Thursday, September 30, 2010

More on the adverse cardiovascular effects of NSAIDs, old and new

And this time, according to a study presented at the recent European Society of Cardiology (ESC) 2010 Congress, the increased risk was for stroke. From the Medscape report:

Short-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) was associated with an increased risk of stroke in a Danish population study including only healthy individuals.

Again, it bears emphasis that these were healthy individuals using the drugs short term! In recent years doctors have become wary of giving NSAIDs to individuals with cardiovascular disease but most docs wouldn't think twice about short term use in healthy folks. That's what's new in this study. The fact that they lead to excess strokes as well as heart attacks should surprise no one.

It was also again noted that the risk extended throughout all NSAIDs. The old ones were as bad as the COX 2s although, as in other studies, Naproxen tended to be safer than some of the others.

Given how often NSAIDs are prescribed and the frequency of over the counter use this may be one of the largest adverse effects in modern medicine.

The CPOE patient safety dogma is gradually coming apart at the seams

Here's a study from two academic medical centers in Philadelphia. The authors looked at the effect of a nearly hard CPOE stop of concurrent orders for warfarin and trimethoprim-sulfamethoxazole, versus the old fashioned method of having the pharmacist call to express concern when such an order was entered:

Results  The proportion of desired responses (ie, not reordering the alert-triggering drug within 10 minutes of firing) was 57.2% (111 of 194 hard stop alerts) in the intervention group and 13.5% (20 of 148) in the control group (adjusted odds ratio, 0.12; 95% confidence interval, 0.045-0.33).


...the study was terminated early because of 4 unintended consequences identified among patients in the intervention group: a delay of treatment with trimethoprim-sulfamethoxazole in 2 patients and a delay of treatment with warfarin in another 2 patients.

One instance was a delay of 3 days in starting the antibiotic (which had been recommended by the ID service!). In looking at the body of the paper, the other instance of antibiotic delay was actually a failure to start the antibiotic at all. Of the warfarin delays, one was a one day delay and the other was a three day.

The study didn't evaluate outcomes.

The boosters of CPOE as a facilitator of patient safety have been driven more by a belief system than evidence. Meanwhile, this year there have been several papers showing negative consequences. This may make my year end top ten list.

More from Med Page Today.

By the way, there's no absolute contraindication to prescribing warfarin and trimethoprim-sulfa together, provided you can monitor the INR frequently, which is easily done in hospitalized patients.

Tuesday, September 28, 2010

Organized push back against TPA for ischemic stroke continues

And again it comes from the house of emergency medicine. The idea is to marshal overwhelming opposition among ER physicians using an on line survey. The problem is, there's only one response you can give---to agree with this statement (my italics):

“Given the controversial evidence that currently exists regarding the efficacy of thrombolytics in ischemic stroke, we the undersigned agree that a decision NOT to administer thrombolytics to a patient with an acute ischemic stroke is reasonable and within the standard of care regardless of the circumstances or the eventual outcome.”

It's a pretty strong statement. Here's the thinking behind the effort:

We get 30,000 emergency physicians to agree that "This is acceptable care. It may not be ideal in all circumstances, but it's not negligent.”

...Our legal system recognizes that a physician's practice will be deemed to be non-negligent if his or her treatment is "what the average physician, who is similarly trained, would do in a similar circumstance."

So if they get enough ER physicians to go on record in agreement with the statement they can, through solidarity and strength in numbers, sway the legal system.

I have mixed feelings about this effort. I hate seeing anything designated as “standard of care” because the whole notion is simplistic and it just gives more fuel to the trial lawyers. On the other hand, if the effort is successful, it will increase the bias against TPA among the very group of providers best positioned to use it effectively. To justify the option not to give TPA regardless of the circumstances is problematic. The findings of NINDS have been reproduced in other studies.

I've opined on TPA in some older posts. Here's my present take:

Strict adherence to exclusion criteria and usage protocol is essential.

Informed consent is important. You need to give patients and families the research data and current recommendations in plain English. This must include explicit information on mortality. That means explaining that the mortality effect is neutral and that this is due to some patients with more severe strokes having just enough improvement in their strokes to stay alive, counterbalanced by some patients dying by a direct effect of TPA induced cerebral bleeds. Families need to understand that some of those deaths may be in direct and dramatic proximity to the administration of TPA.

Consider excluding the very elderly who otherwise meet criteria.

The use of TPA in community hospitals will always be problematic until the system of designated stroke centers is much better developed than what we have now.

Putting aside the issue of TPA for ischemic stroke there's a broader perspective on this effort. While I may disagree with some opinions coming out of emergency medicine I admire their solidarity. Organized emergency medicine seems to recognize that its interests are not inherently conflicted with those of patients. So, it looks after its own. Emergency medicine, unlike hospital medicine, has several professional societies, each of which has put out numerous position statements addressing the professional interests of its members. These statements deal with issues ranging from compensation incentives to boundaries of clinical responsibility and avoidance of areas of liability. Organized hospital medicine has done none of that. In fact, they're doing just the opposite. I think that's a good topic for another post.

Press Ganey scores are meaningless

But hospitals keep using them despite the unintended consequences. This eye opening article in Emergency Physicians Monthly looks at the many flaws in Press Ganey methodology and reports survey data that reached some chilling conclusions about the unintended consequences of patient satisfaction surveys. Although this article is primarily about emergency room providers I believe its conclusions have some applicability to hospitalists. Here are some key points the article made:

The pressures to improve emergency department satisfaction scores may create a significant dilemma with emergency department staff. An online survey of 717 respondents performed by Emergency Physician’s Monthly on its medical blog “WhiteCoat’s Call Room” showed that more than 16% of medical professionals had their employment threatened by low patient satisfaction scores.

That's astounding. We all know these scores have little to do with how good a doctor you are.

Another question in the Emergency Physicians Monthly survey asked respondents to rate on a 1-10 scale how patient satisfaction scoring affects the amount of testing that they perform. Forty one percent of medical professionals decreased the amount of testing performed while 59% increased the amount of testing they performed due to the effect of patient satisfaction surveys. From a numerical standpoint, with “1” representing a “maximum decrease” in testing performed and “10” representing a “maximum increase” in the amount of testing performed due to effects of survey data, the change in amount of testing performed due to satisfaction data averaged a score of 6.3 – a mild increase.

That one's a little more difficult to interpret. Did docs understand that every possible answer on this question indicates an increase or decrease in testing, with a “5” indicating a slight decrease and a “6” indicating a slight increase? Whatever the case, with 717 respondents and some likely scatter in the results an average score of 6.3 raises concern that patient satisfaction surveys drive over testing. Unless you subscribe to Berwick's model of radical consumerism your treatment decisions should be based on evidence. This is the first data I've seen that addresses the influence of patient satisfaction surveys on adherence to evidence. In terms of over testing and over treating it's analogous to defensive medicine and certainly is an area that deserves further study.

