Vital signs are supposed to be objective measurements. Read this White Coat Rant.
Via Kevin M.D.
Friday, February 29, 2008
Thursday, February 28, 2008
Accredited woo for fourth year med students
In the springtime a medical student’s fancy turns to thoughts of woo. It’s almost time again for the AMSA sponsored University of Florida accredited Humanistic Elective in alternative medicine, Activism and Reflective Transformation (HEART).
If last year’s program is any indication students can look forward to sessions on shamanism, Tai-chi, dosha testing, Ayurveda and more.
If last year’s program is any indication students can look forward to sessions on shamanism, Tai-chi, dosha testing, Ayurveda and more.
Wednesday, February 27, 2008
Anticonvulsant hypersensitivity syndrome
Anticonvulsant hypersensitivity syndrome (AHS) was recently reviewed in Pharmacotherapy (free full text via Medscape).
Key points:
AHS belongs on the clinician’s list of dermatologic emergencies.
Phenytoin, carbamazepine, and Phenobarbital lead the list of causative agents
Not only many clinicians, but also computerized pharmacy databases, are unaware of potential cross sensitivity among several anticonvulsants.
Valproic acid, benzodiazepines and other nonaromatic anticonvulsants should be safe. (Rare reports of valproic acid related AHS do exist).
Look for a triad of fever, rash and internal organ involvement (usually in the form of liver function abnormalities). Fever and rash are universal.
AHS may overlap with Stevens-Johnson syndrome of toxic epidermal necrolysis although the rash of AHS can take other forms.
The pathogenesis is complex and, among other mechanisms, involves reactivation of latent viruses (HHV 5,6,7) in the more severe cases.
Treatment consists of removal of the offending drug, general supportive care and, in many cases, corticosteroids.
Key points:
AHS belongs on the clinician’s list of dermatologic emergencies.
Phenytoin, carbamazepine, and Phenobarbital lead the list of causative agents
Not only many clinicians, but also computerized pharmacy databases, are unaware of potential cross sensitivity among several anticonvulsants.
Valproic acid, benzodiazepines and other nonaromatic anticonvulsants should be safe. (Rare reports of valproic acid related AHS do exist).
Look for a triad of fever, rash and internal organ involvement (usually in the form of liver function abnormalities). Fever and rash are universal.
AHS may overlap with Stevens-Johnson syndrome of toxic epidermal necrolysis although the rash of AHS can take other forms.
The pathogenesis is complex and, among other mechanisms, involves reactivation of latent viruses (HHV 5,6,7) in the more severe cases.
Treatment consists of removal of the offending drug, general supportive care and, in many cases, corticosteroids.
Tuesday, February 26, 2008
Painless aortic dissection: an uncommon manifestation of an uncommon disease
Internist Lisa Sanders, M.D., writing for the New York Times Magazine, recently presented an uncommon presentation of an uncommon disease: painless aortic dissection. Actually the patient, later in his brief ER course, did develop ischemic leg pain but for practical purposes the dissection can be considered painless given the absence of typical chest and back pain. In the International Registry of Acute Aortic Dissection such atypical presentations were uncommon (6.4%) and were associated with increased mortality.
DB’s Med Rants linked to the article and attributed the successful outcome to the doctor’s avoidance of premature closure, a frequent cognitive error in diagnosis. (The doctors, apparently, were tempted to start immediate heparin to treat the patient’s ischemic limb). I’m not sure how often that particular error would be made in the real world. Before starting anticoagulation (which could delay the safe performance of limb saving invasive procedures) most clinicians, it would seem to me, would first want some type of vascular imaging study such as CTA or MRA to define anatomy and explore options for urgent limb salvage. Such a study would have likely diagnosed the dissection even if aortic dissection hadn’t been initially suspected.
A situation more likely to lead to premature closure is aortic dissection presenting with chest pain. It’s especially true with today’s convenient substitutes for thought, those handy templates and order sets in which anticoagulants are embedded in the chest pain protocols.
I have a couple of quibbles with the article. Immediately following the onset of symptoms the patient was taken to the ER via ambulance where a CT was performed within moments of arrival:
That’s likely to drive already inflated public expectations of CT scans and other fancy imaging techniques. Given that the CT was performed very early following symptom onset it’s unlikely the scan would have shown a stroke unless it happened to be a hemorrhagic stroke.
