New concepts in status epilepticus

From a review in Emergency Medicine Clinics of North America, here are a few key points:

Definition of SE---

Traditional: 30 minutes of unrelenting seizure(s).

New (proposed): greater than 5 minutes or two or more without intervening full return of consciousness.

Why?

The longer durations traditionally used to define SE were selected based on assumptions about underlying pathophysiology that are now known not to be true rather than on any kind of clinical relevance…

Data from continuous electroencephalographic (EEG) monitoring indicate that the average length of a benign, self-limited, adult generalized tonic-clonic seizure (including pre-tonic-clonic, tonic, and clonic phases) is just longer than a minute and only rarely persists beyond 2 minutes. Patients with seizures that last more than 5 minutes are not likely to improve spontaneously. Consequently, most of these patients are more similar to those with seizures of 30 to 60 minutes' duration than they are to patients with benign seizures of less than 5 minutes' duration. Thus, the new definition is better at discriminating prognostically.

Prehospital treatment by paramedics---effective, safe, reduces likelihood of ICU admission and shows a trend toward reduced mortality.

Initial hospital treatment---

A new accelerated protocol has been proposed in which the previously sequential steps of lorazepam and phenytoin are now stacked and given simultaneously and in which phenobarbital has been omitted. In principle, this accelerated strategy should allow more aggressive treatment of patients who have SE and should reduce the delay to the induction of pharmacologic coma (thereby improving the outcomes) in those with the most refractory seizures. Clinical research to determine if this is true in practice is still required.

The lorazepam dose in the protocol is 0.05-0.1 mg/kg. The phenytoin dose is 18-20 mg/kg with the option to repeat once. Drugs for the induction of pharmacologic coma in refractory SE include midazolam 0.2mg/kg then 1.2 mcg/kg/min. Propofol and pentobarbital are listed as alternatives.

Nonconvulsive SE---need EEG to diagnose.

Alcololic ketoacidisos (AKA)

This is the most recent free full text general topic review I have been able to find.

Key points about AKA:

It is not as benign as popularly believed. It may be a cause of unexplained sudden death in alcoholics.

Acidosis may be severe but if altered LOC occurs suspect another cause.

The treatment is general supportive care and dextrose containing IV fluids (thiamine to go with that, please, and give it first).

The pathophysiology of AKA defies complete understanding. Dr. Daniel Foster, Professor of Endocrinology at UT Southwestern Medical School, believes that AKA is idiosyncratic, with most patients never developing it while a few patients do so repeatedly. A history of recurrent episodes is characteristic. The nature of the idiosyncratic susceptibility is unclear.

Alcohol is metabolized to acetate via sequential steps mediated by alcohol dehydrogenase, and the acetate thus formed can produce acetoacetate. However, the major source of ketone bodies produced in AKA, like DKA, is the catabolic sequence in which free fatty acids (FFA) are released from adipocytes and undergo beta oxidation in the liver mitochondria.

A state of semistarvation (leading to low insulin levels) prevails in patients with AKA in whom alcohol has been their major source of caloric intake. Alcohol intake is often markedly reduced around the time of development of AKA thus accentuating caloric deprivation. If an individual has working beta cells (i.e. does not have DM-1) starvation ketosis is limited and does not progress to ketoacidosis. This is due to a feedback mechanism in which ketones and FFAs feed back on the pancreas, causing it to secrete a small trickle of insulin. In this way, during starvation, the body produces ketones as fuel for the brain (ketones are the brain’s only alternative to glucose) while avoiding fatal ketoacidosis. This regulatory mechanism appears to be ineffective in certain unusual clinical states of which AKA appears to be one. In AKA ketosis continues unfettered. FFAs are much higher than in ordinary starvation ketosis and counter-regulatory hormones are high. Dextrose is therapeutic because it ends the catabolic sequence and shuts off ketosis.

Novel H1N1 influenza in hospitalized patients

JAMA has a recent issue devoted to this topic. Here’s what stands out:

In a series from California admitted patients tended to be younger (27) but of those admitted, those over 50 had the highest mortality (11% overall, 18-20% for those over 50). 66% of chest xrays showed infiltrates and 31% of patients required ICU. Viral pneumonia and ARDS were the most common causes of death. Secondary bacterial infection was only found in 4%.

