Wednesday, December 31, 2008

Top 10 issues in hospital medicine for 2008, issue 1: state of the hospitalist movement

Here’s my very biased take on where things stand at the close of 2008:

The never ending debate over the value of the hospitalist model is moot. Research on hospitaists’ impact on outcomes and efficiency has been inconclusive and is likely to remain so, given that large comparison groups against which to study the model are shrinking fast and will soon be nonexistent.

The security of our niche is based not on any measurable value, but on the mass exodus of traditional practitioners from the hospital. The resulting expansion in hospitalist jobs has outpaced growth in the work force. The trend shows no sign of abating. The current economic crisis will only serve to accelerate this exodus. The inflation of salaries may moderate, but hospitalists’ jobs should remain secure.

Larger threats to the hospitalist movement are turnover and burnout. Although we lack hard data on the magnitude of the problem it is widely apparent. This creates challenges for leaders in hospital medicine who are poised to define the ultimate direction of the movement. Hospitalists are increasingly being asked to go beyond the limits of their training by caring for all hospitalized patients regardless of illness. Moreover, their role as expert clinicians is increasingly threatened by pressure to become business and administrative solutions.

This emerging jack-of-all-trades model for hospitalists is a departure from the original notion of doctors devoting all their professional time caring for inpatients in the realm of their specialty (usually internal medicine) who, because they ascended a steep learning curve, developed unique expertise in hospital medicine. The old model attracted me to the field almost a decade ago because of its promise of professional satisfaction. The new model will be palatable for many of the short timers and moonlighters who increasingly make up the work force of hospital medicine but may not attract the career hospitalists needed to sustain and grow hospital medicine as a specialty.

Top 10 issues in hospital medicine for 2008, issue 2: patient safety and the culture of blame

Just as the quality movement has led to a culture of shame, the safety movement has exacerbated a culture of blame. That’s pretty ironic given that the seminal document of the patient safety movement, IOM’s To Err is Human, viewed the culture of blame as counterproductive and sought to mitigate it. This statement is from the executive summary of the book:

The focus must shift from blaming individuals for past errors to a focus on preventing future errors by designing safety into the system. This does not mean that individuals can be careless. People must still be vigilant and held responsible for their actions. But when an error occurs, blaming an individual does little to make the system safer and prevent someone else from committing the same error.

Why did this unfortunate and unintended consequence come about? It’s an example of what happens when a nuanced and highly complex issue gets thrown into the arena of unenlightened and uninformed public debate. Policy wonks distort it. Media spin it egregiously. Trial lawyers take notice.

We’ve seen the consequences this year. CMS’s ill-conceived and manifestly unfair never events policy went into effect, redefining many unavoidable events in hospitals as errors. With such redefinition comes a strong implication of widespread institutional and individual blame. The idea of patient harm as a “never event” has also spawned a new legal principle in which any patient harm is prima facie evidence of negligence, leading to more law suits and a shift in the burden of proof. Ready for the next malpractice crisis?

Tuesday, December 30, 2008

Top 10 issues in hospital medicine for 2008, issue 3: confusing performance with quality

Dr. Robert Centor, an academic hospitalist, is Division Director of General Internal Medicine at the University Of Alabama School Of Medicine in Birmingham and Associate Dean for the Huntsville Regional Medical Campus. He is also a member of the ACP Board of Regents and past president of the Society of General Internal Medicine. He is perhaps better known to many of us as the blogger at DB’s Medical Rants. There he recently wrote a post titled Quality improvement is a misnomer in which he said:

"Quality improvement" implies that patients will have better outcomes. Yet, few studies exist that show that improving performance measures really improves outcomes.

This model makes the unsubstantiated assumption that improving performance measures equates with improved outcomes, and thus we can label our efforts as quality improvement.

The quality movement has largely failed due to widespread confusion between quality and performance. Why are performance and quality (real quality, things that matter in patient outcomes) fundamentally different? It’s all in the motivation. Real quality is driven by a desire to make a difference for patients, regardless of money or public perception. Performance, on the other hand, focuses entirely on public perception. As Dr. Robert Wachter said in his blog just the other day, performance is driven by shame and embarrassment. He also wrote:

…hospitals are doing organizational cartwheels trying to improve their performance on the publicly reported indicators.

Those words speak volumes. Think for a moment about hospitals doing cartwheels trying to improve their performance. It’s all about putting on a show. A natural consequence of hospitals’ excessive concern for perception is a nearly exclusive focus on publicly reported indicators. Therein lies the failure of today’s “quality” movement.

There’s nothing inherently wrong with publicly reported measures. The problem arises when hospitals focus on them to the exclusion of other measures which, though below the public radar screen, matter more. The result is that hospitals tend to ignore measures with the greatest potential to impact meaningful outcomes such as early goal directed therapy against sepsis and applied hypothermia after cardiac arrest, which have a NNT of about 6 for survival and good neurologic outcome, respectively. Many of the high public profile measures nowadays are either non-evidence based (rapid response teams), have a very poor bang for the buck (pneumococcal vaccine, NNT 50,000), have serious unintended consequences (the 4 hour antibiotic rule) or have failed to improve outcomes in the way they were promulgated (heart failure core measures).

If we want better health related outcomes we must focus on real quality, not performance. But with today’s explosion in web based reporting and hospitals scrambling to improve their image, don’t expect it to happen any time soon.

