From a recent paper in JAMA Internal Medicine:
Methods We conducted a retrospective, observational, inception cohort study of patients 18 years or older from 17 health plans participating in the Mini-Sentinel program who had initiated the use of an ACEI (n = 1 845 138), an ARB (n = 467 313), aliskiren (n = 4867), or a β-blocker (n = 1 592 278) between January 1, 2001, and December 31, 2010. We calculated the cumulative incidence and incidence rate of angioedema during a maximal 365-day follow-up period. Using β-blockers as a reference and a propensity score approach, we estimated the hazard ratios of angioedema separately for ACEIs, ARBs, and aliskiren...
The cumulative incidences per 1000 persons were 1.79 (95% CI, 1.73-1.85) cases for ACEIs, 0.62 (95% CI, 0.55-0.69) cases for ARBs, 1.44 (95% CI, 0.58-2.96) cases for aliskiren, and 0.58 (95% CI, 0.54-0.61) cases for β-blockers. The incidence rates per 1000 person-years were 4.38 (95% CI, 4.24-4.54) cases for ACEIs, 1.66 (95% CI, 1.47-1.86) cases for ARBs, 4.67 (95% CI, 1.88-9.63) cases for aliskiren, and 1.67 (95% CI, 1.56-1.78) cases for β-blockers. Compared with the use of β-blockers, the adjusted hazard ratios were 3.04 (95% CI, 2.81-3.27) for ACEIs, 1.16 (95% CI, 1.00-1.34) for ARBs, and 2.85 (95% CI, 1.34-6.04) for aliskiren.
Conclusions Compared with β-blockers, ACEIs or aliskiren was associated with an approximately 3-fold higher risk for angioedema, although the number of exposed events for aliskiren was small. The risk for angioedema was lower with ARBs than with ACEIs or aliskiren.
From the American Journal of Emergency Medicine:
Results
A total of 92 patients were enrolled in the study. Patients were divided into 2 groups based on whether they were treated (group1, n = 30) or not treated (group 2, n = 62) with sodium bicarbonate. There were no significant differences in demographic characteristics between groups. The median time interval between the administration of CPR and sodium bicarbonate injection was 36.0 minutes (IQR: 30.5-41.8 minutes). The median amount of bicarbonate injection was 100.2 mEq (IQR: 66.8-104.4). Patients who received a sodium bicarbonate injection during prolonged CPR had a higher percentage of return of spontaneous circulation, but not statistical significant (ROSC, 40.0% vs. 32.3%; P = .465). Sustained ROSC was achieved by 2 (6.7%) patients in the sodium bicarbonate treatment group, with no survival to discharge. No significant differences in vital signs after ROSC were detected between the 2 groups (heart rate, P = .124; systolic blood pressure, P = .094). Sodium bicarbonate injection during prolonged CPR was not associated with ROSC after adjust for variables by regression analysis (Table 3; P = .615; odds ratio, 1.270; 95% confidence interval: 0.501-3.219)
Conclusions
The administration of sodium bicarbonate during prolonged CPR did not significantly improve the rate of ROSC in out-of-hospital cardiac arrest.
IAH and ACS are under appreciated. They occur in a variety of medical and surgical critical illnesses. Diagnosis is easy once you think of it. Vigilance is required. The topic was recently reviewed here. Previous blog posts here, here and here.
Why do we need oxygen? Why does cyanide kill?
We've long known that patients are at increased risk early following hospital discharge---for the first 30 days or so. What is less well appreciated is that only about a third of early readmissions are for the same diagnosis as the original admission. Rather, there appears to be a general state of vulnerability and poor reserve early after hospitalization irrespective of the original diagnosis. Hence the notion of post-hospital syndrome. Free access to the perspective piece and audio interview here.
But not ready for prime time. The topic was recently reviewed. From the opening section of the review:
The increased need for MRI in PPM patients has prompted the development of a specifically designed pacemaker and lead system tested for safe use in the MRI environment and in early 2011, the US Food and Drug Administration (FDA) approved the first cardiac pacemaker designed to be used safely but conditionally during MRI examinations.[7]
Historically the hazards of MRI in pacemaker patients have included inhibition, “throwing the reed switch” leading to asynchronous pacing, reprogramming, current induction in the lead causing thermal injury at the tip and even myocardial perforation. And more.