Now here's the kicker:

In the Emergency Physician’s Monthly survey, 48% of health care providers reported altering medical treatment due to the potential for a negative report on a patient satisfaction survey, with 10% of those who altered treatment making changes were medically unnecessary 100% of the time. Examples of medically unnecessary treatment provided to improve satisfaction scores included performing unnecessary testing, prescribing medications that were not indicated, admitting patients to hospitals when they did not need hospital admission and writing work excuses that were not warranted. More importantly, 14% of survey respondents stated that they were aware of adverse patient outcomes that resulted from treatment rendered solely due to a concern with patient satisfaction surveys. These adverse outcomes included allergic reactions to unnecessary medications, resistant infections and clostridium difficile colitis from unnecessary antibiotic prescriptions, kidney damage from contrast dye, and medication overdoses.

Patient satisfaction has turned into a performance game. And according to this survey it's a game that wastes resources and could harm patients.

GruntDoc said:

I have No Idea why hospitals pay for this service, when they could do it themselves for a lot less moolah, have much higher data capture rates, and get actually usable data.

Monday, September 27, 2010

Anticoagulation for superficial vein thrombosis: NEJM reports important study and New York Times misses the boat as usual

First let's take a look at the study:

The efficacy and safety of anticoagulant treatment for patients with acute, symptomatic superficial-vein thrombosis in the legs, but without concomitant deep-vein thrombosis or symptomatic pulmonary embolism at presentation, have not been established.

...we assigned 3002 patients to receive either fondaparinux, administered subcutaneously at a dose of 2.5 mg once daily, or placebo for 45 days. The primary efficacy outcome was a composite of death from any cause or symptomatic pulmonary embolism, symptomatic deep-vein thrombosis, or symptomatic extension to the saphenofemoral junction or symptomatic recurrence of superficial-vein thrombosis at day 47.

The primary efficacy outcome occurred in 13 of 1502 patients (0.9%) in the fondaparinux group and 88 of 1500 patients (5.9%) in the placebo group (relative risk reduction with fondaparinux, 85%; 95% confidence interval [CI], 74 to 92; P less than 0.001). The incidence of each component of the primary efficacy outcome was significantly reduced in the fondaparinux group as compared with the placebo group, except for the outcome of death (0.1% in both groups). The rate of pulmonary embolism or deep-vein thrombosis was 85% lower in the fondaparinux group than in the placebo group (0.2% vs. 1.3%; 95% CI, 50 to 95; P less than 0.001).

The New York Times article, apparently echoing a related NEJM editorial in the same issue, criticized the authors for ignoring cost considerations. That's not entirely fair, because the authors of the paper raised the cost effectiveness red flag themselves by stating that the number needed to treat to prevent a major VTE was 88. You wouldn't even have to do the math to know that's pretty expensive.

But where the NYT article really blew it was in its total lack of perspective. A little background and a more in depth analysis of the study would have been helpful. According to the study findings the rate of progression to major VTE (DVT or PE) untreated was 1.3% at 47 days. That can be extrapolated to about 10% at one year---maybe a little less assuming that the risk wanes over time, but it's still quite a bit, and enough to be considered a state of extreme hypercoagulability by any standard. That finding shouldn't be surprising. Superficial vein thrombosis, when not caused by an IV catheter or varicose veins, is a known red flag for the hypercoagulable states that underly some forms of cancer and vasculitis.

One extremely important point the NYT piece ignored was that the NEJM study was not looking at therapeutic anticoagulation. The dose of fondaparinux used in the study, 2.5 mg daily, was the VTE prophylactic dose of fondaparinux. And the endpoints under discussion in this study are not resolution of the condition being addressed (superficial thrombosis) but prevention of more significant events. So in evaluating this study and comparing the results to what's already known it is important to recognize that this paper was an evaluation of VTE prophylaxis.

So from a cost effectiveness standpoint how does this use of fondaparinux stand up to other data on VTE prophylaxis? If you compare it with medical prophylaxis in hospitalized patients, it holds up quite well. Although pharmacologic VTE prophylaxis in hospitalized medical patients is widely accepted and emerging as a standard, the bang for the buck, when you look at published studies, is quite low. A large repository of studies on this topic can be found in the Chest guideline article on medical VTE prophylaxis. When examining this literature it is essential to note whether symptomatic or asymptomatic VTEs were reported. Symptomatic VTE represents the tip of the iceberg of the total VTE burden. The NEJM paper looked at only symptomatic events. Had they reported asymptomatic events based on screening via compression ultrasound or venography, as many prophylaxis studies have done, the baseline risk would have been much higher. The number needed to treat would have been substantially lower. That would have made the cost effectiveness analysis much more favorable. It's almost certain that the cost to prevent one event using such data would be below $50,000, which is the threshold for cost effectiveness by the usual analysis.

The essential question raised by this analysis is whether asymptomatic DVT is an “outcome that matters.” After all, it's more of a surrogate endpoint than a clinical one. If asymptomatic DVT is not an outcome that matters then you have to go back and question much of the vast literature that's been cited by guideline authors, not to mention guidelines themselves which recommend VTE prophylaxis in hospitalized patients.

For example, in this meta-analysis from Annals of Internal Medicine looking at VTE prophylaxis in medical patients the number needed to treat to prevent one symptomatic DVT was 233. And these were higher risk patients, with all 9 studies looking at select groups, and most studying patients that corresponded to those recommended for prophylaxis in current guidelines. Well, that doesn't make the NNT of 88 look so bad, does it?

Why did the New York Times leave this information out? The cynical side of me would say they wanted to frame this as a case of disease mongering by the pharmaceutical industry, but I'll give them the benefit of the doubt. It's probably more a matter of ignorance and sloppy reporting, as evidenced by their failure to take into account any of the background I've cited above.

A final point bears mention. The NEJM study provides information that can change practice without escalating costs because low molecular weight heparin (Lovenox) has gone generic. You wouldn't be on thin ice to extrapolate the study findings regarding fondaparanux to other pharmacologic agents for VTE prophylaxis, since studies of multiple agents have yielded only minor differences.

DB, who blogged about this study Friday, had a somewhat different take. He wonders whether insurance companies will pay for this treatment. He hopes they don't. The people who make these decisions for insurance companies, like the Obamacare czars, are somewhat challenged when it comes to interpreting clinical studies so who knows what they'll decide. But I think there are more things to consider than whether they'll pay for 45 days of Arixtra. If they don't, many patients can probably afford generic Lovenox out of pocket. And what about 5 days or so of Arixtra or a low molecular weight heparin followed by six to twelve weeks of warfarin? That alternative is plausible and deserves future study.

What's the latest excuse for introducing woo into hospitals?

The reduction of health disparities.

And, despite this disingenuous disclaimer at the end of the article---

The inclusion of an innovation in the Innovations Exchange does not constitute or imply an endorsement by the U.S. Department of Health and Human Services, the Agency for Healthcare Research and Quality, or Westat of the innovation or of the submitter or developer of the innovation.