The article, unfortunately, concludes with this:
Ritter’s doctors won’t be happy with that statement, I’d wager. While this story may contain lessons about premature closure we have no reason to believe his doctors made that error. How do we know Ritter’s doctors considered dissection “too late?” Equally likely, that possibility went through their minds immediately upon Ritter’s presentation, was considered in the brief time available, and rejected when symptoms, risk factors and initial diagnostic tests pointed to acute coronary syndrome as more likely than aortic dissection. Occasional wrong diagnosis is inevitable even with pristine care and does not equal error.
DB’s Med Rants linked to the article and attributed the successful outcome to the doctor’s avoidance of premature closure, a frequent cognitive error in diagnosis. (The doctors, apparently, were tempted to start immediate heparin to treat the patient’s ischemic limb). I’m not sure how often that particular error would be made in the real world. Before starting anticoagulation (which could delay the safe performance of limb saving invasive procedures) most clinicians, it would seem to me, would first want some type of vascular imaging study such as CTA or MRA to define anatomy and explore options for urgent limb salvage. Such a study would have likely diagnosed the dissection even if aortic dissection hadn’t been initially suspected.
A situation more likely to lead to premature closure is aortic dissection presenting with chest pain. It’s especially true with today’s convenient substitutes for thought, those handy templates and order sets in which anticoagulants are embedded in the chest pain protocols.
I have a couple of quibbles with the article. Immediately following the onset of symptoms the patient was taken to the ER via ambulance where a CT was performed within moments of arrival:
A few minutes later the patient-doctor was whisked out of the E.R. to get a CT scan of his head. If this was a stroke, there was a good chance it would show up.
That’s likely to drive already inflated public expectations of CT scans and other fancy imaging techniques. Given that the CT was performed very early following symptom onset it’s unlikely the scan would have shown a stroke unless it happened to be a hemorrhagic stroke.
The article, unfortunately, concludes with this:
An aortic dissection is one of the classic difficult diagnoses in medicine. Far too often it’s not even considered. Or as in the case of John Ritter, who died of a dissection in 2003, it is considered but too late. (That case is now being litigated in a Glendale, Calif., courtroom, with Ritter’s family charging wrongful death.)
Ritter’s doctors won’t be happy with that statement, I’d wager. While this story may contain lessons about premature closure we have no reason to believe his doctors made that error. How do we know Ritter’s doctors considered dissection “too late?” Equally likely, that possibility went through their minds immediately upon Ritter’s presentation, was considered in the brief time available, and rejected when symptoms, risk factors and initial diagnostic tests pointed to acute coronary syndrome as more likely than aortic dissection. Occasional wrong diagnosis is inevitable even with pristine care and does not equal error.
Monday, February 25, 2008
Dismantling evidence based medicine
I’m finding it harder and harder to defend evidence based medicine (EBM) these days. My usual defense is to explain away all the things that are wrong as distortions of EBM rather than EBM itself. And while this defense seems valid, the term EBM has become so synonymous with those distortions that maybe we need a new name. How about Science Based Medicine in recognition of the new blog of the same name? In this post I will present a roundup of blog entries and articles which express important concerns about EBM as it is promoted today.
EBM as originally conceived was a sound notion. What the EBM movement has become is problematic. Sackett and colleagues defined EBM in a classic editorial years ago:
There’s nothing wrong with that basic idea. The key word is judicious. But somewhere in the history of the movement the boosters issued some injudicious rules about how doctors should use evidence. The result was a devaluation of basic science, prior knowledge and pathophysiologic rationale. Plausibility was out the window. Preposterous claims were legitimized as questions for “research.” When chance variation conspired with publication bias, biased Medline indexing and conflicts of interest numerous forms of quackery (often euphemistically termed “complementary and alternative medicine” or CAM) appeared validated. While the evidence was weak it was enough to stimulate the infusion of millions of tax dollars into dubious research. Although unanticipated by EBM’s founders the movement helped fuel a “CAMbrian explosion.”