Top 10 issues in hospital medicine for 2008, issue 4: emergency room handoffs

The handoff between the emergency room physician and the hospitalist is just one of several discontinuities in health care during which patients are vulnerable. Although it has been intuitively known for a good while it earned a place on this year’s top 10 list because of a new study documenting frequent occurrences of patient harm and near misses. This patient safety problem is one of competing agendas: poor communication and handoff errors are driven by administrative pressure on ERs to reduce their wait times and improve “throughput”.

Top 10 issues in hospital medicine for 2008, issue 5: what do we know about glycemic control in hospitalized patients?

Less than we thought we did this time last year, which wasn’t much. Since that time, non-evidence for strict glycemic control has been reported at such a dizzying pace I’ve barely been able to keep up with it. My posts from the past year are here, here, here, here and here.

At the close of 2008 what do we have to support glycemic control in hospitalized patients? Little more than observational studies, pathyphysiologic rationale and common sense. Based on such rationale, what we know reduces down to this:

Hyperglycemia is common in hospitalized patients, many of whom did not have a prior diagnosis of diabetes. It should not be ignored.

Sliding scale insulin should not be the sole means of glycemic control in hospitalized patients. Basal coverage should be included in the regimen.

Insulin drip protocols are appealing for ICU patients because of their rapidity of action, the flexibility they afford and the fact that subcutaneous insulin absorption is unreliable in hypoperfusion states.

Glycemic control does matter, but the best treatment targets are not known, and probably vary from one clinical state to another (sepsis, stroke, acute coronary syndrome, perioperative period).

Top 10 issues in hospital medicine for 2008, issue 6: weaning from ventilators is obsolete

---(with only a few exceptions). Despite this fact the term “weaning” remains popular in critical care. The new thinking is that most patients should not be weaned. Rather, on any given day they are either ready for extubation or they are not. The job of the clinician is to do a daily assessment for readiness.

While this fact has been known for over a decade it made my 2008 top10 list because of a pivotal study this year in which the assessment was validated as an integrated protocol combining the daily sedation interruption with the spontaneous breathing trial, resulting in a striking mortality benefit.

Monday, December 29, 2008

Top 10 issues in hospital medicine for 2008, issue 7: emerging problems in the treatment of MRSA

We live with the fear that suddenly, one day, we will wake up to find vancomycin resistant Staphylococcus aureus (VRSA) in our community. Although rare reports of the sudden appearance of high level vancomycin resistance due to the vanA gene known to cause vancomycin resistance in enterococci have surfaced, the reality is that the major threats are different: vancomycin is gradually wearing out its welcome, by multiple mechanisms, while new strategies evolve. Hospitalists must be aware of these mechanisms and evolving strategies.

The mechanisms:

There are inherent weaknesses in vancomycin compared to beta lactam antibiotics. This relates to less effective killing action and a narrower therapeutic window for vancomycin. This is not a new problem, and accounts for higher mortality in MRSA infections (in which vancomycin is usually administered) than in MSSA infections (in which beta lactam antibiotics are used). This issue is reviewed here.

Vancomycin treatment failures increase in proportion to increasing MICs even well within the “sensitive” range below 2 mcg/ml.

Transient heteroresistance to vancomycin, in which small subpopulations of organisms show vancomycin MICs in the intermediate range, is common and may lead to treatment failure in patients whose isolates test “sensitive”.

Vancomycin tolerance, defined as a wide discrepancy between the MIC and MBC, may lead to treatment failure in patients whose isolates test “sensitive”.

Traditional vancomycin dosing regimens have resulted in low trough levels. This can lead to treatment failure, since vancomycin’s effectiveness is time dependent rather than peak concentration dependant.

Poor penetration of vancomycin in lung tissue, requiring trough levels several fold above MIC.

These concerns have led to a lowering of the vancomycin sensitivity breakpoints for MRSA.

Evolving strategies:

Aiming for higher vancomycin trough levels. Although newer vancomycin preparations have been considered relatively non toxic, recent trends in higher dosing may be producing nephrotoxicity.

Use of other older antibiotics such as trimethoprim/sulfa, clindamycin and tetracyclines. In contrast to HA-MRSA, CA-MRSA isolates are usually sensitive to these antibiotics. Their use as an alternative to vancomycin in serious MRSA infections has been limited, has not been validated in high level studies, and is controversial.

Newer agents. Linezolid has been suggested as an alternative to vancomycin for pneumonia. The jury is still out. Daptomycin has been found non-inferior in intravascular infections. It is not effective against pneumonia. Tygecycline has efficacy against MRSA but is not approved for a wide variety of clinical indications. Limitations are that it is bacteriostatic and may not be effective against infections in which bacteriocidal activity is required. Moreover, serum levels tend to be low, a possible limitation in bacteremic infections.

Acknowledgment: Several issues raised here were covered by Dr. James Pile in his presentation at SHM 2008, which was the inspiration for this post.



Top 10 issues in hospital medicine for 2008, issue 8: resistant gram negative infections

For most of the last two decades gram positive infections have been the focus of attention concerning antibiotic resistance. More recently gram negative resistance has begun to outpace the pipeline of antibiotic development.

In serious infections multiple studies [1] [2] [3] have demonstrated the effect on survival of including the causative pathogen in the initial (“empiric”) antibiotic selection. This generally means very broad initial coverage with two or more agents. For gram positives, vancomycin coverage has become knee jerk. Decision making for gram negative coverage is now more complex. The clinician must take into account changing trends in resistance mechanisms, a wide variety of antibiotics and local resistance patterns.

