a public display of it. Things have been quiet in the blogs after an initial splash, so I decided to search for updates and found a couple of recent news items.


The status of things, it would appear, is up in the air as investigations are ongoing at two levels---the state medical board and the University. Details will eventually be made public.

Resistant hypertension

There's a nice post over at The Kidney Doctor on this topic along with several references. The AHA scientific statement on resistant HT can be accessed here.

Wernicke's encephalopathy

A post about Wernicke's at Renal Fellow Network prompted this literature search.


This article covers CT and MRI findings:

CT and above all MRI of the brain play a fundamental role in diagnosing the condition and ruling out other diseases. MRI is the most sensitive technique and is required in all patients with a clinical suspicion of Wernicke’s encephalopathy. Medial thalami, mamillary bodies, tegmentum, periaqueductal region, and tectal plate are typical sites of abnormal MRI signal. The dorsal medulla, red nuclei, cranial nerve nuclei, cerebellum, corpus callosum, frontal and parietal cerebral cortex are less common sites of involvement although they are more frequently affected in nonalcoholic patients. Paramagnetic contrast material may help to identify lesions not otherwise visible.

This review of WE focuses on imaging findings but also comments on clinical criteria and pathophysiology:

In view of the poor diagnostic performance of the classical triad, new classification criteria have been proposed. These criteria require two of four items including dietary deficiencies, oculomotor abnormalities, cerebellar dysfunction, and an altered mental state or mild memory impairment [13]...

Alcoholism does not directly cause thiamine deficiency, although it may induce such deficiency because of its frequent association with malnourishment. More specifically, the low thiamine absorption rate at the mucosal level, the impaired hepatic function, and the alcohol-related raised thiamine metabolism together may lead to the development of chronic thiamine deficiency [14]. Thiamine-deficient membranes are unable to maintain osmotic gradients, which results in the swelling of intra- and extracellular spaces.

From the discussions in this and other reviews it is apparent that the mechanisms by which thiamine deficiency produce the brain lesions of WE are multifactorial and poorly understood.


This fascinating review explores the controversial and sometimes confusing overlaps between WE, Korsakoff Syndrome (KS) and non-thiamine related alcohol dementia.


This review highlights the increasing recognition of WE as a complication of bariatric surgery.


This article reviews several aspects of the clinical findings, natural history and pathology of WE and KS. It emphasizes the under-diagnosis of WE. This under-diagnosis is due to the fact that only 10-15% of patients present with the classic triad (eye findings, ataxia and mental status changes).


This case series illustrates that WE may be associated with a characteristic acid-base disturbance, combined respiratory alkalosis and wide anion gap metabolic acidosis such as is seen in salicylate intoxication.


Here is a review of the emergency prevention and management of WE in acutely ill patients emphasizing common pitfalls. The discussion of early recognition deals with non-WE presentations of thiamine deficiency such as cardiovascular collapse, heart failure, lactic acidosis and acute abdominal symptoms. Also listed are non-alcohol related conditions now known to be associated with WE: hyperemesis gravidarum, TPN without adequate thiamine supplementation and post-bariatric surgery states. The pathophysiology and biochemistry of WE are described as complex, and the brain lactate accumulation mentioned in the post at Renal Fellow Network is probably but one of several mechanisms of injury.


A 2007 review from Lancet Neurology cites an even wider variety of non-alcohol scenarios that can be associated with WE including fad diets and nutritional imbalances of various sorts, magnesium deficiency (it may induce refractoriness to administered thiamine) and various situations in cancer patients. The review makes the point which, though obvious, bears mention, that WE cannot reliably distinguished from drunkenness. The optimal route for thiamine administration is IV. Although deemed controversial in some of the other reviews this one makes more specific statements about dosing. 100 mg IV daily is common practice, and while this may be appropriate for prophylaxis in at risk patients, the review recommends 500 mg IV tid for patients with strongly suspected or established WE to prevent KS, other brain damage or death. (A banana bag may not be enough!).


The profile of WE has changed. During my training, as now, the diagnosis of WE was primarily clinical. Confirmatory diagnostic testing, however has changed. Then it was done by blood testing (thiamine levels or red cell transketolase assays) whereas now MRI is the diagnostic modality of choice. Neither is useful in the acute situation, as thiamine repletion must begin in the emergency setting before confirmatory test results are available. The epidemiology has changed. Because parenteral thiamine administration in the ER has become almost knee-jerk in alcoholic patients, we may be seeing less alcohol-related WE in comparison to other circumstances such as hyperemesis gravidarum, post-bariatric surgery states and other instances of disturbed nutrition.