I began to realize this early in my blogging career when I wondered why we should even bother with research on homeopathy. I later elaborated on the importance of plausibility in a post citing Steve Barrett’s blistering attack on the Institute of Medicine’s pro-CAM report and Wallace Sampson’s classic paper documenting the promotion and advocacy of quackery in American medical schools. Sampson recognized early on the inability of EBM (or what EBM had become) to critically assess the claims of quackery and said in his paper:
Several years later, in a paper published in The Medical Journal of Australia, Sampson and coauthor Kimball Atwood IV said this about EBM’s inability to evaluate quacky health claims (emphasis mine):
In a recent Medscape Roundtable Discussion, while defending the core notions of EBM I criticized its de-emphasis on basic science and noted some of its other failings.
More recently, in a series of three posts, (the first two of which I discussed here) Atwood provided a more formal and quantitative discussion of the failings of EBM by using Bayesian analysis (warning---not light reading).
On Friday Retired Doc posted an insightful discussion on the consequences of EBM’s dogmatic evidence hierarchy. He quoted this paper by M.R. Tonelli which made the point that EBM has wrongly defined pathophysiologic rationale as “evidence”, then relegated it to the bottom of the hierarchy. That makes it possible for implausible CAM claims to be “validated” when, with the help of chance variation and publication bias, they happen to squeak by and pass the evidentiary test. The evidence, no matter how weak, always trumps basic science rationale even when the claim is clearly (or should be) refuted by the latter.
EBM as originally conceived was a sound notion. What the EBM movement has become is problematic. Sackett and colleagues defined EBM in a classic editorial years ago:
Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients.
There’s nothing wrong with that basic idea. The key word is judicious. But somewhere in the history of the movement the boosters issued some injudicious rules about how doctors should use evidence. The result was a devaluation of basic science, prior knowledge and pathophysiologic rationale. Plausibility was out the window. Preposterous claims were legitimized as questions for “research.” When chance variation conspired with publication bias, biased Medline indexing and conflicts of interest numerous forms of quackery (often euphemistically termed “complementary and alternative medicine” or CAM) appeared validated. While the evidence was weak it was enough to stimulate the infusion of millions of tax dollars into dubious research. Although unanticipated by EBM’s founders the movement helped fuel a “CAMbrian explosion.”
I began to realize this early in my blogging career when I wondered why we should even bother with research on homeopathy. I later elaborated on the importance of plausibility in a post citing Steve Barrett’s blistering attack on the Institute of Medicine’s pro-CAM report and Wallace Sampson’s classic paper documenting the promotion and advocacy of quackery in American medical schools. Sampson recognized early on the inability of EBM (or what EBM had become) to critically assess the claims of quackery and said in his paper:
With inadequate approaches that fail to uphold criteria for validity and plausibility, so called ‘evidence-based’ medicine remains fluid and loses its value to help physicians discern what is truly useful.
Several years later, in a paper published in The Medical Journal of Australia, Sampson and coauthor Kimball Atwood IV said this about EBM’s inability to evaluate quacky health claims (emphasis mine):
Evidence-based medicine (EBM), relying on results of randomised trials, should be a bulwark against the Absurd. However, the heterogeneity of clinical trial methods and designs, differing population bases, and varying endpoints often result in heterogeneity of outcomes. This has precluded systematic reviews of CAM methods from defining a line of inefficacy. EBM also does not include plausibility or consistency with basic science in its methods and reviews, leaving each to physician and patient interpretation. Moreover, there are no solid criteria for evaluating the quality of trials and reviews, especially for detecting erroneous, manipulated, and faked data. Thus, most CAM systems remain in an indeterminate limbo state, awaiting enough negative clinical trials to return consensus opinion to the state of decades prior.
In a recent Medscape Roundtable Discussion, while defending the core notions of EBM I criticized its de-emphasis on basic science and noted some of its other failings.
More recently, in a series of three posts, (the first two of which I discussed here) Atwood provided a more formal and quantitative discussion of the failings of EBM by using Bayesian analysis (warning---not light reading).