This review outlines newly emerging resistance threats. Extended spectrum beta lactamases (ESBLs) and carbapenemases along with other resistance mechanisms may result in resistance to all commonly prescribed antibiotics, necessitating consideration of alternatives such as tygecycline or the older and largely abandoned class of polymyxin antibiotics. (More information on the polymyxins can be found here).

ESBLs concentrate in the periplasmic space of gram negative bacilli and consequently may overwhelm the beta lactamase inhibitors present in two currently available antibiotic combinations. For this reason, and because ESBLs inactivate late generation cephalosporins, carbapenems are increasingly included in initial therapy. A carbapenem review is referenced here. Additional posts from last year with recent literature citations can be found here and here.

Top 10 issues in hospital medicine for 2008, issue 9: palliative care

Hospitalists talk a great deal about palliative care even though no one seems to know (or articulate) exactly what it is. This year Bob Wachter described the success of the program at UCSF and this study demonstrated that palliative care programs save hospitals money. Nevertheless the concept remains poorly defined. This, as I explained in a recent post, is a source of confusion for clinicians and may be a barrier to more widespread adoption. Characterizations are variable, ranging from descriptions of terminal care to definitive care for a variety of illnesses. To confuse things further proponents use nebulous terms like patient centered as if they are unique to palliative care, but which should characterize medical care in general. (I’m reminded of the woo-meisters who hijacked the notion of the whole person for their own promotional use, but I digress). What the various descriptions of palliative care have in common are attributes all of health care aspires to: quality of life, symptom relief (palliation means helping things get better, after all), excellence and efficiency (avoiding high tech, expensive care for those who won’t benefit). Palliative care, then, is just good old fashioned doctoring. Why does it require a special service?

Several commenters, trying to help carve out a definition, merely talked around the concept. This one came close:

The underlying premise is that the patient has a "life-limiting" disease (what used to be referred to as a terminal disease), but that unlike hospice, there is a role for palliative care early on in the disease course, mostly for symptom management and social & spiritual support, even as the patient receives disease-modifying or curative treatment concurrently….There are times when you would not get palliative care involved, for example, with a 20 year old patient with pyelonephritis or a 45 year old with an acute MI.

That still leaves COPD, dementia, cerebrovascular disease, heart failure, easily 90% of internal medicine, under the umbrella of palliative care. This is something the entire hospitalist service, not a just special team, should be doing.

Sunday, December 28, 2008

Top 10 issues in hospital medicine for 2008, issue 10: How should hospitalists respond to the pseudoscientific invasion?

Suppose an integrative medicine consult service is introduced at your hospital with plans to offer Therapeutic Touch, Reiki, acupuncture and Tai Chi. You are the medical director of the hospitalist program. The CEO, knowing that your program accounts for most of the consult requests and hoping for a nice revenue stream from the new service, asks for your support. What do you do?

While integrative medicine programs commonly offer harmless treatments whose modest benefits are self evident (relaxation modalities, music therapy) these tend to be mixed with other claims which are scientifically unsound. As hospitalists we are (or claim to be) all about ethics and scientific integrity. As quackery spreads throughout mainstream academic and community medical institutions like cancer the individual hospitalist is increasingly likely to confront the issue.

At the organizational level there has been little discussion. I have attended one hospital medicine course sponsored by a large academic institution which promoted non-evidence based alternative medicine. The Society of Hospital Medicine has been silent. It’s time to take a stand.

Tolerance for the promotion of quackery in mainstream medicine is a violation of fiduciary duty.

Top 10 issues in hospital medicine for 2008

About this time every year I compile a top 10 list of issues I think were important for hospitalists. This listing is subjective and very biased. As in past years it covers both organizational and clinical issues in hospital medicine. It will be presented as a series of posts, in more or less reverse order of importance, over the next few days.

Friday, December 26, 2008

Liberation from mechanical ventilation in patients with neurologic disorders

Protocol driven assessment for liberation from mechanical ventilation is well established for patients with respiratory failure, but relatively little has been written concerning patients with neurologic impairment. Patients with impaired consciousness present special problems with regard to clearance of secretions and ability to maintain an airway. The November issue of Critical Care Medicine reports an assessment tool for patients with neurologic disorders.

Update in the treatment of pressure ulcers---nothing to get excited about

A gazillion treatments are promoted for pressure ulcers but according to this JAMA review none of them, including nutritional supplements, are evidence based.

Wednesday, December 24, 2008

Wake up and breathe!

The benefits of spontaneous breathing trials and sedation interruptions (spontaneous awakening trials) in mechanically ventilated patients have been known for years. A recent pivotal study showed that combining both trials in an integrated protocol provides additional benefits including decreased mortality. One of the study authors discussed the practical aspects of the integrated protocol, popularly known as the wake up and breathe protocol, in a recent Medscape interview.

Patient falls

An article in ACP Hospitalist profiles the aggressive multidisciplinary efforts of several institutions to reduce fall risks. Their success? One effort reduced falls by 27% (note that’s not 100%). Another resulted in 143 consecutive fall free days. (Impressive, but somebody fell on day 144). Falls as a never event? Absurd.

Tuesday, December 23, 2008

Does Michael Jackson have alpha-1 antitrypsin deficiency?