Long term azithromycin to prevent COPD exacerbations?

In this NEJM study the effect was modest (9 months to first exacerbation as opposed to 6 months) and at the price of hearing impairment developing in a few patients at 1 year. The impact on antimicrobial resistance, though a concern, is unknown.


Via Hospital Medicine Quick Hits.

FDA warning on Zofran and QT prolongation

This is surprising. It is unusual nowadays to see QT problems surface long after a drug has been on the market, since drugs are routinely tested in vitro for K+ channel blocking effects early in development.


The Arizona CERT, which is the definitive repository of information on QT prolonging and torsades inducing drugs, puts Zofran in an intermediate risk category:

Drugs with a Possible Risk of Torsades de Pointes

Drugs that prolong the QT interval and/or in some reports have been associated with torsades de pointes but at this time lack substantial evidence for causing torsades de pointes.

Zofran use is ubiquitous on the wards. I'm aware of no reports of it causing torsades. On the other hand, how many patients with unexplained arrests on the wards are getting Zofran?


The FDA is making some significant labeling revisions:

The labels are being revised to include a warning to avoid use in patients with congenital long QT syndrome because these patients are at particular risk for Torsade. Recommendations for ECG monitoring in patients with electrolyte abnormalities (e.g., hypokalemia or hypomagnesemia), congestive heart failure, bradyarrhythmias, or in patients taking other medications that can lead to QT prolongation, are being included in the labels.

That represents a lot of patients being monitored!


HT to Hospital Medicine Quick Hits.

Global ST elevation: pericarditis or massive STEMI?

Global ST segment elevation (seemingly not confined to a vascular territory) is a differential clue favoring pericarditis over STEMI. The rule, however, is not absolute, because very proximal occlusion of a wrap around LAD variant would threaten the anterior, inferior and lateral walls, leading to widespread ST segment elevation.


Accompanying a tracing showing pericarditis at Dr. Smith's ECG blog is a discussion of other electrocardiographic features in the differential. PR segment depression is a well known clue to pericarditis. Less well known is a QTc of at least 372 ms in nearly all cases of anterior STEMI and reciprocal ST segment depression in nearly all cases of inferior STEMI, features not characteristically present in pericarditis.

More evidence of cardiovascular harm from NSAIDs

---in this study.

Are cardiologists doing too many PCIs?

For the most part, no according to this study, which looked at both acute and non acute indications.

The Million Hearts initiative

This, a promotional piece about a new government initiative, and one of dubious value at that, does not belong in a scientific journal IMHO.


The Million Hearts initiative takes some low hanging fruit concerning cardiovascular hygiene (good diet, smoking avoidance, BP control), turns it into a set of performance measures and throws government money at it. There's not a shred of evidence that this sort of sound-good, feel-good approach will work. Moreover, our experience with these sorts of performance measures over the past decade suggests that in all likelihood it will not work.


Dr. Wes weighs in:

Now I do not hold a Masters in public health or public policy, but I do know a thing or two about evidenced-based medicine and cardiology. So it seems only appropriate that a cardiologist should comment on the proclamations made by an infectious disease specialist and pediatrician who promise to "save a million hearts," especially when we consider the billions of taxpayer dollars that have been or will be allocated to their programs.

Even more from Dr. John M.

Theocracy hysteria

This post is worth the read if only for the concluding sentence:

Theocracy is forever descending on the United States, but somehow it always lands in the Middle East.

A Cochrane review on P4P

Here were the findings:

Six of the seven studies showed positive but modest effects on quality of care for some primary outcome measures, but not all. One study found no effect on quality of care. Poor study design led to substantial risk of bias in most studies. In particular, none of the studies addressed issues of selection bias as a result of the ability of primary care physicians to select into or out of the incentive scheme or health plan.

At best, then, these results are “modest” and mixed. When looked at alongside significant design flaws, particularly the failure to take into account selection bias, there is no convincing evidence, conclude the review authors, that P4P consistently improves quality of care.