A Canadian series looked at critically ill patients. Mean age was 32 and 28 day mortality was 14%. Patients’ illnesses progressed rapidly with a mean of 1 day from hospital admission to ICU transfer. Shock and nonpulmonary organ failure were common. Hypoxemia tended to be severe with the mean PO2/FiO2 of 147. 81% got mechanical ventilation with a mean duration of 12 days. Lung rescue therapies were commonly used.

A series from Mexico reported similar outcomes with additional findings of note: 31% were obese and antiviral treatment (adjusting for those with no opportunity for treatment due to early death) improved survival.

Investigators from Australia and New Zealand reported on a series of patients referred for ECMO. Those patients had a 21% mortality by study end. Patients transitioning to ECMO had a median PO2/FiO2 of 56 on a median of 18cm PEEP.

An editorial, commenting on a trial published in the same issue showing non-inferiority of surgical masks compared with N-95s noted that we still don’t have enough evidence on this issue and the controversy will continue.

Recognition of focused practice in HM

Here's more info from The Hospitalist. When I posted about this a couple of months ago I wondered when we would see some resources to help with preparation. In article Scott Flanders said:

“SHM has to help develop the tools and resources hospitalists will need to successfully prepare for and pass this test,” he says. He expects educational resources and self-assessment modules will be available on SHM’s Web site (www.hospitalmedicine.org) and at HM10, April 8-11 in Washington, D.C.

Most hospitalists will work through the RFP process as part of their 10 year recert. What about those who are grandfathered in with lifetime certification? They don't have to take the test but they can. Details on how that will work are unclear.

AHA 2009: chronic pacemaker mediated cardiomyopathy?

We've long known that right ventricular pacing is not physiologic. PACE study investigators, presenting at AHA 2009, looked at the difference between RV and BiV pacing in terms of EF after one year in patients with normal or nearly normal systolic function at baseline.

By one year there was no difference in 6 minute walk performance or quality of life indicators, but patients in the RV pacing group dropped their EF (by 7%) whereas those in the BiV group did not. For a patient starting with a normal EF, a 7% drop may not seem like much, but consider the impact of a few % per year!

RV pacing leads to cardiac remodeling. BiV pacing prevents it. Based on these findings, chronic RV pacing is a bit like depriving some patients of ACE inhibitors.

If you've taken care of many patients with pacemakers you've probably seen pacemaker mediated cardiomyopathy. The hypothesis needs further study before we implant BiV pacers in all patients, but for now there is an important take home message---minimize RV pacing via rate and AV interval programming and be aware that patients in whom this is not possible, because they are RV pacer dependent, may be at special risk to develop dilated cardiomyopathy.

For details on this fascinating study:

Presentation slides.

Discussant slides.

Presentation audio.

Discussant audio.

Summary slide.

Homeopathy is woo. Green Journal.

I love the courage of the Green Journal in calling out quackery. You wouldn't find an article like this in JAMA or the Annals. Of note, one of the authors is identified with a department of complementary medicine. All the same, he knows things that go quack.

Patient safety 10 years after “To Err is Human”

Commentary from key leaders in the latest issue of The Hospitalist reflects on where we've come in the decade since the Institute of Medicine released its patient safety report. Though the article is mainly congratulatory there has been spirited debate about the success (or lack thereof) of the patient safety movement. A recent report by the Consumers Union declared the movement a failure. Although the report lacked data on safety breaches and was based on a faulty premise (equating the continued high rate of hospital associated infections to unsafe practice) it correctly pointed out that we have done little to implement the IOM's recommendations.

Why haven't we done more? Maybe because the IOM's recommendations were predicated on a culture of transparency while over the past decade we have devolved into a culture of blame. These are mutually exclusive outcomes. I pointed that out here and in other posts as my own reason for giving the movement a failing grade.

Meanwhile Bob Wachter gives the patient safety movement less than glowing reviews but apparently for the opposite reason. He seems to believe we have achieved a no blame culture and not only that, it has gone too far. He opened his September 30 blog post with:

In this week’s New England Journal, Peter Pronovost and I make the case for striking a new balance between “no blame” and accountability. Come on folks, it’s time.

Why the seemingly divergent conclusions? Because we've conflated the ideas of accountability and blame. Blame is finger pointing when something goes wrong. The ad below reflects our culture of blame. Note the implied finger pointing: if the patient gets VAP it's someone else's fault.



That's the attitude that pervades medicine today and it's so counterproductive! But it's not the accountability Bob's talking about. If we make careful distinctions between accountability and blame Bob and I are not that far apart. He believes there should be consequences for stubborn, deliberate violation of known safety measures such as hand washing and time outs. I couldn't agree more. It's a form of disruptive behavior, for which Joint Commission already requires “zero tolerance”.