The story’s been all over the blogs today. Fox news says the story’s fake, that Jacko’s fine. Even if true it’s sloppy reporting. This post is typical:

Halperin says Jackson is battling an inherited condition called A1AD — alpha-1 anti-trypsin deficiency — where those affected by it lack a protein that helps protect the lungs. Halperin says that due to the ailment, Jackson “can barely speak” and that the “vision in his left eye is 95 percent gone.”

And while the breathing woes are surely something to worry about, Halperin claims that “it’s the bleeding that’s the most problematic part. It could kill him.”

The posts also say Jackson desperately needs a lung transplant.

While it’s true alpha-1 has extrapulmonary manifestations and disease associations (cirrhosis, necrotizing panniculitis, dementia) there’s no link to visual loss or bleeding. The statements, lacking in internal consistency, are offered without explanation.

I’d wager the claim is fake. Too goofy to be true.

Sunday, December 21, 2008

Intensive glycemic control in critically ill medical and surgical patients

Add this paper to the litany of negative studies.

On a related note, this paper in the same issue of Critical Care Medicine showed adverse cerebral metabolic effects of intensive glycemic control in patients with severe brain injury, which correlated with increased mortality.

Glycemic control and macrovascular outcomes in DM 2: the VADT

This was presented at a meeting a while back, but just published on line in NEJM:

The primary outcome was the time from randomization to the first occurrence of a major cardiovascular event, a composite of myocardial infarction, stroke, death from cardiovascular causes, congestive heart failure, surgery for vascular disease, inoperable coronary disease, and amputation for ischemic gangrene.

Results The median follow-up was 5.6 years. Median glycated hemoglobin levels were 8.4% in the standard-therapy group and 6.9% in the intensive-therapy group. The primary outcome occurred in 264 patients in the standard-therapy group and 235 patients in the intensive-therapy group (hazard ratio in the intensive-therapy group, 0.88; 95% confidence interval [CI], 0.74 to 1.05; P=0.14). There was no significant difference between the two groups in any component of the primary outcome or in the rate of death from any cause (hazard ratio, 1.07; 95% CI, 0.81 to 1.42; P=0.62). No differences between the two groups were observed for microvascular complications.


Though a bit disappointing it’s no surprise, and consistent with what we already knew, that intensive glycemic control had no impact on macrovascular outcomes over the first 5 years or so of treatment. It was mildly surprising that microvascular disease was not impacted. What we recently learned from the long term follow up of the UKPDS was that it may take up to 10 years to realize beneficial clinical outcomes. If the FDA insists on “hard” clinical outcomes the development of new diabetes drugs may be doomed. A related editorial in the Journal of Clinical Endocrinology and Metabolism makes the same point here.

Friday, December 19, 2008

Speaking of thrombolytic therapy for patients presenting in cardiac arrest

This just came out in NEJM:

In a double-blind, multicenter trial, we randomly assigned adult patients with witnessed out-of-hospital cardiac arrest to receive tenecteplase or placebo during cardiopulmonary resuscitation…. the data and safety monitoring board recommended discontinuation of enrollment of asystolic patients because of low survival, and the protocol was amended. Subsequently, the trial was terminated prematurely for futility after enrolling a total of 1050 patients… We did not detect any significant differences between tenecteplase and placebo in the primary end point of 30-day survival (14.7% vs. 17.0%; P=0.36; relative risk, 0.87; 95% confidence interval, 0.65 to 1.15) or in the secondary end points of hospital admission (53.5% vs. 55.0%, P=0.67), return of spontaneous circulation (55.0% vs. 54.6%, P=0.96), 24-hour survival (30.6% vs. 33.3%, P=0.39), survival to hospital discharge (15.1% vs. 17.5%, P=0.33), or neurologic outcome (P=0.69). There were more intracranial hemorrhages in the tenecteplase group.

Of note, patients initially suspected of having PE were not randomized and give open label thrombolytic therapy. Patients presenting in cardiac arrest with PEA as the presenting finding should be considered for thrombolytic therapy.

When anticoagulation is not enough for PE

This topic is discussed in the January 2009 issue of the American Journal of Emergency Medicine.

There is no controversy about the fact that patients with acute PE who are hemodynamically stable need anticoagulation with heparin (or low molecular weight heparin) and not thrombolytic therapy. For patients who present with hypotension (massive PE) the consensus (although not without some controversy) favors thrombolytic therapy.

Two other situations present more difficulty in decision making: the patient with evidence of right ventricular dysfunction who is hemodynamically stable and the patient with suspected massive PE presenting in cardiac arrest. These two situations are the focus of the paper which, although not a systematic review, is the best evidence synthesis I’ve seen on the topic so far.

Points of interest:

The responsibility for hemodynamic stratification and choice of treatment often falls to the emergency room physician.

Apparently hemodynamically stable patients should have cardiac biomarkers performed (troponin and BNP or proBNP).

Those with elevated biomarkers should be evaluated for RV dysfunction via echocardiography.

Patients with echocardiographic evidence of RV dysfunction should be considered for systemic thrombolytic therapy based on careful clinical assessment of multiple factors.

Around half of patients with witnessed arrests whose presenting rhythm is PEA have massive PE. The British Thoracic Society guidelines recommend thrombolytic therapy in such patients, in whom a diagnosis of PE is suspected on clinical grounds. Fears of bleeding related to the trauma of CPR have been unfounded.