---it is, from all appearances, being endorsed by the AHRQ. Just look at the introductory paragraph:

The following is a profile of a practice innovation presented by The Health Care Innovations Exchange (HCIE) from the US Agency for Healthcare Research and Quality (AHRQ). HCIE is a comprehensive program designed to accelerate the development and adoption of innovations in healthcare delivery. It aims to increase awareness of innovative strategies and activities among health care providers in a timely manner. This program supports the agency's mission to improve the safety, effectiveness, patient-centeredness, timeliness, efficiency, and equity of care -- with a particular emphasis on reducing disparities in health care and health among racial, ethnic, and socioeconomic groups.

So what kind of woo is being promoted? It's the use of shamans for Hmong patients when they or their families request their presence at Mercy Medical Center Merced, an acute care hospital in Merced, California.

So what's the big deal? Anyone's free to visit a patient, right? Right. And you wouldn't prohibit a patient's Hmong spiritual advisor or healer from visiting anymore than you would prohibit a Catholic priest or a Baptist minister from visiting, would you? Of course not. But this program is different. The shamans become members of the hospital staff. They are given hospital badges. They perform healing rituals based on their own pseudoscientific traditional medical principles. The ceremonies are even approved by the medical center!

Approved ceremonies. The medical center has preapproved 9 ceremonies that can be conducted in the patient's hospital room, emergency department, or preoperative unit. The ceremonies are brief, quiet and do not require a private environment.

Even worse, the shamans periodically “educate” physicians about their pseudoscientific traditional methods. A shaman even serves on the hospital advisory board.

But thank goodness for this (my italics):

Hmong shamans receive a 40-hour intensive orientation on Western medicine where they learn about Western biomedical practices, germ theory, and disease symptomatology;

So if the shamans buy into this Western notion of germ theory maybe they'll at least wash their hands.

And what level of evidence backs up this AHRQ program? A few anecdotes:

Anecdotal reports suggest the program has reduced cultural conflicts and miscommunications between Hmong patients and physicians, and increased Hmong support of Western medicine, physician acceptance of traditional medicine, and satisfaction among Hmong patients.

And what was the anecdotal evidence that the shamanistic rituals were effective?

The concept for the shaman program stemmed from an incident in 1996, when a prominent 55-year old Hmong businessman with gastrointestinal problems refused surgery because of cultural and linguistic communication difficulties between his extended family and his physicians. This patient postponed medical care until all of his body systems failed; many Hmong gathered outside of the patient's room and requested that a shaman perform traditional healing ceremonies and blessings. These community members ultimately succeeded and the ceremonies were performed. While physicians had no hope that this man would survive, he did, which had a powerful impact on hospital administrators and providers regarding the potency of traditional medicine.

Well, so much for evidence based medicine at AHRQ!

Medicine must address cultural disparities. There are many ways this can be done without promoting and adopting pseudoscientific woo. Adopting shamanistic rituals in US hospitals to address cultural disparity may fit right in with Donald Berwick's notion of patient centered care. I contend that it's disingenuous, unethical, and undermines the scientific integrity of mainstream institutions. Were this nutty idea to be applied consistently across all the cultures represented by our patients, American health care systems would have to abandon their scientific foundations and become institutions of the eclectic healing arts.

It's just the latest pretext (and, unfortunately, a very politically correct one) for the abandonment of science based medicine.

What does the latest AP poll on Obamacare mean?

Maybe that the Republicans need to be careful how they frame the debate. But it's difficult to tell from the scattered news reports and blogs I've found. The big picture is that Obama's job approval is low (nothing new there) and that folks tend to be opposed to Obamacare. But not always for the reasons you might think. Here's where the devil's in the details. Again, you might have to read between the lines of these reports.

A report from The Hill reflects the popular spin:

Voters who say the new health reform law was too conservative outnumber by 2 to 1 those supporting repeal, according to a poll released Saturday.
About 40 percent of respondents said the law was too timid in overhauling the nation's healthcare system, while 20 percent said they'd like to see it scrapped...
Among the other key findings:
30 percent of respondents said they support the legislation; 40 percent oppose it; and the remaining 30 percent declined to weigh in one way or the other.

This ABC News report offers a little more detail (my italics):

The poll found that about four in 10 adults think the new law did not go far enough to change the health care system, regardless of whether they support the law, oppose it or remain neutral. On the other side, about one in five say they oppose the law because they think the federal government should not be involved in health care at all.

So if that last phrase in any way reflects the wording of the question, what's really surprising about this survey is that so many respondents (20%) don't think the government should be involved in health care at all.

What about the 40% who thought the law should have done more? What more would they want done? I'm sure there would be a spectrum of opinions with the more left leaning among them wishing we had passed single payer. That wouldn't fly right now, as our culture and our economy wouldn't tolerate it. But Marcia Angell, a senior lecturer in the department of social medicine at Harvard and one who opposes Obamacare in favor of a single payer system, expressed a different idea in a recent interview with Martin Samuels. She thinks we should gradually implement a single payer system by just lowering the Medicare age a few years every decade. On its face the idea has some appeal. It's simple and clean in concept. Its gradual implementation would help ease the shock. It would allow time to allow all those nifty cost saving ideas about integrated care and the efficiencies of the EMR to come to fruition. I remain skeptical.

For another take on the poll and an interesting comment thread see this post from Wesley Smith's blog.

Friday, September 24, 2010

Obamacare will bend the cost curve

---but in the wrong direction. That's why the Republicans have released their Top 6 reasons to repeal.

Via Gateway Pundit.

STEMI versus NSTEMI---meaningless distinction??

Brendan Phibbs, ever the towering intellect and still in possession of a steel trap mind at over 90 years of age, continues to contribute to the medical literature. His latest paper, in the July 2010 issue of Annals of Noninvasive Electrocardiography, is quite remarkable. It is titled Differential Classification of Acute Myocardial Infarction into ST- and Non-ST Segment Elevation Is Not Valid or Rational. Phibbs is being true to form. Never one for weasel words, he makes strong declarative statements. I don't have access to the full text of the paper, but let's look at the abstract:

Background: The distinction between ST elevation and nonST elevation infarcts is widely accepted and is employed as a guide to management...

Finding: The pathology of the two subsets is identical as are the morbidity, mortality and clinical course. Non-ST elevation infarcts are likely to be subsequent, to occur in older patients and to involve the circumflex artery: this subset therefore includes a high-risk group. ST deviation in any part of the electric field of the heart will predictably be accompanied by reciprocal deviation if the entire field of the heart is mapped. Further, ST deviation of infarction is often transient, resolving in minutes so that infarcts will be predictably misclassified. ST deviation per se is therefore not a rational basis for classification of infarcts. In fact, invasive therapy is indicated in both subsets with identical results.

Conclusion: The distinction between ST elevation and non-ST elevation infarcts is baseless. The high risk subgroup included in the non-ST elevation infarct set should not be denied the benefit of early invasive therapy.