All the manufacturers are working on MRI compatible devices and the field is evolving rapidly.
With emphasis on newer models and the modes available.
From a recent paper in JAMA Internal Medicine:
Methods To determine whether preoperative hyponatremia is a predictor of 30-day perioperative morbidity and mortality, we conducted a cohort study using the American College of Surgeons National Surgical Quality Improvement Program database...
Results..Preoperative hyponatremia was associated with a higher risk of 30-day mortality (5.2% vs 1.3%; adjusted odds ratio [aOR], 1.44; 95% CI, 1.38-1.50), and this finding was consistent in all the subgroups. This association was particularly marked in patients undergoing nonemergency surgery (aOR, 1.59; 95% CI, 1.50-1.69; P less than .001 for interaction) and American Society of Anesthesiologists class 1 and 2 patients (aOR, 1.93; 95% CI, 1.57-2.36; P less than .001 for interaction). Furthermore, hyponatremia was associated with a greater risk of perioperative major coronary events (1.8% vs 0.7%; aOR, 1.21; 95% CI, 1.14-1.29), wound infections (7.4% vs 4.6%; 1.24; 1.20-1.28), and pneumonia (3.7% vs 1.5%; 1.17; 1.12-1.22) and prolonged median lengths of stay by approximately 1 day.
Hyponatremia seems to be a marker of frailty. There is no evidence here that correction of hyponatremia would reduce these complications.
High quality does not mean lower cost. In fact the relationship is all over the map in this analysis.
Well, the idea seems to be that character and other intangible attributes of applicants are important and not just academic performance according to this NEJM piece. It's true, of course, although it's nothing new. It's what admissions committees have been after for decades and has long been the focus of applicant interviews and letters of recommendation. But in the minds of some these matters are getting more attention which is refreshing given our rising obsession with measurement in medical education.
In the audio segment accompanying the article the discussant points to a common fallacy in discussions of this topic: the false dichotomy between academic prowess in the sciences and the humanistic qualities desirable in a physician.
A few months ago marked the twentieth anniversary of the launch of evidence based medicine (EBM). Now seems a good time for a retrospective. After twenty years what does EBM mean? Where has it taken us? What are the distortions and unintended consequences? You might be surprised.
What I intend to do is start with a little of the history of EBM, talk about the essential notion as originally conceived by the founders, and mention a little about the process as applied to clinical practice today. Then I'll deal with some distortions and misconceptions as well as some surprising unintended consequences.
EBM was launched on November 4 1992 with the publication of this paper in JAMA. I don't recall noticing the paper coming out but when discussions of EBM as a new movement became popular I wondered what was so new about it. After all I thought I had always made clinical decisions based on evidence. I recalled so many of the clinical trials I had applied in my practice through the years. Practicing doctors for the most part, I thought, were conscientious in applying this evidence to their clinical decisions.
What I later learned was that it was not the reliance on evidence but the manner in which it was applied that was new. EBM sought to take things to a new level with a more systematic and rigorous approach to the application of research data.
Very soon after the publication of the JAMA paper, however, misconceptions began to fly. These mainly centered around the idea that EBM was “one size fits all” or “cookie cutter” medicine. That distortion persists today. More on that below. But it prompted some of the founders to publish another paper, which I regard as the second founding document, a paper in BMJ titled Evidence based medicine: what it is and what it is and what it isn't. In it we find what is most widely quoted today among aficionados as the essential definition:
It's about integrating individual clinical expertise and the best external evidence...
Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients.
Note that EBM is about individual expertise and judgment and about the individual patient. More on that below.
What about the process? It's useful to take a look at that because it can be rather onerous and I suspect that not many of us today practice it in its pure form chiefly because of the time it takes. I covered the process of EBM in a couple of long posts a few years ago. Suffice it to say here that it starts with asking a clinical question focused on your patient and converting it into a set of search terms that can be applied to a search engine such as PubMed. Citations thus retrieved are appraised according to a set of criteria after the model of the EBM pyramid. There are several variations on the basic pyramid theme, an example of which is shown here. Using the criteria the list of citations is trimmed down to those articles that are current and deemed of sufficient quality. The final step involves taking the information thus selected and applying it to the patient's idiosyncrasies including circumstances, preferences and values.