Thursday, December 18, 2008

The great existential question for bloggers these days

---is “Should I twitter?”

DB has been pondering it.

Reasons to twitter:

I can express my stream of consciousness in real time.

I can promote my blog and increase traffic.

It’s a quick way to share thoughts when I don’t have much time.

Breaking medical news appears early on twitter.



Reasons not to twitter:

How many people really want to tap into my stream of consciousness, anyway?

Why worry about blog traffic? After all, I’m blogging for me, right?

I don’t need to twitter to write quick posts in real time. I can do it on my blog. It’s worked well for Instapundit.

There’s very little truly breaking medical news. Medical sound bites are always distorted.


I choose not to twitter, at least for now. There’s barely enough time to blog. Why add something else to my plate?

Hospitalists as bed control officers?

Yes, at least at Johns Hopkins Bayview. Doctors there reported their experience recently in the Annals of Internal Medicine. ER wait times were shortened and everyone seemed happy. Bob Wachter, although circumspect (not every program should tackle this, he said) had a generally positive reaction:

The American Hospital Association just released its 2008 estimates, and the number of hospitalists is now pegged at 27,000, which makes the field larger than cardiology or emergency medicine – the largest non-primary care field in Internal Medicine, and the fastest growing field in the history of medicine. This is staggering (next time, please remind me to trademark a term when I coin it), and owes to the fact that when most docs are running in the other direction, hospitalists step up to the plate and fix problems that need fixin’.

So a shout out to Eric Howell and the Hopkins Bayview crew for adding one more arrow to the hospitalist Quiver of Indispensability.

According to a conversation between Bob and the leaders at Bayview hospitalists were considered dispensable before the start of the bed control initiative. Now they’re considered indispensable.

This system is working well at Hopkins Bayview and might be a good fit at a few other hospitals, but it represents another step in the wrong direction for the hospitalist movement in general. When I made the move from traditional internist to hospitalist in 1999 hospitalists were considered clinicians (usually internal medicine trained) who, because they spent all or nearly all their professional time caring for inpatients, could ascend to extraordinary heights on the learning curve of inpatient medicine. The special expertise thus provided, along with the flexibility it afforded primary care physicians who chose not to round in hospitals, was the basis for their value. Over time things changed as leaders in the field thought up increasingly diverse tasks (clinical, procedural and administrative) to add to the hospitalist’s repertoire. Increasingly the specialty of hospital medicine is being viewed as a cadre of providers whose primary role is to offer business and administrative solutions to hospitals, with clinical expertise diminishing in importance.

There is little or no evidence to back up my opinions as to what’s “right” or “wrong” for the hospitalist movement. This developing model of hospitalist as jack of all trades might appeal to short timers looking for a good paying job while they decide what they really want to do, or until they land a fellowship. But I would wager that it is not what most of us looking for hospital medicine as a rewarding clinical career signed up for.

Related:

Hospital medicine: A mile wide and an inch deep?

More on SHM and hospitalist career satisfaction.

How to bring woo to an academic medical center

This paper, which could have come straight out of the Quackademic Medicine playbook, tells how it was done at two institutions in Canada. To successfully integrate woo into an academic medical center you need a promoter and a Trojan horse.

The promoter, aka the champion:

Our results suggest that a highly respected champion is necessary for the development of a new integrative medicine program. Both these programs were highly dependent on the efforts of champions with visions who were able to mobilize a wide range of individuals at many different levels within the health care system in order to facilitate the actualization of these integrative medicine programs..... What is most important is that the champion has credibility within the host institution, as well as with patients and clinicians who will work together in the integrative medicine program.

The Trojan horse (italics mine):

CARE began with only a consult service and to date does not include a chiropractor among the team members despite the high use of chiropractic among children. Similarly, the chiropractors in the SMH clinic began by explicitly limiting their legally-defined wide scope of practice to musculoskeletal conditions. However, as referrals and comfort levels increased over time, the SMH chiropractors have seen a wider range of referrals and increasingly have been asked to provide 'second opinion' level service when their physicians are unsure of the diagnosis (ie, because of diagnostic uncertainty, they will defer the diagnostic opinion to the chiropractors). This suggests an evolution in the physicians' level of trust and confidence towards the chiropractors. In both settings, the CAM providers were being integrated into conventional medicine contexts and as such, there was a degree of conventional medicine dominance created by the existing structures as has been described previously. In both clinics, the CAM providers were required to initially limit the scope of their activities in order to gain access to the integrative setting.

“Trojan horse” is a figure of speech I borrowed from Orac, who invoked the concept about a year ago to describe how pseudoscience gets its foot in the door of the academic medical center:

In reality, what bothers me about the whole concept of CAM is that it's basically a Trojan horse through which some therapies that might be evidence-based and could easily be integrated into our standard armamentarium of medical therapies are the "foot in the door" behind which hardcore woo lumped together as CAM follow, woo such as homeopathy, craniosacral therapy, reiki, and even reflexology, all of which I have encountered on wepages for academic centers devoted to CAM.

Wednesday, December 17, 2008

When a mainstream medical journal has the courage to call out pseudoscience

---it’s a rare and beautiful thing. Most journals are too PC to tackle it, choosing to be neutral or, in many cases promotional. So here’s a tip of the RW hat to the “Green Journal” for their recent review of acupuncture, concluding with:

So, after 3 decades of intensive research, is the end of acupuncture nigh? Given its many supporters, acupuncture is bound to survive the current wave of negative evidence, as it has survived previous threats. What has changed, however, is that, for the first time in its long history, acupuncture has been submitted to rigorous science—and conclusively failed the test.