Low blame and high accountability are not conflicting goals. What we have now is too much blame and not enough accountability! In its report the IOM noted that transparency would be essential to effective process improvements for patient safety. The report also stated that such transparency would require movement toward a blame free culture. But, due to misinterpretation of research data and a blunder in the use of language the IOM report had the opposite effect! I explained here:

Ironically, the IOM, with the issuance of its report, undermined its own aspirations for a culture of transparency right out of the gate! They did this by indiscriminately referring to a broad spectrum of adverse patient outcomes as “errors.” This unfortunate attribution, based on faulty analysis of a landmark study on adverse hospital events, I have argued, did much to sabotage the cause of patient safety in the decade that followed. (For the original investigator’s own criticism of the IOM’s interpretation see this editorial). Instead of an era of transparency we entered a heightened culture of blame and finger pointing. The most vivid example of this, of course, is Medicare’s never events policy, of which we are just beginning to realize the adverse consequences.

Now we have a domino effect of more and more unintended consequences. Already in the works is a new legal standard which shifts the burden of proof to hospitals in certain malpractice cases. So much for transparency!

At a recent UWGrand Rounds presentation Bob described what he called a “masterful bit of spin” by the IOM in equating the rate of adverse events in health care to one commercial air crash per day. But the IOM did worse than spin data. They spun assumptions based on faulty interpretation of data. Masterful but unfortunate.

Mitosis

I was taught to remember the acronym IPMAT.

Interphase

Prophase

Metaphase

Anaphase

Telophase

(There’s also preprophase and prometaphase).

Many school kids in the 1960s learned about it from The Thread of Life, one of the Bell Laboratories science films. Clip below.

Novel H1N1 vaccine safety

Monitoring has been intense but there have been no unusual concerns to date according to two reports.

Has public reporting impacted health care at all?

Public reporting of health care performance measures has been a hot topic for several years. It already had a good head of steam in 2005, my first year of blogging, when policy mavens hoped it would be transformative. Last year Bob Wachter even wondered if we were entering a golden age of transparency.

But how was it supposed to work? The conventional wisdom was that it would work by influencing consumers' choices. That never came to pass, though, and Bob suggested another effect:

Shockingly, in the past five years, these mantras have proven to be way off the mark. Instead,

1.Some rudimentary quality data has been placed on the Web
2.Few people are looking at these data, and virtually no real patients are making their healthcare purchasing decisions based on them.
3.And yet… hospitals are doing organizational cartwheels trying to improve their performance on the publicly reported indicators.

Although #2 is surprising, #3 is truly flabbergasting -- it demonstrates the power of shame and embarrassment as motivating forces.

So, shame and embarrassment are motivating hospitals! Yes, it's true, but is it a good thing? In my view such motivation amounts to little more than a form of institutional narcissism---it's all about us (the institution) and our report cards, and has little to do with patients. (As regular readers know I believe that, with few exceptions, performance measures are weak, sometimes non-evidence based and occasionally even harmful).

OK, all cynicism aside: has this transparency movement had any meaningful impact at all? Up to now we've had no evidence one way or the other. That brings me to the EFFECT study, presented at AHA 2009 and published on line in JAMA. The conclusion in the published abstract doesn't give you the real flavor of the study but here's what it said:

Results The publication of the early feedback hospital report card did not result in a significant systemwide improvement in the early feedback group in either the composite AMI process-of-care indicator (absolute change, 1.5%; 95% confidence interval [CI], –2.2% to 5.1%; P=.43) or the composite CHF process-of-care indicator (absolute change, 0.6%; 95% CI, –4.5% to 5.7%; P=.81). During the follow-up period, the mean 30-day AMI mortality rates were 2.5% lower (95% CI, 0.1% to 4.9%; P=.045) in the early feedback group compared with the delayed feedback group. The hospital mortality rates for CHF were not significantly different.

Conclusion Public release of hospital-specific quality indicators did not significantly improve composite process-of-care indicators for AMI or CHF.

So, all in all, public reporting had little impact. I'll get back to that barely statistically significant improvement in MI mortality in a moment.

This study had a somewhat roundabout design. Both comparison groups of hospitals were subject to public reporting. The difference was, in the “intervention group” the reporting was early and accompanied by a media blitz. In the comparison group the reporting was later and there was no media blitz. According to post reporting surveys the intervention hospitals did scramble to enhance their performance, but in a heterogeneous and disorganized manner, accounting for the lack of measured difference in overall adherence to indicators between the comparison groups.