The studies cited in the review looked mainly at performance. What's missing from the discussion in the review is any attempt to distinguish between performance and real quality. If we have learned anything at all from our experience with core measures and public report cards it's that performance does not equal quality. If the evidence that P4P improves performance is scant it's somewhere between slim and none for quality.


More from Medscape and DB's Med Rants.

Massive patient privacy breach at Stanford

---attributable to an electronic billing service.

More from Health Care Renewal.

CT negative for SAH. Is LP the next step?

That's been the traditional teaching. But that teaching is based on low level data, much of it from the era of early generation CT scanners. This new study in BMJ sought to determine the sensitivity of present day CT scanners as a function of time. The findings:

Of the 3132 patients enrolled (mean age 45.1, 2571 (82.1%) with worst headache ever), 240 had subarachnoid haemorrhage (7.7%). The sensitivity of computed tomography overall for subarachnoid haemorrhage was 92.9% (95% confidence interval 89.0% to 95.5%), the specificity was 100% (99.9% to 100%), the negative predictive value was 99.4% (99.1% to 99.6%), and the positive predictive value was 100% (98.3% to 100%). For the 953 patients scanned within six hours of headache onset, all 121 patients with subarachnoid haemorrhage were identified by computed tomography, yielding a sensitivity of 100% (97.0% to 100.0%), specificity of 100% (99.5% to 100%), negative predictive value of 100% (99.5% to 100%), and positive predictive value of 100% (96.9% to 100%).

The results of this study suggest that if CT using a late generation scanner is done within 6 hours, LP is not necessary to rule out SAH.

Via Hospital Medicine Quick Hits.

Decline in catheter associated UTIs noted long before Medicare's blame game

---according to this study. The study period was 1990 through 2007. Medicare's blame game, the no pay for adverse events program, was announced in 2007 but didn't start until 2008.

Via Hospital Medicine Quick Hits.

How should hospitalists collaborate with consultants and what's the risk?

The relationship between the attending physician and the consultant has never been perfectly clear. It varies with different people's expectations and certainly from hospital to hospital. The concept of comanagement has, in many settings, taken it from unclear to nebulous.

Dr. Brad Flansbaum, blogging at The Hospitalist Leader, pointed me to this article illustrative of how the collaboration can go wrong. The article is so poorly written, as Dr. Flansbaum points out, that it's difficult to know what really happened, but perhaps there are some lessons.

Important questions are raised. When is it appropriate to order a consult? To what extent should the rules for comanagememt be hammered out in advance and what are the key issues?

For my twelve year hospitalist career I've worked in only one program although I've seen different styles. Some hospitalists consult liberally, others sparingly. Either style can go to the extreme, to a fault. I've heard of hospitalists who consult for every deranged organ system, others who hunker down and feel they can handle anything. Some consults are for a legitimate clinical question. Others are for a procedure. Many are CYA---sometimes with good reason. After all, if there is a bad outcome, the specialty talent was available and you didn't utilize it, then what?

Chronic meds disappear from the list at discharge

---as documented in this recent paper. Important meds, like antiplatelet agents and statins. And it was even worse if the patient was in the ICU.

The study period was 1997 to 2009. Although systems initiatives (computer generated med lists, collaboration with the hospital pharmacy) to help improve discharge medication instructions were well in place by 1997 med rec as we now know it was not introduced until 2005. These processes all required someone to pick and choose from an array of medications followed by computer generation of a list for the patient. Good intentions, the systematization of the process, added steps to the old method of ordering “patient to continue meds per previous home routine with the following changes:...” Those added steps complicated the loop and created opportunities for error.

Via Hospital Medicine Quick Hits.

Righthaven meltdown?

As the blogosphere breathes just a little easier. For now.

Doctors need help to make decisions---but what kind of help?

Brad Flansbaum addressed this topic recently, blogging at The Hospitalist Leader. The post, interestingly, had little to do with the blog's overall focus on leading hospitalist groups. One implication of the post seemed to be a pitch for a greater role of policy and expert panels weighing in on patient care decisions. Was he talking about government leaders, guideline authors or something else? He didn't say. If I knew of any particular political leanings on Dr. Flansbaum's part perhaps I could make a guess, but I don't.

Somehow the post rubs me the wrong way. It's difficult to criticize because though it asks provocative questions, talks around many things and implies many things it doesn't make a declarative statement about much of anything.