Obesity and asthma

The in vitro response to glucocorticoids is reduced in peripheral blood monocytes and BAL cells in obese as opposed to lean asthmatics. TNF expression was also increased in obese patients. Via American Journal of Respiratory and Critical Care Medicine.

The findings help explain link between obesity and asthma.

Tuesday, December 16, 2008

EMR angst

We’re all too familiar with the stress of transitioning from paper to the electronic medical record. It may work the other way around. What if you relocate form an area of high information technology to one of lower technology? Here’s what Vanderbilt researchers found:

After controlling for confounding effects, the authors found that graduates who transitioned to lower-HIT institutions reported feeling less able to practice safe patient care (P = .02), to utilize evidence at the point of care (P = .05), to work efficiently (P < .001), to share and communicate information (P = .03), and to work effectively within the local system (P = .007).

Bibliographic retrieval databases

It’s not just Pub Med. Here’s a repository from Student BMJ, along with a list of free journal collections and searching tips.

Monday, December 15, 2008

Influenza update

The Cleveland Clinic Journal of Medicine has a very helpful update in its December issue.

Points of interest:

The efficacy of last year’s vaccine was unusually low at 40%. This year’s vaccine is expected to perform better.

Although oseltamivir (Tamiflu) is still recommended, last season saw a concerning rise in resistance. Virtually no resistance has been seen with zanamivir (Relenza).

Forget amantadine (Symmetrel) or rimantadine (Flumadine). Resistance is way too high.

The predictive value of clinical assessment of patients is poor. Use point of care testing.

The author states: Health care providers should offer vaccination at every opportunity between October and May. This means going beyond the core performance measures for hospitalized patients.

There is now a vaccine against H5N1 (bird flu).

CDC recommendations regarding influenza are here.

Wikipedia has some nice images and graphics.

Wernicke Encephalopathy---not just in alcoholics

Wernicke encephalopathy an internist's (and hospitalist's) dream, as treatment is easy and gratifying, while consequences of non-treatment are grave. Although usually discussed in the context of alcoholism, it can occur in a variety of settings of nutritional depletion. Examples reported in the literature include hyperemesis gravidarum and administration of TPN without thiamine supplementation. Nowadays it is increasingly seen following bariatric surgery. It usually occurs in the first month post operatively in the setting of protracted vomiting. The topic is reviewed in the Annals of Surgery, accessible via Medscape.

Friday, December 12, 2008

More about Joint Commission’s disruptive behavior policy

Chris Rangel wrote a provocative post about Joint Commission’s new disruptive behavior policy set to go into effect in 2009. He’s concerned that the definition of disruptive behavior (for which the JC recommends a zero tolerance policy) is a little vague, particularly this language (italics mine):

Intimidating and disruptive behaviors include overt actions such as verbal outbursts and physical threats, as well as passive activities such as refusing to perform assigned tasks or quietly exhibiting uncooperative attitudes during routine activities. Intimidating and disruptive behaviors are often manifested by health care professionals in positions of power. Such behaviors include reluctance or refusal to answer questions, return phone calls or pages; condescending language or voice intonation; and impatience with questions.

He points out:

Wait a minute! What this second part means is that basically, if you are having a bad day, then you’re a disruptive physician. If you have a bad bedside manner or you are not chummy with the hospital staff then you are disruptive. If you are distracted by a personal or professional crisis, then you are being disruptive. As one AMA delegate put it, if you are perceived as being disruptive to any particular staff member then you ARE disruptive.

By this definition a hospital administration could invoke the disruptive behavior policy to sanction anyone they don’t happen to like.

He goes on to point out an important unintended consequence of such a policy, which is to suppress strong opinions and concerns about hospital operations which may impact patient care. As I first noted here, such whistle blowing on the part of physicians, even legitimate expressions of concern, may be construed as disruptive.

He concludes:

The JC shouldn’t be trying to codify specific behaviors. Each case is unique and should be decided without specific description of behaviors leading to unfair bias while loosing sight of the endpoint of this whole endeavor. Neither should we expect every person in a high stress job where people’s lives are on the line to walk around like a smiling jackass in some hall monitor’s idea of the perfect Stepford Wives-like medical nightmare where everyone is pleasant and totally incompetent. Given the choice, I’d rather be treated by the brilliant asshole* then Dr. Smiley Mannequin. So far the AMA has asked the JC to reconsider their proposal. Let’s hope that the JC grows some CS.

While I agree with Rangel for the most part he failed to mention that the new JC policy is no respecter of persons---it applies equally to nurses, pharmacists, doctors and administrators. There’s no double standard. Everyone in the health care environment is expected to be civil. It’s not just about doctors anymore. As I pointed out in a recent post Alan H. Rosenstein, MD, MBA, an expert who has written a great deal on this subject, said that many doctors are the recipients rather than the perpetrators of disruptive behavior.


The Joint Commission, much to its credit, recognizes that fact. The Sentinel Event Alert regarding the new standard is careful to avoid the term “disruptive physician” and says:

While most formal research centers on intimidating and disruptive behaviors among physicians and nurses, there is evidence that these behaviors occur among other health care professionals, such as pharmacists, therapists, and support staff, as well as among administrators.