That last piece is often lost in discussions today when EBM is invoked to guide public policy. Herein lies one of the more pervasive distortions of EBM. Public policy discussions about the direction of health care got into high gear early in the Obama administration when the gimmicky phrase “comparative effectiveness research” entered the lexicon and debates raged about health care reform. There were diverse arguments about the direction health care should go but many of them sought to homogenize it, citing such things as the Dartmouth Atlas data and other sources which showed variation in delivery. The idea was that through various forms of central control one could minimize the variation which after all many believed to be the enemy of quality and efficiency. Pathways, performance measures, positive incentives and negative incentives all seek to do this and many proponents try to bolster their arguments by appealing to EBM. They thereby only reflect their ignorance about what EBM is. Maybe you like central control and can make some good arguments for it but you can't invoke EBM to support those arguments. EBM is diametrically opposed to central control. If you've any doubt about whether EBM concerns primarily individual decision makers and individual patients, watch this interview with David Sackett, one of the movement's founders:
I don't purpose to argue against central control here. Maybe it has something to recommend it but by definition the more external forces encroach on your decision making the less you will practice EBM. Just by definition.
But even when EBM is practiced according to its core principles there are unintended consequences. These relate to a fatal flaw of EBM found in that pyramid I referenced earlier. What I am referring to is that though not intended by its founders, application of EBM has led to numerous promotions of quackery. I have cited examples of this many times before as have David Gorski and other bloggers. It has to do with placing scientific plausibility at the bottom of the EBM pyramid, as I once explained:
...that this failure of EBM is more than just one of occasional unintended consequences. While it may have been unintended in the minds of the original founders, now it's systematic.
The problem is illustrated by the evidence pyramids, which are at the very core of the teaching about EBM. There are numerous versions of these pyramids, and Gorski links to a few examples, but what they have in common is that they put biologic plausibility (variously termed basic science, physiologic rationale, etc) at the bottom if they include it at all.
A casual observer might think that putting basic scientific rationale at the bottom means it's intended to be foundational (remember the old stepped care diagrams for treatment of hypertension and rheumatoid arthritis?). But that's not the way the EBM hierarchies of evidence are designed. Instead, higher levels on the pyramid trump those below. Students of EBM are taught to start at the top of the pyramid and “drill down,” level-by-level, until they find the evidence they want, and stop there.
Kimbal Atwood had a good example of how this has been applied to promote nutty ideas like homeopathy, in which occasional weak clinical trials which appear to favor homeopathy by chance variation trump overwhelming basic science information against it:
When this sort of evidence is weighed against the equivocal clinical trial literature, it is abundantly clear that homeopathic “remedies” have no specific, biological effects. Yet EBM relegates such evidence to “Level 5”: the lowest in the scheme. How persuasive is the evidence that EBM dismisses? The “infinitesimals” claim alone is the equivalent of a proposal for a perpetual motion machine. The same medical academics who call for more studies of homeopathy would be embarrassed, one hopes, to be found insisting upon “studies” of perpetual motion machines. Basic chemistry is still a prerequisite for medical school, as far as I’m aware.
The way we got into this fix is that the founders of EBM realized we couldn't rely only on scientific rationale. That has gotten us into trouble in the past. High level outcome based evidence is needed to be placed in the mix to address that problem. But what the EBM apologists left out was the fact that while scientific plausibility couldn't be the sole basis for making clinical decisions it couldn't be ignored. It needed to be a prerequisite.
Solutions? A group of physicians and scientists have recognized that EBM's unintended consequence could be avoided by giving basic scientific plausibility its due place while following the other EBM principles. You can find out lots more about that at their website.
So what do you think about EBM 20 years later? The verdict is mixed but it hasn't lived up to its promise. Maybe with the help of science based medicine (SBM) we'll get there.