On Friday Retired Doc posted an insightful discussion on the consequences of EBM’s dogmatic evidence hierarchy. He quoted this paper by M.R. Tonelli which made the point that EBM has wrongly defined pathophysiologic rationale as “evidence”, then relegated it to the bottom of the hierarchy. That makes it possible for implausible CAM claims to be “validated” when, with the help of chance variation and publication bias, they happen to squeak by and pass the evidentiary test. The evidence, no matter how weak, always trumps basic science rationale even when the claim is clearly (or should be) refuted by the latter.
Friday, February 22, 2008
Medicare payment and hospital “mistakes”
Ever since my initial rant about the new Medicare policy I’ve waited for Bob Wachter’s take. Wachter is an expert on safety and quality and does his share of preaching about it. Yet, he approaches the subject with a degree of skepticism and humor I find refreshing. You can tell he’s not far from the trenches of day to day patient care.
He finally weighed in with a post on February 11 along with a link to this article he coauthored in The Joint Commission Journal on Quality and Patient Safety. His conclusion was more optimistic than mine despite the fact that he cited virtually all the negatives I did.
Wachter noted four conditions to be met for the policy to be reasonable:
Clearly the policy as written fails to meet condition number one, particularly for decubitus ulcers and patient falls (which Wachter believes should be off the list). Condition number four is problematic. The POA provision will result in system gaming. (Take it for granted that creative hospital charting will rise to a new level).
In his article, Wachter suggests that the policy creates a business case for patient safety. But that implies hospitals didn’t have a business incentive already. A recent paper in JAMA went so far as to say hospitals are currently incentivized to allow adverse events by means of coding modifiers that provide increased DRG payments for complications. I posted a strong disagreement with that thinking and gave the example of hospital acquired sepsis:
And how strong is the business case, really, for prevention efforts? How, for example, and at what expense, can hospitals make patient fall injury a “never event”? Given today’s anti-restraint culture and the recent banning of Vail beds hospitals’ only recourse (unless they want to adopt Happy Hospitalist’s mandatory helmet policy) is to hire a full time sitters for all hospitalized elderly patients. From a purely business point of view (not the point of view I would advocate) hospitals might be better off doing nothing.
Wachter concludes his article with this statement:
That implies that when the unintended consequences surface Medicare will take steps to mitigate them and if the experiment is a failure Medicare will dismantle it. Somehow I’m not comforted. In the 63 year history of this grand experiment’s unintended consequences and abuses, what’s been the track record?
He finally weighed in with a post on February 11 along with a link to this article he coauthored in The Joint Commission Journal on Quality and Patient Safety. His conclusion was more optimistic than mine despite the fact that he cited virtually all the negatives I did.
Wachter noted four conditions to be met for the policy to be reasonable:
Evidence demonstrates that the adverse events in question can largely be prevented by widespread adoption of achievable practices.
The events can be measured accurately, in a way that is auditable.
The events resulted in clinically significant patient harm.
It is possible, through chart review, to differentiate adverse events that began in the hospital from those that were “present on admission” (POA).
Clearly the policy as written fails to meet condition number one, particularly for decubitus ulcers and patient falls (which Wachter believes should be off the list). Condition number four is problematic. The POA provision will result in system gaming. (Take it for granted that creative hospital charting will rise to a new level).
In his article, Wachter suggests that the policy creates a business case for patient safety. But that implies hospitals didn’t have a business incentive already. A recent paper in JAMA went so far as to say hospitals are currently incentivized to allow adverse events by means of coding modifiers that provide increased DRG payments for complications. I posted a strong disagreement with that thinking and gave the example of hospital acquired sepsis:
So they’re saying, in effect, that hospitals have been incentivized to allow patients to experience complications! But that’s based on the dubious assumption that the increase in DRG reimbursement exceeds the added cost of caring for patients who have experienced complications in the hospital. The example given assumes that an extra $3468.77 would more than pay for an episode of sepsis. But what if the patient’s sepsis requires 10 days of big gun antibiotics, the use of activated protein C, consumes the resources of an early goal directed therapy team and requires 5 days in the ICU? Hospital resource managers know better and, ever since the advent of DRGs in 1984, have considered such events to be costly.