The report recommends several actions including (italics mine):

Educate all team members – both physicians and non-physician staff – on appropriate professional behavior defined by the organization’s code of conduct.

Hold all team members accountable for modeling desirable behaviors, and enforce the code consistently and equitably among all staff regardless of seniority or clinical discipline…

If you’ve worked in a hospital for any length of time you know that this disruptive behavior thing works both ways. That’s why I’m more than a little disappointed in the New York Times distortion of the issue in their recent article Arrogant, Abusive and Disruptive — and a Doctor. It’s a one sided portrayal of the stereotypical instrument throwing physician who intimidates everyone else on the health care team:

Still, every nurse has a story about obnoxious doctors. A few say they have ducked scalpels thrown across the operating room by angry surgeons. More frequently, though, they are belittled, insulted or yelled at — often in front of patients and other staff members — and made to feel like the bottom of the food chain. A third of the nurses in Dr. Rosenstein’s study were aware of a nurse who had left a hospital because of a disruptive physician.

With JC’s broad definition of disruptive behavior applied across the whole spectrum of health care providers the possibilities are endless. If a nurse grudgingly carries out a doctor’s orders, if an attending leans a little too heavily on a medical student or if administration is unreceptive to expressed concerns about patient care, one can invoke the disruptive behavior policy.

Thursday, December 11, 2008

American Academy of Pediatrics statement on CAM

About the only thing informative about this report from the AAP is its documentation of the spread of woo like a cancer throughout academic and community medicine. Otherwise it’s pretty much a fluff piece, or so it seems to me.

Walmart’s generic drug list

Seems there’s never a copy around when I need one, so I’ll link it here.

Wednesday, December 10, 2008

Change coming to the White House

You mean it won’t be smoke free anymore? Who knew?



Not much mainstream coverage about this, but some bloggers have weighed in.

Dr. Wes

Happy Hospitalist

BOSO


I mean, it’s all about leading by example for the public good, right?

Lotrel outdoes Lotensin/HCTZ in ACCOMPLISH

This was a high risk population of hypertensives. The study was published in NEJM. Despite nearly identical BP control, outcomes were better in the Lotrel group:

There were 552 primary-outcome events in the benazepril–amlodipine group (9.6% and 679 in the benazepril–hydrochlorothiazide group (11.8%), representing an absolute risk reduction with benazepril–amlodipine therapy of 2.2% and a relative risk reduction of 19.6% (hazard ratio, 0.80, 95% confidence interval [CI], 0.72 to 0.90; P<0.001).

In a Medscape piece concerning the study Dr Franz Messerli commented:

"This landmark study unequivocally relegates hydrochlorothiazide from first-line to third-line therapy at least in a patient population with similar demographic and clinical features as in ACCOMPLISH," said Messerli. "The issue is not to be taken lightly, since hydrochlorothiazide remains one of the most commonly prescribed antihypertensive drugs….”

Venous thromboembolism and pregnancy

---is reviewed in NEJM. Very comprehensive and helpful.

Monday, December 08, 2008

Maybe I could get excited about palliative care

---if someone would tell me what it is.

Bob Wachter describes a wonderful clinical service at UCSF---one that is well organized, delivers excellent care and is rated highly by patients, families and house staff. He calls it the palliative care service but doesn’t quite define what it is, leaving me wondering about the whole concept. Think I’m nit picking? Try asking your colleagues, or searching the literature on what palliative care really is. Good luck in getting a coherent answer.

Even the usually straightforward Wikpedia is vague, describing palliative care as something which is delivered in the context of both curative care and hospice care. So what is it, exactly?

Bob’s post is not explicit but from his title (My Patients Are Dying… And I’ve Never Been Prouder) he’s talking about end of life care. But Mount Sinai School of Medicine Professor R. Sean Morrison, MD, who has written a great deal about palliative care, said in a recent Medscape video editorial that “Unlike hospice, hospital palliative care is not dependent on prognosis.” Moreover, in an earlier NEJM article Morrison’s description of palliative care does not preclude curative care as implied by this statement: “Palliative care should be offered simultaneously with all other medical treatment.” In this recently published study the majority of patients on palliative care services were discharged alive. So, again, what is it?

The closest thing you’ll find to a definition (and it’s not really satisfactory) is something like the one in the NEJM article:

Palliative care aims to relieve suffering and improve the quality of life for patients with advanced illnesses and their families through specific knowledge and skills, including communication with patients and family members; management of pain and other symptoms; psychosocial, spiritual, and bereavement support; and coordination of an array of medical and social services.

OK. Palliation means making the patient’s illness get better while paying attention to the surrounding psycho-social and spiritual issues. It’s what we should be doing for all our patients all the time, so why does a hospital need a special service? (The focus on patients with advanced illness doesn’t really narrow things down much; most hospitalized patients have advanced illness). My reading suggests that palliative care is simply hospital medicine raised to a higher level of excellence, efficiency, organization and patient centeredness. It sounds a lot like what the Institute of Medicine has been harping at all of us to do. The idea of a palliative care “program” suggests a separate team to deliver this excellent care while the rest of us settle for mediocrity! Palliative care claims to have distinctive attributes, but they really shouldn’t be distinctive. They should be the norm.