But at the risk of erecting the straw man (with apologies in advance if I do) I'll try to parse it out. First, the background for the post is a new study in the Journal of General Internal Medicine (JGIM) which compared the way a sample of doctors and a sample of patients looked at numbers from a hypothetical clinical trial:

Respondents were asked to interpret the results of a hypothetical clinical trial comparing an old and a new drug. They were randomly assigned to the following framing formats: absolute survival (new drug: 96% versus old drug: 94%), absolute mortality (4% versus 6%), relative mortality reduction (reduction by a third) or all three (fully informed condition). The new drug was reported to cause more side-effects...

RESULTS

The proportions of doctors who rated the new drug as more effective varied by risk presentation format (abolute survival 51.8%, absolute mortality 68.3%, relative mortality reduction 93.8%, and fully informed condition 69.8%, p less than 0.001). In patients these proportions were similar (abolute survival 51.7%, absolute mortality 66.8%, relative mortality reduction 89.3%, and fully informed condition 71.2%, p less than 0.001). In both doctors (p = 0.72) and patients (p = 0.23) the fully informed condition was similar to the absolute risk format, but it differed significantly from the other conditions (all p less than 0.01). None of the differences between doctors and patients were significant (all p greater than 0.1).

There's a lot we could unpack here but what are the essential findings of the study? First, we all, doctors and patients alike, are subject to framing bias. No surprise there. Then there was the fact that docs and patients responded similarly when presented only the relative risk reduction. No surprise there, either. In fact it says very little because the information presented to the respondents provided no test of critical analytic skill. With only the relative risk reduction presented the respondent has no way to assess the effect of framing. The astute response to such a scenario would be “it depends” (on the baseline risk, raw numbers, etc) but I'm sure the survey questions didn't offer that option. What might raise some eyebrows is that when absolute risk reduction and comprehensive information were presented patients and doctors still responded similarly.

The authors of the paper were appropriately guarded in their conclusion:

CONCLUSIONS

Framing bias affects doctors and patients similarly. Describing clinical trial results as absolute risks is the least biased format, for both doctors and patients. Presenting several risk formats (on both absolute and relative scales) should be encouraged.

This paper addressed framing bias. It did not address whether doctors are better in the real world at critically appraising the medical literature than patients. It did not purport to do so. The hypothetical scenarios presented were too simple to be a meaningful test of critical appraisal. To conclude that doctors are no better at interpreting medical literature than the lay public is not only ridiculous on its face (a little Bayesian thinking might be in order here) but goes far beyond anything demonstrated by the study. Yet Dr. Flansbaum dances around that very idea.

So, again trying hard to avoid the straw man, here are my reactions to a couple of the other questions raised in Dr. Flansbaum's post:

Are auto mechanics more worthy of their fiduciary duty than doctors?

The opening sentences of Dr. Flansbaum's post read:

I assume, incorrectly perhaps, that mechanics have a basic knowledge of their craft such that routine auto repairs require little effort. The tasks do not supersede the expected competency of the repairperson, and the customer can expect a car that operates at the time of pick up. A small percentage of jobs may stretch that assumption, but that is okay by me.

But the snark in the next two paragraphs hint that he doesn't feel quite the same about doctors.

Do doctors need policy setting expert panels in order to practice EBM?

From Dr. Flansbaum's post:

I also observe that politicians object to “meddling” when EBM-based policies from expert committees passively (or actively) affect the doctor-patient relationship, especially as it relates to decision-making and the counsel we provide. Just watch the nightly news—sound bites abound. This relationship is sacrosanct after all, and our advice is authoritative and 98.7% correct. Who would question a physician after all?

Well, first, I know of no pundits or politicians who assert that we should never question doctors, or that doctors are authoritative or 97% correct. Now if Dr. Flansbaum is pitching for more policy-based control of physicians' practices it's strange that he would invoke EBM. EBM, much like “patient safety” and “antibiotic stewardship,” is one of those catchy terms all too easily used to bolster a specious argument.

The true notion of EBM does not apply here at all. In fact, according to David Sackett's original definition, EBM can only be applied with individual clinical expertise at the level of the individual patient. So there can be no such thing as “EBM based policies from expert committees.” I've heard many arguments in favor of more central control of doctors' practices. Though I disagree with that position I respect many of the arguments. Just don't invoke EBM. However much there may be to like about central control of medical practice, it isn't EBM.