And how strong is the business case, really, for prevention efforts? How, for example, and at what expense, can hospitals make patient fall injury a “never event”? Given today’s anti-restraint culture and the recent banning of Vail beds hospitals’ only recourse (unless they want to adopt Happy Hospitalist’s mandatory helmet policy) is to hire a full time sitters for all hospitalized elderly patients. From a purely business point of view (not the point of view I would advocate) hospitals might be better off doing nothing.
Wachter concludes his article with this statement:
In light of all of this uncertainty and risk, “not paying for errors” should be viewed as a bold experiment and its initial implementation a pilot study, whose consequences should be carefully monitored.
That implies that when the unintended consequences surface Medicare will take steps to mitigate them and if the experiment is a failure Medicare will dismantle it. Somehow I’m not comforted. In the 63 year history of this grand experiment’s unintended consequences and abuses, what’s been the track record?
DB weighs in here.
Kevin’s take on Pete Stark
This needs no elaboration:
Wish I’d said it.
Mr. Stark's profound ignorance of medical issues is stunning and dangerous. It is frightening that a politician of his stature is so openly biased and antagonistic against physicians.
Wish I’d said it.
Thursday, February 21, 2008
Quackademic medicine
---is proliferating faster than Orac can update his on line hall of shame, the Academic Woo Aggregator. His February 18 post notes some observations by David Colquhoun, author of DC’s Improbable Science, on just how rampant quackery promotion is in U.S. academic medical institutions. Both posts make for compelling reading.
Medicare and “never events”
Performance enhancing drugs for docs?
When I glanced at the title and abstract of this JAMA study the other day I decided to skip the rest of the article. It looked pretty ho-hum. Investigators found that survival from in hospital cardiac arrest was lower at night and on week ends. Well, duh. But after reading this post from Dr. Wes about the article I thought I’d give it a closer look. At the end of the discussion section the authors suggest the use of performance enhancing drugs for night shift workers: Chronobiologic scheduling, naps, or use of medications such as modafinil may also improve nighttime staff performance. Modafinil, in case you don’t know, is Provigil, a wakefulness promoting drug used in patients with narcolepsy and sleepiness associated with sleep apnea. Before you decide this suggestion is completely off the wall, note that Provigil is approved for shift work sleep disorder (ICD-9 307.45).
Another interesting tidbit, from the paper’s introduction, is the authors’ suggestion that the night and weekend deaths are a result of “medical error.” I can see the next Medicare initiative coming: DRG payment penalties for unexpected night and weekend deaths.
Another interesting tidbit, from the paper’s introduction, is the authors’ suggestion that the night and weekend deaths are a result of “medical error.” I can see the next Medicare initiative coming: DRG payment penalties for unexpected night and weekend deaths.
Wednesday, February 20, 2008
ARDS and ALI: Is recruitment PEEP better than conventional PEEP?
A few years ago an ARDS network study said no for mortality and ventilator free days. Two recent studies published in JAMA revisited the question. In neither study was there a difference in mortality. One study attributed a reduction in refractory hypoxemia to the high peep strategy and the other one demonstrated that the high peep strategy was associated with more ventilator free days and organ failure free days.
Two related editorials were published in the same issue. The one by Gattinoni and Caironi was favorable to the high PEEP strategy for patients with more severe hypoxemia. The other one by Chiche and Angus was more reserved, citing the difficulties in interpreting studies of complex interventions, and suggesting that high PEEP strategies may ultimately emerge in clinical practice.
Taken together, what do these studies mean for real world practice? In neither study did there appear to be harm, and effects on secondary endpoints were encouraging, so why not implement the strategy? For the LOV study, at least, the devil may be in the details. Their protocol involved recruitment maneuvers and allowed plateau pressures to rise as high as 40(!), pretty dicey stuff if you’re not an expert. This is the type of thing that will likely perform better in the hands of expert clinical trialists than in the community.
On the other hand, the protocol used by the Express investigators looks much more doable. I look forward to more discussion and expert opinion on this topic to help us synthesize these findings with what we knew before and to help us decide how to incorporate them into real world practice.
Retired Doc offers some perspective here.