In the May 17 2012 issue of the NEJM Ray et al reported an increased risk of sudden cardiac death attributable to the use of azithromycin. I blogged that issue here. The study was limited, being a cohort study based on administrative data and the absolute risk was low but its findings were compelling, particularly in regard to the timing of SCD in relation to the use of azithromycin. A more recent paper in the Journal failed to uphold the association of cardiac risk with azithromycin. A perspective piece in the same issue addresses the discrepancy between these studies. According to their analysis the findings of Ray et al are real and the discrepancy between the two studies may be attributable to differing patient populations and in the more recent paper a survival advantage attributable to azithromycin in the treatment of pneumonia that may have counterbalanced any adverse cardiac effect. It has long been known, of course, that macrolides as a class prolong the QT interval. Although that problem may not extend equally across the class there is plausibility to a risk of sudden cardiac death attributable to azithromycin.
They also point out findings in the Ray paper suggesting that levofloxacin has similar cardiac risk to azithromycin but not ciprofloxacin. Quinolones have been implicated in QT interval prolongation and Torsades but the risk appears not to extend equally across the class.
So what are we to make of all this? There are several points worth noting:
In the perspective piece the authors point out the FDA's statement regarding azithromycin:
On the basis of its review, the FDA approved revisions to azithromycin product labels regarding risks of QT-interval prolongation and the associated ventricular arrhythmia torsades de pointes. The revised labels advise against using azithromycin in patients with known risk factors such as QT-interval prolongation, hypokalemia, hypomagnesemia, bradycardia, or use of certain antiarrhythmic agents, including class IA (e.g., quinidine and procainamide) and class III (e.g., dofetilide, amiodarone, and sotalol) — drugs that can prolong the QT interval.
I would submit that those concerns would apply to the use of all macrolides as well as all quinolones with the possible exception of ciprofloxacin. That makes them somewhat impractical to implement but there are precautions that can be taken, in terms of minimizing the other risk factors I note below.
While the absolute risk of antibiotic induced QT prolongation and Torsades is low it is magnified by other risk factors that may interact and conspire to produce a catastrophic event. Hospitalization is a likely setting for the perfect storm that may bring these factors together. Hypomagnesemia and hypokalemia, both of which are powerful risk factors for QT prolongation, are common in hospitalized patients. Administration of proton pump inhibitors as “GI prophylaxis” to patients with pneumonia or other acute respiratory conditions causes hypomagnesemia. Poor oral intake, the common use of diuretics in the hospital and the use of normal saline as the default IV fluid may all produce hypokalemia. The concomitant use of other drugs known to prolong the QT interval (eg haloperidol and ondansetron) is common in hospitalized patients. So just being hospitalized may invite a combination of risk factors.
Recall as I pointed out year before last that patients who die while hospitalized with pneumonia tend to do so suddenly rather than according to any expected trajectory of hypoxia or organ failure. That observation just heightens the concerns mentioned above.
Finally, all that's new about this issue is the hype. The concerns have existed for a long time and over five years ago I cited a paper making the case that close attention to the electrocardiogram was warranted for any patient being treated for infection (or beyond that for most all patients sick enough to be hospitalized).
This is from the JAMA series on information for patients and families and is a nice easy to read summary of what they can expect as they navigate through the transition process.
As pointed out in this review, the classic form is a pediatric entity. When cases arise in adults they are less typical and the distinction from TTP is blurred. These cases are probably best termed TTP-HUS and should not argue against plasma exchange therapy.
Often in my professional development I am taught to consider the source. Information presented by pharmaceutical companies is to be rejected. Blogs are to be read with an extra measure of caution. A journal's reputation means something. Not so much anymore. Now we have to evaluate medical claims on their own merits regardless of the source. That demands a little more effort. Why do I say this? A case in point is the trend over the last few years in so called top tier medical journals toward the promotion of quackery. Just recently the Annals of Internal Medicine published this study on acupuncture for treatment of seasonal allergic rhinitis. The paper is cosmetically scientific with all the jargon and trappings of evidence based medicine:
Results: Compared with sham acupuncture and with RM, acupuncture was associated with improvement in RQLQ score (sham vs. acupuncture mean difference, 0.5 point [97.5% CI, 0.2 to 0.8 point; P less than 0.001]; RM vs. acupuncture mean difference, 0.7 point [97.5% CI, 0.4 to 1.0 point; P less than 0.001]) and RMS (sham vs. acupuncture mean difference, 1.1 points [97.5% CI, 0.4 to 1.9 points; P less than 0.001]; RM vs. acupuncture mean difference, 1.5 points [97.5% CI, 0.8 to 2.2 points; P less than 0.001]). There were no differences after 16 weeks in the first year. After the 8-week follow-up phase in the second year, small improvements favoring real acupuncture over the sham procedure were noted (RQLQ mean difference, 0.3 point [95% CI, 0.03 to 0.6 point; P = 0.032]; RMS mean difference, 1.0 point [95% CI, 0.2 to 1.9 points; P = 0.018]).