So here's what he's saying: In his review of the world's literature, clinical and pathological correlations do not support a meaningful electrocardiographic distinction between STEMI and NSTEMI. At first that seems counterintuitive but as I think about it I can think of several explanations for why the distinction would be artificial. He's not arguing that there's no such thing as a STEMI or a NSTEMI (after all, some MI patients have ST elevations and some don't), but that the distinction is not clinically or pathologically meaningful. There might be a number of reasons.

First, many circumflex occlusions (epicardial coronary artery occlusion was long believed to be the pathologic correlate of STEMI) are associated with no or subtle ST elevation. Second, the presence or absence of ST elevation often depends on time to presentation with ST segments elevated one minute and isoelectric the next in the same patient, or vice versa, reflecting the unstable coronary plaque in a dynamic state of thrombosis and lysis. Third, there are several known “STEMI equivalents” which represent acute coronary occlusion without ST elevation, such as “true posterior” infarctions and hyperacute T wave infarctions seen in the very early stages of coronary occlusion. Finally, certain conditions which displace the ST segments such as bundle branch block and left ventricular strain may play “tug-o-war on the stylus” and mask ST elevation.

So do ST segment elevations have meaning at all? Of course. They are the most powerful initial diagnostic finding in acute MI. Often they help localize the culprit lesion and predict outcome. But if the distinction is meaningless how does one know whether to send the patient to the cath lab? In Phibbs' line of reasoning, absent contraindications, all patients with acute MI should go promptly to the cath lab. But in the real world it's usually only the ones who declare their diagnosis at the door who are eligible---and who are those patients? The ones with ST segment elevation! So is this paper of any practical importance? Maybe, in that it informs us that we should not be so rigid in our categorization. Furthermore, some patients without ST segment elevation but with a strong clinical picture or early biomarker elevation should be sent to the lab (remember what Grunt Doc did).

I think the distinction between STEMI and NSTEMI will persist for a while, just out of convenience. After all, once Phibbs' view gains traction it will open up a can of worms. The guidelines, which now lump NSTEMI with unstable angina, will have to be reorganized.

But I have a feeling it will eventually gain traction, because I think Phibbs is right. We wrestled with Phibbs in the area of electrocardiographic classification of MI once before and he won. In 1999 he published a paper demonstrating that the distinction between Q wave and non Q wave MI was meaningless. That view was not immediately accepted either, and Phibbs published several more papers on the subject over the next several years, until the concept of Q wave versus non Q wave infarction became obsolete. R.I.P.

Are state medical board panels qualified to make judgments about opiate prescribing?

This survey suggests that biases and beliefs more than expertise influence board members' attitudes.

Lactic acidosis

Among hospitalist, critical care, nephrology and emergency medicine circles I frequent this is a subject of some confusion as to how to treat. This review from The Journal of Hospital Medicine may offer some help.

Points of interest:

In hypoperfusion states lactic acidosis may be adaptive.

Not only metformin but linezolid can cause lactic acidosis.

Lactic acidosis is powerfully associated with bad outcomes but it is the underlying condition rather than the lactate itself which produces the bad outcome.

What about bicarb administration? In general, although there are exceptions, the literature does not support its use. There are theoretical harmful effects: intracellular acidosis, the Bohr effect (making hemoglobin stingy) and decreased ionized calcium (negative inotropy).

Bicarb therapy and hemodialysis have been generally recommended in cases of metformin toxicity. Special situations such as salicylism and TCA overdose, in which bicarb therapy is strongly recommended, were not addressed in the review even though lactic acidosis may be an accompanyment.

Thursday, September 23, 2010

Unintended consequences of Obamacare come to light

Nancy Pelosi said we'd find out what this bill would do after passage.

Via Gateway Pundit.

More on the new CPR (CCR) from the 36th Annual Tutorials in the Tetons Update in Cardiovascular Disease

I'm usually a strong advocate for guideline based care. Almost all the studies I've examined on the effects of guideline adherence show outcomes to be improved. There's one notable exception: the AHA guidelines for CPR and emergency cardiac care. Dr. Ewy spoke at the 2010 Tutorials on this topic and I mentioned his talk briefly here.

Many folks are familiar with Ewy's recommendations for chest compression only bystander CPR which has been more widely adopted since publication of the AHA Science Advisory allowing it as an option for out of hospital cardiac arrest.

Less well known, and thus far adopted in portions of only three states, is Ewy's protocol for ACLS. This paper in Current Opinion in Cardiology summarizes the protocol. It applies to adult patients with out of hospital cardiac arrest (not pediatric or suspected respiratory arrest) who are believed to be in the circulatory phase (down for greater than 5 minutes). It features no rescue breathing, intubation delayed until at least three CPR cycles and use of the AED only after 200 compressions.

The protocol has yielded rates of survival to hospital discharge of almost 40%. Rates for patients treated according to the 2005 guidelines have been much lower, on the order of 20-25%. Using statistics on the number of out of hospital cardiac arrests in the US and the improved survival rates using his protocol Dr. Ewy did a little math and estimated that 63,000 lives could be saved each year in America by implementing the changes.

Ewy briefly mentioned post resuscitation care, specifically the post resuscitation bundle which includes therapeutic hypothermia and early cardiac catheterization (within 24 hours), even during coma while the patient is being cooled and even in patients lacking classic electrocardiographic findings of STEMI. In some communities fire departments are diverting codes to hospitals that employ the bundle even when it involves some delay in getting them there.

So what do the new protocols mean for the hospitalist? In-hospital arrests are different and Ewy's protocol changes may not be as applicable. First, many in-hospital arrests, at least those in the ER and the ICU, can be treated in the electrical phase (first 5 minutes) during which time prompt defibrillation remains paramount, just as recommended in the guidelines. Second, the epidemiology of arrests in the hospital is different, with more codes being respiratory codes, in which Ewy's protocol does not apply.

The new ACLS guidelines are due out very soon. What will they look like? It's hard to say, although historically they have stayed years behind the best resuscitation science.

CPOE, medical ethics, patient safety

Read this post. Just read it. 'Nuff said.

Dabigatran a slam dunk in FDA advisory panel

From Medscape:

Barring any unforeseen damning revelations about the drug, the FDA's approval of the oral thrombin inhibitor dabigatran (Pradaxa, Boehringer Ingelheim) for stroke prevention in atrial fibrillation (AF) is all but certain.

Does that mean warfarin genotyping will be ready for prime time no sooner than it becomes obsolete? I doubt it. Dabigatran will only be approved for stroke prevention in atrial fibrillation. It may be years before it's validated for treatment of VTE.

Consumers want more care, not necessarily evidence based care

--according to this Health Affairs report.

Which is why Berwick's notion of patient-centered care is incompatible with Obamacare and why single payer care would never fly in the U.S.

Wednesday, September 22, 2010

Hospital management of acute decompensated heart failure---odds and ends from the Tutorials in the Tetons 36th Annual Update in Cardiovascular Disease

I know this is a little late to be blogging on a session which was held August 14. This topic was too complex and nuanced to live blog or tweet, and life has been very busy since my return home from this meeting. Besides that I needed time to go and check out some primary sources.