So back to the title of the post. What kind of help do we really need? As I've said before the focus needs to be on improving access to educational resources so doctors can more quickly and easily apply the best external evidence to individual patient care.

Oh, BTW---were the editors of JGIM in too big a hurry to get this paper out or were the spell checkers at the Journal on the blink that day?

Obamacare's popularity continues its decline

Health Care BS posts this and writes:

The Obama administration has made real history with ObamaCare. They have created the only nanny-state entitlement in history that gets less popular as time goes on.

Accountable care organizations: managed care on steroids

Accountable care organizations (ACOs) are being touted by policy elitists as the way to integrate health care services, improve quality and reduce costs. To many in the trenches of health care who have experienced the law of unintended consequences this view is naïve. We know that more intrusion from government means more conflicts and more pressure to game the system. According to this Pajamas Media piece by Paul Hsieh ACOs will merely bring new and more perverse cost incentives leading to cherry picking of patients along with new and creative ways to abuse the system:

Less scrupulous providers will thus be tempted to manipulate the assignment rules to avoid these burdensome “ACO lepers.” Consulting firms are already advising prospective ACOs on the pros and cons of various patient assignment systems. Because the financial stakes are so high, some will inevitably seek to exploit these rules to their advantage, even if it’s at their patients’ expense...

Under ObamaCare, the winners will be those lobbyists, consultants, and less-scrupulous hospitals and doctors willing to “game” the system to their advantage. The losers will be those doctors unwilling to play those games — and their patients.

Woo promoting article in The Atlantic

This is an article about the growth of quackademic medicine in our teaching institutions and it's celebratory more than critical. It profiles the integrative medicine clinic of Dr. Brian Berman. That's right, this Dr. Berman. I blogged about him four years ago and it seems his clinic at the University of Maryland is still going strong. Stronger, apparently.

The article, like integrative medicine itself, is a mixture of quackery and general distortion with a little science and pseudo skepticism thrown in. A central premise is that no matter how nutty the idea, you can't call it quackery if it carries the imprimatur of a respected academic institution:

Concerns of outright malpractice or naked hucksterism seem grossly misplaced when applied to a clinic like Berman’s.

Below are a few more of the distortions contained in the article:

The false dichotomy between the conventional medicine approach and “healing.”

The claim that conventional medicine ignores prevention.

The notion that the principles of conventional medical science are obsolete because they originated in the era when acute infectious diseases were the leading killers.

The idea that medical science has failed to make significant advances in the care of chronic diseases. (Tom Sullivan debunks that popular canard here).

By and large the purported benefits of integrative medicine, as illustrated by the numerous testimonials in the article, are the result of the placebo effect and the generous time and personal attention lavished on the patients who attend. So, some might ask, what's the problem? Aren't those reasons enough to justify integrative medicine?

Not when those benefits are attributed to a quacky intervention. It's just unethical. As Steve Novella, interviewed for the piece, said:

Novella is a highly respected Yale neurologist, and the editor of Science-Based Medicine, an influential blog that has tirelessly gone after alternative medicine. I met with him in his home outside New Haven, Connecticut, where he argued that claims about the practitioner-patient relationship are only intended to draw attention away from the fact that randomized trials have by and large failed to show that alternative treatments work better than placebos. And while he concedes that sham treatments can give patients a more positive attitude, which can confer real health benefits, he is adamant that providing sham treatments at all—essentially fooling patients into believing they’re being helped—is highly unethical. “Alternative practitioners have a big advantage,” says Novella. “They can lie to patients. I can’t.”

Aside from the ethical considerations cited by Novella the argument raises another false dichotomy: that spending lots of time with patients and approaching them as whole persons is somehow uniquely inherent to integrative medicine and foreign to conventional medicine. For many counter-examples to that argument just read DB's many posts on the true nature of mainstream internal medicine or my post here where I cite the example of the late Thomas Brittingham as the exemplar.

No, it's not the pure notion of the whole person or spending time with patients that's unique to integrative medicine. So what is integrative medicine's uniqueness? I would submit that, in part, it's the fact that it makes quacky claims that are so appealing and sensational to the uncritical public that patients are willing to pay handsomely for it out of pocket. That eliminates some of the time pressure that exists under the reimbursement system for conventional medicine.