Limitation: The study was not powered to detect rare adverse events, and the RQLQ and RMS values were low at baseline.
Conclusion: Acupuncture led to statistically significant improvements in disease-specific quality of life and antihistamine use measures after 8 weeks of treatment compared with sham acupuncture and with RM alone, but the improvements may not be clinically significant.
Initially I just glanced casually at the study. This type of thing is not so unusual anymore. It was just another promotion of a nutty idea by a mainstream medical journal under the guise of evidence based medicine. It was so dense with scientific verbiage and so circumspect sounding I knew it would take a little effort to expose it. And at the time I was busy. And tired.
Well, fortunately Mark Crislip over at Science Based Medicine did it for me. When you read his post I suggest you skip down to the middle where he begins the actual analysis of the paper. The real devil is in the details and he unpacks them nicely:
The big difference is that acupuncture is a form of magic that is likely to get published in formerly reliable journals complete with positive spin: Acupuncture in Patients With Seasonal Allergic Rhinitis. A Randomized Trial...
A careful and critical reading of the paper gives compelling evidence that acupuncture does nothing, in line with all the other well-designed acupuncture studies. The cognitive disconnect between the editorial and conclusion and the data presented in the paper is a wonder to behold. And most people will read only the spin in the abstract and the editorial, not noticing the fatal flaws, and erroneously conclude that acupuncture has efficacy.
Yet another reason why I am glad I let my Annals subscription lapse years ago.
It's all quite ridiculous. One of the more unintentionally funny papers in the medical literature. Or was it intentional? It's hard to know from just reading the paper whether or not it's a parody. But apparently it was intended to be taken seriously because in an accompanying editorial the journal elevates it to the realm of public policy, specifically “comparative effectiveness research.”
This type of nonsense has been going on in high impact medical journals for several years now and it is getting worse. It started out in BMJ about a decade ago and over time has metastasized to other journals. Over at Quackwatch Steve Barrett put BMJ on his black list years ago and subsequently added the Annals.
But the Annals and BMJ have managed to maintain a good reputation, so now a journal's reputation means little. Whether it's indexed in Medline means little. The same can be said of broad categories such as journals and blogs. It's strictly buyer beware. I've said for a long time that relying on the source to evaluate the quality of information is intellectually lazy. Now, as illustrated by the paper and editorial in question, it's flat out unreliable.
There's not much being done to stop the trend but as time and energy permit I'll do what I can to expose it. In the meantime maybe there's a positive here. It means, more than ever before, that we have to evaluate medical information on its own merits rather than considering too strongly the source. Something we should have been doing all along.
Not warranted in critically ill patients requiring volume resuscitation according to new JAMA meta-analysis.
According to this Mayo Clinic Proceedings review:
Milk-alkali syndrome (MAS) consists of hypercalcemia, various degrees of renal failure, and metabolic alkalosis as a result of ingestion of large amounts of calcium and absorbable alkali. This syndrome was discovered in the 1930s after treatment of peptic ulcer disease with milk and sodium bicarbonate had become common.1 Initially considered a rare condition, MAS is now believed to be the third most common cause of in-hospital hypercalcemia, after hyperparathyroidism and malignant neoplasms.2
Nowadays it might better be named calcium-alkali syndrome. The old culprits, milk and baking soda, once used to treat peptic ulcer, have been replaced by calcium carbonate antacids. Re-emergence of the syndrome is due to increasing popular awareness of the problem of osteoporosis.
Another review was published more recently. I should point out an error in that review. Calcitriol is mentioned as an adjunctive treatment. I think they meant to say calcitonin.
Patient centered decision making is a core principle of evidence based medicine (EBM). A recent Annals paper looked at patient centered decision making and demonstrated a positive effect on outcomes:
Background: Patient-centered decision making (PCDM) is the process of identifying clinically relevant, patient-specific circumstances and behaviors to formulate a contextually appropriate care plan.