Anyway, on August 14 John O'Connell, MD, executive director of the heart failure program at St. Joseph's Heart and Vascular Institute in Atlanta discussed some recent evidence on acute decompensated heart failure (ADHF).

First an observation of my own. Speakers on this topic are fond of saying that, in contrast to the long term management of heart failure, there's practically no evidence to guide us in the management of ADHF. Although that's not entirely true (see here and here) the recommendations for ADHF in the 2009 Focused Update for the ACCF/AHA heart failure guidelines are based largely on expert opinion (level C). 76% of the recommendations were level C, 19% were level B (single small RCT) and only 5% are considered based on high level evidence (level A).

According to Dr. O'Connell's update there has been little in the way of new evidence to change practice, as most recent trial results in ADHF have been negative or inconclusive.

Here are some highlights:

ASCEND HF, underway now and estimated to be completed at the end of this year, is a large RCT of nesiritide versus placebo, both alongside standard heart failure treatment. Major clinical outcomes will be recorded and it is hoped that this will put to rest the controversy that has surrounded nesiritide the last several years.

In EVEREST (reported in these two papers) several soft short term outcomes but not major clinical outcomes (mortality or heart failure related morbidity) were improved by the vasopressin antagonist tolvaptan. Accordingly, the FDA has approved it only for euvolemic hyponatremia.

The use of loop diuretics, though tried and true in the management of ADHF, is supported mainly by tradition and expert opinion. Two studies reported this year compared dosing strategies (comparative effectiveness studies, get that?!). This study found no difference in short term outcomes between bolus and continuous infusion dosing at equivalent doses of furosemide. DOSE, looking at high dose versus low dose furosemide both in continuous and bolus dosing forms, presented at ACC 2010, found no difference in the primary outcome which was a global clinical assessment. Secondary endpoints in the high dose group (dyspnea, fluid loss and biomarker levels) were improved at 72 hours at the price of more renal deterioration but that was transient. All in all there seems to be little difference in dosing strategies and we may have little to guide us that's any better than Samuel Shem's rule: Lasix dose=age+BUN or the old adage that we give the patient “enough.”

Dr. O'Connell reminded the audience that loop diuretics have some negative consequences. At the same time a brisk diuresis ensues an acute fall in GFR occurs. However, the relationship between diuresis and worsening renal function, as well as the pathophysiology of the cardiorenal syndrome, are complex. One fascinating paper he cited from last year sought to determine the factors causing decreased renal function during diuresis for acute heart failure. Only high CVP readings at the beginning and end of hospital treatment predicted worsening renal function. So venous congestion in the kidney may be more important than decreased cardiac output. To the extent this is true one would expect better renal outcomes with more aggressive fluid removal.

A related issue is the use of ultrafiltration (UF) in the treatment of ADHF. The UNLOAD trial (a comparative effectiveness study conducted before comparative effectiveness research was a catch phrase) showed superiority of ultrafiltration over standard loop diuretic therapy for weight loss, net fluid removal and 90 day readmissions. Why? There are several likely reasons. UF addresses refractoriness to loop diuretics. A diuretic holiday allows reversal of renal epithelial cell changes induced by the loop diuretic. Also, loop diuretics remove approximately one third normal saline, as observation of the common appearance of “lasix urine” will attest. UF on the other hand removes isotonic fluid.

Dr. O'Connell concluded his talk and commented in the Q&A on the vexing problem of readmissions. He expressed some reservations when I asked him specifically about the effects of the hospitalist model. He listed some key objectives to be met in every ADHF admission:

1) Achieve adequate fluid removal---in other words, completely decongest the patient. Many heart failure patients are discharged before this is accomplished.
2) Initiate life prolonging neurohumoral antagonists.
3) Assess the patient for candidacy for evidence based invasive therapies such as device or revascularization therapies.
4) Educate the patient.
5) Arrange for continuity with post hospital care. Initiation of neurohumoral antagonists is not enough. They need to be sequentially added and titrated to evidence based goals in a timely manner, and this is primarily done in the out patient setting.

The hospitalist model, with its fragmentation of care and its agenda to discharge patients more quickly, may be adverse to goals 1, 3 and 5.

The Paul Levy controversy is about to heat up---again

A Massachusetts health care union and the NOW are raising a stink. They are launching a media campaign and plan to demonstrate at BIDMC's annual board meeting tomorrow. They have leveled numerous allegations that go beyond Levy's inappropriate relationship with a female subordinate, implying abuses of the CEO position and lack of accountability of the office.

It's hard to form opinions without more information about what really happened, but as this plays out on the national stage there may be forthcoming lessons regarding accountability of hospital CEOs.

First Annual International Pain Summit reemphasizes the 5th vital sign

---and several other provisions:

In its “Declaration that Access to Pain Management is a Fundamental Human Right,” delegates to the inaugural International Pain Summit proposed that all people:

1. Have a right to the access to pain management without discrimination.
2. Have a right to be both informed about how their pain can be assessed through the recording of a fifth vital sign, and informed about the possibilities for treatment.
3. Have a right to access an appropriate range of effective pain management strategies supported by policies and procedures appropriate for the particular setting of health care and the health professionals employing them.
4. Have a right to access appropriate medicines, including but not limited to opioids, and to access health professionals skilled in the use of such medicines.
5. Have a right to assessment and treatment by an appropriately educated and trained interdisciplinary team at all levels of care.
6. Have the right to a health policy framework that, in governing pain relief treatment in the social, economic and regulatory environment, is compassionate, empathetic and well-informed.
7. Have a right to access best-practice, non-medication methods of pain management (ranging from relaxation and physiotherapy methods to more complex cognitive behavioral treatment) and to specialist-performed interventional methods, depending upon resources of the country.
8. Have a right to be recognized as having a disease entity, requiring access to management akin to other chronic diseases.

Additionally, the declaration proposes that:

1. Healthcare professionals have an obligation to offer a patient in pain the management that would be offered by a reasonably careful and competent healthcare professional.
2. Governments and all healthcare institutions establish laws, policies and systems that will help promote — not inhibit — access to pain management.

When the nurse calls and says a patient's BP is 70/50 I know I have to drop what I'm doing and go attend to that patient immediately, because that patient is in trouble. When the nurse calls and says a patient is voicing “ten out of ten pain” the same onus is on me, but the patient may or may not be in any distress. We all use the numeric pain scale because Joint Commission and our institutional policies say we have too, but at the same time we know (most of us, anyway) that the scale is subjective and, in most cases, meaningless.

This initiative, with apologies to Yogi Berra, is Déjà vu all over again. A pain management movement of sorts gained traction in the US around 1999 with the recognition that we weren't treating pain well. Unfortunately the corrective efforts that ensued were driven more by public pressure than science, and the “education” delivered to doctors was about 80% dogma-based medicine.

The unintended consequences have since been realized. Epidemiologic and research evidence has uncovered patient deaths attributable to the changes in pain treatment strategies.

We need to be constantly looking for better ways to treat pain but it needs to be driven by science, not activism. With this new initiative I'm concerned we may be exacerbating this decade old safety problem just when we were beginning to get a handle on it.