Now what about that improvement in MI mortality? It turns out that it was largely attributable to an improvement in STEMI mortality. Although the percentage of hospitals achieving time-to-reperfusion benchmarks didn't differ between the two groups the findings suggested that in the intervention group there may have been a shorter time to reperfusion. If so it appears to have been driven entirely by time to administration of thrombolytic agents (PCI was used infrequently, but, hey, this was Canada). The only difference in process indicators attributable to the intervention was the frequency of thrombolytics administered in the ER, before transfer to intensive care. Of note, the survey indicated that ten hospitals in the intervention group decided, after the reporting, to allow ER physicians to administer thrombolytics without specialty consultation.

Although I believe performance measures tend to be weak, time to reperfusion is a notable exception. The process change by which hospitals gave ER docs autonomy in the administration of thrombolytics may have made a difference.

So, after all these years and all this momentum, evidence for an impact of public reporting is slim. Institutional narcissism, up to now, has been largely ineffective, being driven by weak and perfunctory process measures. The quality movement needs to adopt a more thoughtful and nuanced approach to improvement.

AHA 09: the POPE study

Hospitalists involved in the care of CABG patients will find this study of interest. Pericardial irritation occurs post CABG. Pericarditis can cause arrhythmias as well as lead to effusion progressing to tampanade. Frequently NSAIDs are given to reduce these complications. Evidence to support this strategy has been lacking. The POPE study, presented at AHA 09, looked at the use of diclofenac to reduce the volume of pericardial effusion. The findings, from the press release:

A non-steroidal anti-inflammatory drug, diclofenac, failed to reduce fluid accumulation around the heart after cardiac surgery.

The NSAID after heart surgery also did not reduce the serious problem of cardiac tamponade, compression of the heart by fluid.

Only patients with pericardial effusion at baseline were enrolled. The investigators concluded:

The use of NSAIDs in post-cardiac surgery patients is useless in this setting.

As pointed out in the presentation slides NSAID use post CABG has been common even though not supported by good evidence, and in spite of known adverse effects including increased renal failure, heart failure and myocardial infarction.

Amyloid cardiomyopathy

This Clinical Perspective piece in Circulation stresses the little appreciated fact that there are actually three types of cardiac amyloidosis: the AL type that we’re used to thinking of as well as two types of transthyretin related disease, the mutant type (of which there are over 100 mutations) and the wild type seen almost exclusively in older men. The three types differ in clinical features and prognosis.

EMRs don't improve health care---yet

Claims made over the last several years that EMRs lead to better quality of care have been devoid of supporting evidence. Now we have evidence from a large study that EMRs in fact don't improve quality. I apologize for not having a better source for this than a New York Times article, which reports that the findings were to have been reported at a conference in Boston. Unfortunately, the article didn't provide a link to the conference proceedings and didn't name the conference. Maybe I'll find the primary source later. In the mean time the article reports:

But a new study comparing 3,000 hospitals at various stages in the adoption of computerized health records has found little difference in the cost and quality of care.

“The way electronic medical records are used now has not yet had a real impact on the quality or cost of health care,” said Dr. Ashish K. Jha, an assistant professor at the Harvard School of Public Health, who led the research project.

Unfortunately the study looked at performance measures, and performance measures do not equal quality. But the study still makes a strong statement because performance measures represent the bare minimum standards, the lowest of the low hanging fruit. So if EMRs didn't improve performance measures you can be darn sure they had little or no impact on real quality.

I agree with the comments of the interviewees in the article, that we have years to go before we utilize EMRs effectively, in a way that will improve patient care.

Autoimmune polyendocrine syndromes

Reviewed here (Expert Review of Endocrinology and Metabolism).

Colchicine toxicity

Brief review and lessons from the courtroom.

AHA 09: the FOCUS study

This study addressed an issue that often plagues hospitalists who are involved in co-management of patients undergoing hip fracture repair: when the patient's hemoglobin and hematocrit drop following surgery, what is the appropriate transfusion target in patients with cardiovascular disease or risk factors for CVD? While a H/H target of 8/24 has been validated for patients across the board, conventional wisdom has it that 10/30 is a more appropriate target for patients with cardiovascular disease. FOCUS compared strategies utilizing these two targets and found no advantage of the more aggressive transfusion strategy in terms of death or cardiac event rate. Results concerning the effect on functional outcomes have yet to be announced.