Medicine by central control as is being pushed by many today cannot accommodate patient-specific factors and is thus in conflict with patient-centered decision making and EBM.
More from the article:
Objective: To ascertain whether encounters in which PCDM occurs are followed by improved health care outcomes compared with encounters where there is inattention to patient context.
Design: Patients surreptitiously audio-recorded encounters with their physicians. Medical records of these encounters were then screened for “contextual red flags,” such as deteriorating self-management of a chronic condition, that could reflect such underlying contextual factors as competing responsibilities or loss of social support. When a contextual factor was identified, either as a result of physician questioning or because a patient volunteered information, physicians were scored on the basis of whether they adapted the care plan to it...
Results: Among 548 contextual red flags, 208 contextual factors were confirmed, either when physicians probed or patients volunteered information. Physician attention to contextual factors (both probing for them and addressing them in care plans) varied according to the presenting contextual red flags. Outcome data were available for 157 contextual factors, of which PCDM was found to address 96. Of these, health care outcomes improved in 68 (71%), compared with 28 (46%) of the 61 that were not addressed by PCDM (P = 0.002).
Here's a nice review from CCJM.
A review was recently published in the Annals of Internal Medicine.
It's difficult to parse because it only cites other reviews and policy documents, not primary sources. It lists ten measures “strongly encouraged” and twelve “encouraged” for “adoption now.”
The strongly encouraged measures are:
1) Pre-op and anesthesia checklists
2) Central line checklists and other bundles
3) Process interventions to reduce urinary catheter use (reminders, etc.)
4) VAP bundles
5) Hand cleaning
6) Do not use abbreviation lists
7) Interventions to reduce pressure ulcers
8) Barrier precautions
9) Ultrasound guidance for central line placement
10) Interventions to increase VTE prophylaxis
Items 1 and 2 have good evidence to support them. Anesthesia should be singled out as a remarkable success story but that effort was started decades ago and predates what we think of today as the patient safety movement. And it was done quietly, without the hype and public policy intrusions that characterize today's effort.
Interventions to reduce urinary catheter use (item 3) seem reasonable even if not evidence based. I have not formally reviewed the topic but have followed it closely and am aware of no strong research evidence that such interventions actually improve outcomes. Things are going in the right direction, though (somebody must be doing something right) based on a study I cited over a year ago demonstrating a decline in catheter related UTI. The trend cannot be attributed to Medicare's “no pay for errors” initiative concerning catheters, however, because it long predated the policy.
The evidence has been mixed concerning item 4 (VAP bundles). We are on a learning curve as to which components are most effective.
Item 5, hand washing, has been recognized as beneficial for over a century. Efforts to improve adherence are laudable. Giving it the status of a reportable measure, however, may distract from other equally if not more important infection control measures. The stethoscope, for example, of little clinical use today due to vanishing operator skill, remains in heavy use as a CPT coding instrument and is arguably as important as the hands in spreading infection (one in three stethoscopes carry MRSA).
I won't go over the rest of the top ten point by point. All are good ideas but suffer from lack of supporting evidence and/or the unintended consequences of turning them into reportable measures. Most have already been widely adopted for years if not decades.
Put mildly, items 11-22 are a little more interesting:
11) Multicomponent interventions to reduce falls
12) Use of clinical pharmacists to reduce adverse drug events
13) Documentation of patient preferences for life sustaining treatments
14) Obtaining informed consent for procedures
15) Team training
16) Medication reconciliation
17) Practices to reduce radiation exposure
18) The use of surgical outcome measures and report cards
19) Rapid response systems
20) Use of complementary methods to detect adverse events and medical errors
21) Computerized physician order entry
22) Simulation exercises
My head swims. OK, let's go through it.
11 and 12....check. We've been doing them for years.
13....pretty much implemented by law in 1990 and a nearly universal practice for many years.
14, 15....not exactly new ideas
16....med rec? Hmmm. Seems I recall that becoming a Joint Commission standard seven years ago. A wonderful idea in the abstract but a failure in the real world. Not that we shouldn't keep trying, but it's been a failure.
17....OK, why not?
18....Evidence in support of public reporting has been mixed but largely negative. It's loaded with unintended consequences.