The article additionally points out the alarming degree to which quackademics are infiltrating the renowned Mayo Clinic, to a greater degree than even I was aware. Even the dean of the medical school is on board.

Some of the Mayo doctors quoted in the article are in favor of integrative medicine but their arguments are mainly sophistry. Though superficially appealing the defects and half-truths in their statements become apparent once a little critical thought is applied.

What's up with all the drug shortages?

As hospitalists we brace ourselves for the shortage of the month. It's usually an older drug, often a generic, and one you'd least expect.

A pharmacist blogging over at Science Based Medicine offers an interesting analysis. The supply chain is complex and, it seems, the problem is multifactorial, but with a common theme: under increasing regulatory and economic pressure industry players are consolidating and restructuring. So now we need a new field. If pharmacokinetics and pharmacodynamics address what happens once a drug is inside the patient, what about getting the drug to the patient? Pharmacologistics?

More on the differential diagnosis of wide complex tachycardia

A commenter on my last post on this topic pointed me to a search that uncovered two interesting and helpful papers I was not aware of.

This review traces the history of methods distinguishing between VT and aberrancy on the surface electrocardiogram. The tried and true method, which assesses for AV dissociation (including that evidenced by fusion and non aberrant capture) or VA conduction with block, is accurate and conceptually sound. However, it is difficult to use with faster ventricular rates, at which atrial impulses are often not well seen. The use of morphologic analysis has gradually improved. Unreliability of early criteria drove the emphasis on analysis of AV relationships. Simple criteria based on QRS width or axis have fallen out of favor. Various early criteria were based on the resemblance of the QRS complex to either bundle branch block. These were popular because they were intuitive, but suffered from low sensitivity and specificity. Several improved methods were developed leading up to the popular Brugada criteria which established morphologic analysis as a more reliable method. More recently criteria involving only lead aVR have been validated.

The aVR method, as explained in this paper, is comparable in accuracy to the Brugada method and appealing in its simplicity.

Gout management in patients with CKD

An update from CCJM.

Effect of a MRSA bundle for hospitalized patients

From a NEJM report:

The bundle consisted of universal nasal surveillance for MRSA, contact precautions for patients colonized or infected with MRSA, hand hygiene, and a change in the institutional culture whereby infection control would become the responsibility of everyone who had contact with patients. Each month, personnel at each facility entered into a central database aggregate data on adherence to surveillance practice, the prevalence of MRSA colonization or infection, and health care–associated transmissions of and infections with MRSA...

During this period, the percentage of patients who were screened at admission increased from 82% to 96%, and the percentage who were screened at transfer or discharge increased from 72% to 93%. The mean (±SD) prevalence of MRSA colonization or infection at the time of hospital admission was 13.6±3.7%. The rates of health care–associated MRSA infections in ICUs had not changed in the 2 years before October 2007 (P=0.50 for trend) but declined with implementation of the bundle, from 1.64 infections per 1000 patient-days in October 2007 to 0.62 per 1000 patient-days in June 2010, a decrease of 62% (P less than 0.001 for trend). During this same period, the rates of health care–associated MRSA infections in non-ICUs fell from 0.47 per 1000 patient-days to 0.26 per 1000 patient-days, a decrease of 45% (P less than 0.001 for trend).

Platelet disorders in pregnancy

Free full text review.

Warfarin nephropathy: a newly described entity

Think of it in any patient on warfarin (INR can be high, low or therapeutic) with AKI (usually AKI on CKD).  A  post at Nephron Power has the key points and primary sources.

Management of uremic bleeding disorder

A free full text evidence based review was published in Nature Clinical Practice Nephrology.

Commentary here from Renal Fellow Network.

Hospitalized patients die with hyponatremia more than from it

---according to this study.

Death was far more often due to associated conditions than to neurologic damage attributable to the hyponatremia. There was also a U shaped curve, with mortality increasing as sodium levels decreased, but the trend reversed at sodium levels below 120. This apparently means that underlying medical conditions are generally associated with levels of 120-134. Levels lower than that are more likely to be caused by external factors (medications, etc) rather than severe underlying medical illnesses.

Via Uremic Frost.