A common thread in many descriptions of palliative care relates to the quality of communication. Discussions go beyond DNR status and whether the patient has a living will to the education of patients and families on the big picture of the patient’s health and realistic expectations concerning the limitations of treatment. This leads to greater patient satisfaction, more informed and rational decision making, and often the avoidance of ICU care, feeding tubes and other technologies which, in many patients, serve only to decrease quality of life. While these interventions are ineffective in many patients they are costly, which is probably why palliative care programs save hospitals money. Lots of money. But again, why should good communication with patients and families require a special care service?

Like so many other concepts in medicine, the word “palliative” has been hijacked. The idea of palliative care has been administratively defined by people with agendas. For clinicians it’s been an exercise in obfuscation.

The excellence and the efficiency of what is called palliative care is something to get excited about. It’s something we should all strive for. I would like to see our hospitalist program spearhead a multidisciplinary effort to take these ideas to a new level of excellence for all of patient care. But I don’t think I’d call it palliative care. I’d call it something else. I’m not sure what, but something with more meaning.

Sunday, December 07, 2008

Cardiac precautions for methadone prescribing

Some guidelines are finally out, issued by the American College of Physicians. Medscape provides a summary here. Among the recommendations:

Recommendation 1 (Disclosure): When clinicians prescribe methadone, they should inform patients about arrhythmia risk.

Recommendation 2 (Clinical History): Clinicians should ask patients about any history of structural heart disease, arrhythmia, or syncope.

Recommendation 3 (Screening): All patients should have a pretreatment electrocardiogram (ECG) to measure QTc interval and a follow-up ECG within 30 days and each year.

I wonder how many people are actually doing this. I started harping about it way back here.

Google hacks

A slide presentation is presented here via Clinical Cases and Images blog.

Also check out these resources.

Here’s one of my old posts on Google vs PubMed.

Saturday, December 06, 2008

Should doctors interact with drug reps?

That’s the topic of the latest Medscape Roundtable Discussion. I took the libertarian view: Let individual doctors decide for themselves.

Friday, December 05, 2008

Drug induced nephropathy

American Family Physician has a review and some recommendations. Unfortunately the journal is no longer open access so I can’t link to the article (not even the abstract). But here’s a Medscape CME piece which summarizes the review. (Fair and balanced? Yes, as far as I can tell, and no industry support!).

This issue has garnered increasing recent attention in hospital medicine. The new emphasis is on lowering the threshold for detecting renal injury. Changes in serum creatinine formerly considered modest should prompt a review of medications and a search for means to mitigate renal damage.

Thursday, December 04, 2008

Rapid response teams disappoint---again

This may be the biggest study yet, from St. Luke’s, Kansas City, MO.

Conclusion In this large single-institution study, rapid response team implementation was not associated with reductions in hospital-wide code rates or mortality.

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.

Wednesday, December 03, 2008

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.

Tuesday, December 02, 2008

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.

Monday, December 01, 2008

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.

Thursday, November 27, 2008

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%.

Wednesday, November 26, 2008

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.

Tuesday, November 25, 2008

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.

Sunday, November 23, 2008

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.

Saturday, November 22, 2008

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.

Friday, November 21, 2008

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.

What’s ahead in gram negative infections?

An article from Expert Review of Anti-Infective Therapy examines the emerging threats of resistant gram negative organisms and what we have now, or in the pipeline, to deal with them. In general there are few gram negative agents in late stages of development.

At present, Tygecycline is a consideration for Acinetobacter baumannii infections although its role is uncertain. A. baumannii frequently causes pulmonary infections. In that connection the recently reported failure of Tygecycline in the phase III HAP/VAP trial is concerning.

Is it woo or is it real?

Maybe a little of both?

This demonstration took place on I've Got a Secret, a popular CBS game show from the early 60’s

Neurologists, psychiatrists, skeptics, what’s going on?

(Don’t try this at home).


Thursday, November 20, 2008

Discharge planning after glycemic control in hospitalized patients

So you’ve done a good job controlling your critically ill patient’s blood sugar with an insulin drip. The patient has recovered and discharge is approaching. Now what? This CME approved Medscape article provides some tips for the transition to out patient care.

A while back, after an exchange with Dr. Daniel Carlat, author of the Carlat Psychiatry Blog (really more of a pharma-critical site than a psychiatry blog) I vowed to asses all Medscape CME offerings I post for bias, imbalance and non-evidence based content. This has gotten to be a competition between collections of anecdotes (which, mind you, do not equal evidence).

The activity in question is based entirely on an article from the Medscape Journal of Medicine. Editorial assistance for the article was provided by the makers of Lantus. (Does that mean it is one of those dreaded ghost written articles?). The author received no financial support from industry. The CME activity itself is non-industry supported.

Ghost written or not, the article can easily be critically appraised by examination of primary sources of evidence. The only thing I found that was non-evidence based and unbalanced was the discussion of glycemic control via insulin drips in the initial phase of critical illness and acute coronary syndrome. Specifically, the article selectively cites evidence in favor of tight glycemic targets while tending to ignore negative studies and the prevailing controversy surrounding in patient glucose control.

The principal focus of the article is on the transitions from insulin drip to sub q insulin to discharge. Those sections contain helpful tables and text on basal bolus regimens. Although they mention the pharmacokinetic advantages of the newer insulins none are mentioned by brand name and no clear recommendation for one over others is made.

My final take? The only unbalanced portion of this presentation was the promotion of plain old regular insulin and had nothing to do with the company which was in a position to influence content.