19....Evidence for benefit from rapid response systems weighs slightly in favor of them but it is fairly weak. Almost all hospitals already have them due to Joint Commission's standard for systems to summon help for deteriorating patients.
20....OK
21....Ahh yes. CPOE. Almost all the research in support of it involves artificial surrogates. There is little if any evidence that it improves meaningful clinical outcomes. There is some evidence that it may be harmful early after adoption. In essence CPOE adds secretarial duties to the doctor's work flow thus replacing the unit secretary. Proponents argue that it eliminates a processing step thereby eliminating an opportunity for error. It is equally plausible that the eliminated step (the unit secretary) is a layer of safety and that the secretarial duties distract the doctor from clinical decision making. Well, whatever one's belief about benefit versus harm it's a moot point because we are well on our way to universal adoption. If experience with CPOE has taught us anything it's that haste magnifies the unintended consequences, so to use it for all it's worth and avoid harm we must go slow in development, training and implementation. That's why I am uncomfortable with any pressure for “adoption now” as a safety measure.
22....Simulation exercises? Sounds like a great idea. Resource intensive though. Where's the evidence?
Aside from the problem that much of the above lacks evidential support, there are no new ideas presented. Most of the measures, evidence based or not, have been widely adopted for some time. So I would find these recommendations to be of little help in advancing the cause of patient safety. But the paper does shed light on why the patient safety movement has failed to live up to its promise. The Consumers Union declared the patient safety movement a failure a decade after the IOM report which many credit with the start of the movement. More recently Bob Wachter, one of the authors of the Annals paper and an ardent systems guy to boot worried that the patient safety movement is in danger of flickering out. He cites physician burnout as one of the reasons.
So why in the world would physicians burn out on patient safety? I think it's because doctors want tools, not rules. They recognize that rules as promulgated by today's systems approaches to patient safety, being onerous and loaded with unintended consequences, should be supported by good evidence. But they're not, for the most part. And as important as systems of care are (yes, I do believe we need a systems approach to patient safety) doctors all too often see them as substitutes for thought and judgment.
Speaking of unintended consequences I'll conclude with one that deserves special mention. When the Institute of Medicine launched the patient safety movement its intention was to de-emphasize blame (as implied in the title of its report To Err is Human) in order to create a culture of transparency and facilitate reporting and analysis of adverse outcomes. But the IOM got carried away in its zeal and egregiously hyped the data on medical harm by equating it to a jumbo jet crashing daily. Even worse than hyping, the IOM actually misrepresented the study on which it based its claims, prompting a lead author of the original report to issue, in the New England Journal of Medicine, a criticism of their spin. A retraction of sorts. But it received little notice and the IOM hype took on a life of its own leading to a heightened culture of blame concerning patient safety, the opposite effect to what was originally intended. I've detailed the whole mess here and other places.
From a recent paper in JAMA Internal Medicine:
Methods Patients received enoxaparin sodium, 1 mg/kg, every 12 hours or 1.5 mg/kg once daily between June 1 and November 30, 2009. Moderate renal impairment was defined as creatinine clearance (CrCl) of 30 to 50 mL/min. Normal renal function was defined as CrCl greater than 80 mL/min. The primary outcome was major bleeding, defined as any bleeding resulting in death, hospital admission, lengthened hospital stay, or an emergency department visit. The secondary outcome was thromboembolism.
Results A total of 164 patients met the inclusion criteria: 105 with normal renal function and 59 with moderate renal impairment. The primary outcome occurred in 6 of 105 patients (5.7%) with normal renal function vs 13 of 59 patients (22.0%) with moderate renal impairment, representing an unadjusted odds ratio of 4.7 (95% CI, 1.7-13.0; P = .002).
That's rather concerning. FDA approved labeling calls for no adjustment until the clearance is below 30 ml/min. So the patients in the reduced renal function group all received the drug “appropriately” according to the approved labeling. Alternatives to address this situation might include the use of unfractionated heparin or enoxaparin dose adjustment based on antiXa monitoring.
From a recent meta-analysis:
In a pooled analysis of data of 31 RCTs measuring the effect of CCBs on stroke, CCBs reduced stroke more than placebo and β-adrenergic blockers, but were not different than ACEIs and diuretics. More head to head RCTs are warranted.