This is one of those rare instances when I'm going to have to disagree with Wesley Smith, who alerted me to the pain summit. I think I know where he's coming from---consistently adequate pain control for patients with advanced illnesses might lower the demand for assisted suicide and euthanasia. I am in sympathy with that view, but there have to be better ways of fixing the problem.

Tuesday, September 21, 2010

And the winner is---Medscape

Here are the top five medical sites doctors visit, according to a survey, in descending order:







A while back I talked about pseudohypercreatininemia. Far less common but better known is pseudohyperkalemia, the subject of two posts at Renal Fellow Network and this recent review. Pseudohyperkalemia is a falsely high potassium reading that occurs in patients with extreme thrombocytosis or in leukemic patients with very high white blood cell counts. I was always taught that it was caused by cells being trapped in the clot after the blood was introduced into the tube. The resulting lysis of the unusually large number of cells released more potassium into the serum. The work around, when this was suspected, was to obtain a plasma sample.

According to these articles that's not the only mechanism. It seems leukemic cells are fragile and trauma during transport to the lab (e.g. via pneumatic tubes) may play a role. The solution? Hand carry the specimen to the lab.

What malpractice risks do hospitalists face?

Ten plus years into the hospitalist movement a data base is accumulating and we're finally seeing some patterns. Here are a few high risk situations noted from a recent article in Today's Hospitalist:

Opiate poisoning, especially with dilaudid.

Comanagement situations if it's not explicitly defined who's responsible for what.

Transitions---ER to ward, ward to OR, OR to ward, etc.

Just being there, as the article explains:

Hospitalists worry that attorneys will take a "scattershot" approach and name everyone on the chart. Is that what you're seeing?

That does happen, at least initially, and there's not much we can do about it. Plaintiff attorneys are going to name everyone they see in the record.

Old rock stars re-lyricing

Bobby Darin: Splish-splash, I Was Havin' a Flash!

Herman's Hermits: Mrs. Brown, You've Got a Lovely Walker!

Ringo Starr: I Get By With a Little Help From Depends!

Hilarious. Read the rest.

NDM-1: a plasmid transmitted gene that codes for a new carbapenemase

Medscape video here.

Monday, September 20, 2010

Martin Samuels launches Lighthouse Learning and the spin cycle begins

Martin Samuels is helping start a new CME company. That fact by itself is interesting enough. Samuels is more than a popular speaker; he's one of medicine's great teachers.

But because Lighthouse Learning intends to provide its content without any support from the pharmaceutical industry Daniel Carlat has taken an opportunity to apply a bit of spin : Harvard's Top Neurologist Just Says “No” to Commercial CME. In his post Carlat talks around the issue a great deal but seems to imply the Samuels, former medical director of a provider of industry supported CME, has had some sort of an epiphany and joined the ranks of the pharmascolds although there's no direct evidence that it's true. Samuels, for example, is on the editorial board and serves as a frequent host for the industry supported medical education provider ReachMD. If he's had such an epiphany you'd expect him to resign from that company but he hasn't, at least not yet, because he's hosting a program there today.

Meanwhile the Boston Globe has covered it here, Medical Marketing and Media here and Thomas Sullivan here. The Medical Marketing and Media post quotes Samuels' partner in the new enterprise, Joe Leibowitz:

“We believe there is a good degree of cynicism in the marketplace and that it's time for the presentation of a new fresh model, one that is free from commercial and industry support,” Jon Leibowitz, president and CEO of the new organization, told MM&M.

If the quote is accurate it's an extreme example of an argumentum ad populum (extreme because cynicism, as opposed to skepticism, seeks to knock things down without regard to facts). But the assumptions here regarding popular belief may not be accurate. For example, the Globe quotes Samuels as saying that doctors have lost confidence in supported CME.

Although that's widely believed in some circles, research evidence overwhelmingly says the opposite.

Dr. Carlat thinks he understands Samuels' motives in starting Lighthouse Learning (well, he is a psychiatrist) and offers his interpretation. But maybe Samuels just thinks that if docs have lost confidence in supported CME they'll go for his product. For-pay CME can be a profitable enterprise. Just ask the folks at UptoDate.

I'm anxious to see what Lighthouse Learning will offer. With Samuels behind it I know it'll be good. He seems to be assembling an all star cast, so it will probably be very expensive. One of the non-evidence based but very popular beliefs in the CME funding debate is that for some lofty reason doctors “should” pay for their own CME.

When it comes to non-industry supported offerings, if they're any good at all, you pay a lot. Again, just look at UptoDate. Because most doctors have to be mindful of their budgets (as do the medical groups that provide their CME stipends) therein lies an unintended consequence: if industry support goes away entirely, doctors' CME choices will be limited.

Long term functional outcomes and quality of life after critical illness

---were poor in this study. Long term cognitive and physical rehab will assume increasing importance in these patients.

Long term cognitive impairment after critical illness

---was common in this study---71% at 12 months (!)---and delirium duration was predictive.

How does dialysis work?

Here's an interesting YouTube presentation at PascaleLane's Stream of Thought.

Can you avoid ESRD by how you eat?

I don't know, and I can't validate this, but here's an embedded booklet posted by Uremic Frost.

Genetic disorders causing hypertension

Liddle's syndrome, Gordon's syndrome and others. Via Renal Fellow Network.

There's no alternative medicine

---says George Lundberg.

Yeah, I know, there's only medicine that's been proven to work and that which hasn't. Well, Lundberg actually talks about three categories:

But actually there are three piles:

You have a test or treatment that has itself been tested and found to be safe and effective. Use it; pay for it.

You have a test or treatment that has been found to be unsafe or ineffective. Don’t use it; don’t pay for it.

You have a test or treatment that is scientifically plausible, meaning not preposterous. Test it and then put it into one of the other two piles.

But what about the fourth category, which is scientifically implausible claims? What do you do with nutty ideas? Well, if you're the NCCAM, study 'em. But that phony “research” has done nothing but fuel the growing industry of quackademic medicine.

Sunday, September 19, 2010

Old Mevacor commercial

Back before we had direct to consumer advertising the drug companies ran ads for doctors, mainly on Lifetime Medical Television. This one for Mevacor (nowadays a $4 generic) was probably from LMT.

In those days, as reflected in the ad, statins were only approved to treat hypercholesterolemia, not ACS or atherosclerosis.

Friday, September 17, 2010

The FDA is strengthening its labeling about gadolinium based contrast agents

---concerning the risk of nephrogenic systemic fibrosis. Via MedPage Today.

Patients have inflated expectations of elective PCI

From the Annals of Internal Medicine:

Almost three quarters of patients thought that without PCI, they would probably have MI within 5 years, and 88% believed that PCI would reduce risk for MI. Patients were more likely than physicians to believe that PCI would prevent MI (prevalence ratio, 4.25 [95% CI, 2.31 to 7.79]) or fatal MI (prevalence ratio, 4.83 [CI, 2.23 to 10.46])...

Conclusion: Cardiologists' beliefs about PCI reflect trial results, but patients' beliefs do not. Discussions with patients before PCI should better explain anticipated benefits.

Somebody needs to spend more time talking with patients.

COPD exacerbations impact overall course of disease

---in several ways according to this article.

One underappreciated but well documented point made in the paper is that acute pulmonary function declines associated with exacerbations tend to persist long after the infection or other precipitant clears, with some patients requiring weeks to return to baseline lung function. Thus it's easy to imagine how frequent exacerbations, each occurring before full recovery from the last one, can accelerate the patient's overall decline.

Is there a “profile” for initial presentation of CA-MRSA pneumonia?

Not really, in this study:

Results: Fifteen patients with CA-MRSA CAP were identified during the 28-month period. Only one of the 14 patients tested had evidence of preceding influenza, and no seasonal pattern was seen. Seven patients were never admitted to the ICU. Eight of 14 with chest CT scans had evidence of lung necrosis. Nine of 15 had evidence of pleural effusions early in their hospital course, and five of nine required at least one pleural drainage procedure. Seven of 15 were immunocompromised (three HIV, one acute lymphocytic leukemia [ALL], one high-dose steroids, and two immunoglobulin deficiency) with an additional three patients with diabetes. Mortality was only 13% (two of 15); both deaths occurred in patients with severe immunocompromise (ALL post chemotherapy and AIDS). Fourteen of 15 patients were treated with antimicrobials that inhibit exotoxin production (clindamycin or linezolid).

Conclusions: CA-MRSA pneumonia is not necessarily a post-influenza infection. Despite necrotizing features in many, the mortality of CA-MRSA pneumonia in our series is lower than previously reported, and patients do not routinely require ICU care. Treatment with antibiotics that inhibit exotoxin production and/or nontoxigenic strains may explain this improved outcome.

Apparently CT was useful in identifying a necrotizing process in some patients, but when it comes to seasonality, post-influenza status and the usual risk factors all bets were off in this study.

Where do we stray from best evidence in the tretment of COPD exacerbations?

In three areas according to this Today's Hospitalist article:

Using IV steroids over PO; using quinolones over macrolids; and delays in starting antibiotics.

Thursday, September 16, 2010

Berwick dances around all sides of issues

From the Washington Post:

The nation's health system can't be transformed by rationing medical care, President Barack Obama's new Medicare chief said Monday in his first major speech.

So we should “ration with out eyes open” but the health system “can't be transformed” by rationing. Bob Wachter was right when he said that Berwick was intellectually nimble.


Berwick broke his silence Monday, telling an audience of health insurance industry representatives that pushing back against unsustainable costs cannot and should not involve "withholding from us, or our neighbors, any care that helps" or "harming a hair on any patient's head."

If only it were possible. Pure Kool-Aid.

H/T to Secondhand Smoke.

Might comparative effectiveness research lead to more expensive care?

This is purely tongue in cheek. I say tongue in cheek because it's based on this newspaper article which provides insufficient substance or background to really understand the research findings, and I haven't been able to find the primary source or a more reliable source. It purports that new comparative effectiveness research proves CABG to be superior to stenting in terms of mortality and major events. But it's sloppy. This statement was a red flag:

The new study, reported Sunday at a Geneva meeting of the European Association for Cardio-Thoracic Surgery, is the first large trial to compare stenting and coronary-artery bypass grafts directly.

No it's not! Sloppy, sloppy, sloppy.

That's why this is tongue in cheek, but suppose, for the sake of discussion, that it's true. If so it's an example of CER validating more expensive care, which leads Wesley Smith to ask:

This raises an interesting question. Bypass surgery is much more expensive than putting in stents. Would the Obamacare cost/benefit panels strongly recommend to cardiologists that they perform more bypass surgeries based on the evidence that it saves more lives, even though the cost is exponentially higher? To be consistent, they should. But I doubt they would.

The popular belief is that CER will lead to better and cheaper care. Is cheaper really better, or even as good? Sometimes it is, sometimes it isn't. In the aggregate, nobody knows. But the Obamacare policy wonks have an agenda to leverage CER, and the interpretation of CER's findings, for cheaper care, so Smith has a point here.

Wednesday, September 15, 2010

Non-evidence based conventional medicine, woo, and Donald Berwick

If you have any interest on this topic, which I covered in a post on Friday, by all means read the comment thread, which is more interesting than the post itself.

It all started with
Kimball Atwood's Health Care Renewal post criticizing the infiltration of woo into purportedly scientific mainstream institutions (like the Institute of Medicine) and its promotion by thought leaders, particularly CMS chief Donald Berwick.

Shannon Brownlee posted a
critical response. At the risk of oversimplification, her point was that it was silly to fret over harmless alternative medicine when there's plenty of conventional medicine (note her inappropriate use of the anachronistic and derisive term “allopathic”) that's not based on best evidence. It was a red herring, beside the point of Atwood's post, but I got sucked into a long back-and-forth anyway, about what's wrong with conventional medicine and why. Although some of her examples of unscientific conventional medicine were factually incorrect (I was able to think of better examples than she was!) we were able to agree that a significant problem exists. I have blogged critically many times about poor adherence to evidence in the house of conventional medicine. It's a complex, multidimensional problem. It has no easy fix. Woo, on the other hand, has an easy fix: we can just say no to nutty ideas. That need not distract in any way from the tougher, more complex problems of inappropriate care in conventional medicine.

For obesity related CKD

---otherwise known, apparently, as obesity related glomerulopathy (ORG), weight loss may help. H/T to Uremic Frost.

Med school is not always smooth sailing

22% reported experiencing a life crisis in this survey.

Should you get an ID consult on every patient with Staph aureus bacteremia?

From a new study:

Infectious diseases consultation was associated with a 56% reduction in 28-day mortality (adjusted hazard ratio, 0.44; 95% CI, 0.22-0.89).

I would not advocate for a rigid rule, but what this study and others with similar findings reflects is that in the treatment of Staph aureus bacteremia there are process issues and nuances in antibiotic treatment that are not well known among generalists.

Elevated hair cortisol levels as an indicator of chronic stress as a risk factor for myocardial infarction

From the journal Stress:

We aimed to evaluate the hypothesis that chronic stress, as assessed by hair cortisol content, is associated with the development of AMI. A prospective case–control study included 56 patients admitted to hospital with AMI and 56 control patients, admitted to internal medicine wards for other indications. An enzyme immunoassay technique was used to measure cortisol in the most proximal 3 cm of hair, considered to represent the most recent 3 months of exposure. Median hair cortisol contents (range) were 295.3 (105.4–809.3)ng/g in AMI patients and 224.9 (76.58–949.9)ng/g in controls (p = 0.006, Mann–Whitney U-test). After controlling for other risk factors for AMI using multiple logistic regression, log-transformed hair cortisol content remained the strongest predictor (OR 17.4, 95% CI 2.15–140.5; p = 0.007). We demonstrated elevated hair cortisol concentrations in patients with AMI. This suggests that chronic stress, as assessed by increased hair cortisol in the 3 months prior to the event, may be a contributing factor for AMI.

Short term stress in the form of extreme fright or acute emotional upheaval has been well established as a cause of acute cardiac disease mediated by catecholamine myocardial injury, manifested clinically as sudden cardiac death and Takotsubo cardiomyopathy, and histopathologically as contraction band necrosis. Suspected but less well established is the role of short term stress in acute myocardial infarction.

Even more speculative has been the role of chronic stress, which may take such forms as vigilance, depression or chronic anxiety, in myocardial infarction. The suspected role of cortisol was based on sound pathophysiologic rationale but direct evidence to support such a role was lacking. This study makes an important contribution. I'll have more to say about this in future posts about stress and cardiovascular disease in connection with my recent attendance at this meeting.

Tuesday, September 14, 2010

Causes of hypercalcemia

Concept map via Nephron Power.

Long term psychological stress and cardiovascular risk

We have pretty good evidence for the influence of short term stress (fright, acute emotional surge) on sudden cardiac death with contraction band necrosis, Takotsubo cardiomyopathy and probably myocardial infarction. Long term stress is a different story. Although we have always suspected it as an antecedent of cardiovascular disease evidence has been harder to come by.

My interest in this field originated with the influence of the late Robert S. Eliot, as a result of my attendance at this meeting (which I have continued to attend almost every year since 1981---I'll be blogging in more detail about my experience at the 2010 meeting soon). Eliot long ago believed that long term stress contributed to cardiovascular disease in a manner independent of traditional risk factors. He was prescient. Evidence is slowly accumulating. Chronic stress induced hypercortisolism appears to be an important mechanism.

Today I found this recent paper and this background reference on the topic. I've never heard the term vital exhaustion before but it's apt. Most of us physicians can easily identify with the concept.

Docs who shun drug reps in their offices hobnob with them elsewhere

---and often will incorporate the information so acquired in their practices according to a Pri-Med study. Dunno what that means, exactly, but it's interesting.

Spontaneous breathing and gasping after cardiac arrest

Gordon Ewy and his Arizona colleagues made these interesting observations in swine:

We analyzed the spontaneous ventilatory activity during the first several minutes of ventricular fibrillation (VF) in our isoflurane anesthesized swine model of out-of-hospital cardiac arrest. The frequency and type of ventilatory activity was monitored by pneumotachometer and main stream infrared capnometer and analyzed in 61 swine during the first 3 to 6 minutes of untreated VF.

During the first minute of VF, the air flow pattern in all 61 swine was similar to those recorded during regular spontaneous breathing during anesthesia and was clearly different from the patterns of gasping. The average rate of continued breathing during the first minute of untreated VF was 10 breaths per minute. During the second minute of untreated VF, spontaneous breathing activity either stopped or became typical of gasping. During minutes 2 to 5 of untreated VF, most animals exhibited very slow spontaneous ventilatory activity with a pattern typical of gasping; and the pattern of gasping was crescendo-decrescendo, as has been previously reported. In the absence of therapy, all ventilatory activity stopped 6 minutes after VF cardiac arrest.

The significance of this observation is as follows:

If you find someone “down” don't be too quick to dismiss cardiac arrest just because they appear to be “breathing.”

This observation provides yet another explanation for why, in primary cardiac arrest, compression only CPR, as well as delayed intubation, is associated with better outcomes.

At this meeting (which I will be blogging about in more detail soon) Ewy made the anecdotal observation that in human resuscitation good compressions, good enough to at least perfuse the medula oblongata, may prolong the duration of spontaneous gasping.

Monday, September 13, 2010

Fake seizures in the ER

Via Your ER Doc.

City of Quincy using garbage and used tampons to fill tree stump holes?


Sebelius: Stop blaming Obamacare or else

It seems HHS secretary Kathleen Sebelius is upset with insurance companies warning patients of impending rate hikes in the wake of passage of the Affordable Care Act. Here's the warning letter she sent. It's rich. It reads in part:

It has come to my attention that several health insurer carriers are sending letters to their enrollees falsely blaming premium increases for 2011 on the patient protections in the Affordable Care Act. I urge you to inform your members that there will be zero tolerance for this type of misinformation and unjustified rate increases...

Simply stated, we will not stand idly by as insurers blame their premium hikes and increased profits on the requirement that they provide consumers with basic protection.

(By the way, why would you want to blame increased profits on anything? She must have been smokin' steamin' mad when she fired off the letter).

So they'll have zero tolerance for particular attributions made by insurance companies about their rates and won't stand idly by??? So what are they going to do? It seems to me they'd have some free speech issues to contend with. I'd love to see them try something.

Here's an excerpt from Wesley Smith's post on this topic:

Obamacare prohibits companies from underwriting for different health conditions and requires them to accept all comers. That will require premiums for many policies to go up, or the whole thing will become economically unfeasible. Besides, the insurance industry is already regulated, and that includes the amount of premiums they can charge.

That point aside, this is really outlandish and unacceptable bullying from a high government official–particularly when reliable reports indicate that Obamacare will cause costs to increase. That is a debatable point to be sure, but one insurance companies should be able to make in a free country without fear of government retaliation.

Threatening to put companies out of business–because that is what would happen if they couldn’t participate in the exchanges–for expressing perspectives the government doesn’t approve or seeking to make a profits in a difficult market made worse by Obamacare, is beyond the pale and has no place in a free and open society.

Yet another quacky paper in PLoS ONE

It's titled The Brain Effects of Laser Acupuncture in Healthy Individuals: An fMRI Investigation. The findings? Shine a laser pointer on the skin and it lights up on MRI. Shine it on different skin areas and different areas of the brain light up. It works whether you shine the laser on acupuncture points or a control (non-acupuncture) point.

Orac's take is here. He concludes and I agree:

Having read this study, I found it to be a steaming, stinking pile of fetid dingo kidneys, even by the usual low, low, low standards of typical CAM studies. My guess for what happened is this: The authors knew this study didn't meet the standards for a real neuroscience journal. Neither did they want to relegate it to the scientific ghetto of the CAM literature, where editorial standards are so low that they're subterranean and attempts at actual science are intermingled with the purest woo, like homeopathy and reiki. So what to do? Well, PLoS ONE bills itself as a journal where only the science counts, where the reviewers don't make judgments on the import of the science being presented but rather only assure that it is sound, boasting a 60-70% acceptance rate for manuscripts. I can see how PLoS ONE might be a tempting place for a quactitioner to drop off her latest attempt at quackademic medicine. Unfortunately, somehow these latest bits of tooth fairy science on acupuncture belie the scientific rigor that PLoS ONE claims for itself. Seeing these articles in PLoS ONE make me even more certain than I was before that I no longer wish to submit any manuscripts to PLoS ONE.

As I said before, this is particularly ironic since the PloS journals are purported to be so scientifically rigorous and above conflict and all. This is the second quacky article in a short time. It's as if NEJM said “come on in, the water's fine”, so PloS took the plunge.

By the way, I like the new term “quactitioner.”