Two related editorials were published in the same issue. The one by Gattinoni and Caironi was favorable to the high PEEP strategy for patients with more severe hypoxemia. The other one by Chiche and Angus was more reserved, citing the difficulties in interpreting studies of complex interventions, and suggesting that high PEEP strategies may ultimately emerge in clinical practice.
Taken together, what do these studies mean for real world practice? In neither study did there appear to be harm, and effects on secondary endpoints were encouraging, so why not implement the strategy? For the LOV study, at least, the devil may be in the details. Their protocol involved recruitment maneuvers and allowed plateau pressures to rise as high as 40(!), pretty dicey stuff if you’re not an expert. This is the type of thing that will likely perform better in the hands of expert clinical trialists than in the community.
On the other hand, the protocol used by the Express investigators looks much more doable. I look forward to more discussion and expert opinion on this topic to help us synthesize these findings with what we knew before and to help us decide how to incorporate them into real world practice.
Retired Doc offers some perspective here.
Tuesday, February 19, 2008
Evidence based medicine does not equal science based medicine
That’s right, I said it. I’ve tried really hard over the last several years to learn about, read about and practice EBM. Along the way I’ve noticed something peculiar: evidence based medicine (EBM) has become a powerful enabler of complementary and alternative medicine (CAM). I touched on this briefly in a post in which I pondered the reasons why woo has so successfully corrupted academic medicine:
The problem may be a form of extreme empiricism applied to clinical questions. Empiricism, according to the dictionary, regards direct experience and observation as the only source of knowledge. In medicine, according to the definition, empiricism “disregards scientific theory and relies solely on practical experience.” That is not a core principle of EBM as I understand it, but it is a popular and pervasive distortion.
How many times, for example, have you heard the old saw “there is no alternative medicine; there is only medicine which has been shown to work and medicine which has not been shown to work?” That may be appealing at first glance, but EBM’s obsession with finding out what treatments “work”, with total disregard for biologic plausibility and prior knowledge, has spawned an explosion of dubious “clinical studies” on all sorts of woo, from acupuncture to those wooiest forms of woo such as homeopathy and Reiki. Seldom is anything solved by such studies. No claims are ever proven, nor are they totally dismissed. The lingering doubt perpetually fuels more inconclusive “research.” The track record of the National Center for Complementary and Alternative Medicine speaks for itself in this regard.
I examined some of the failings of EBM in a post last year. Methodologic flaws in CAM research, chance variation combined with positive publication bias and biased Medline indexing are just a few of the reasons. But I’m afraid I didn’t make these points nearly as well as Kimball Atwood recently did in two wonderful posts in the Science Based Medicine blog.
He points out that treatments must pass not only the evidentiary test but also the test of scientific plausibility. Because EBM devalues the latter it is inadequate for the evaluation of implausible claims even though it may perform well in evaluating plausible ones. This fundamental error is built into EBM’s system of analysis as illustrated by its evidence hierarchy, which places physiologic rationale and scientific principles at the bottom of the heap. Atwood illustrates the consequences of such faulty analysis in the first of his two posts:
Using the example of homeopathy, the focus of the first of his two posts, Atwood goes through a long list of fundamental scientific principles in opposition to the claims of homeopathy and then asks:
In the second post Atwood gives the issue a more quantitative treatment by contrasting EBM’s use of popular frequentist statistics with Bayesian statistical analysis which seeks to determine how new evidence modifies prior knowledge (such as basic science principles, physiologic rationale, etc.). Most of us are familiar with the use of Bayesian analysis in evaluating laboratory test results in individual patients because it is widely advocated and taught as a tool for diagnosis. Although equally valid (and superior in many ways to the popular frequentist approach) for analysis of clinical trial data for evaluation of treatments, it is not a tool of EBM.
Atwood issues a plea for incorporation of Bayesian thinking in the evaluation of clinical claims because it takes into account scientific plausibility. According to Bayes’ theorem, whether you’re evaluating the probability of disease in a patient or the probability that a health claim is true the prior probability, P(A), based on what was known before, occupies the numerator of the equation. Thus if P(A) is zero no amount of observational data could establish the hypothesis as true. If P(A) is infinitesimally small nothing short of overwhelming experimental evidence could establish the hypothesis as true.
Homeopathy, Reiki and Therapeutic Touch immediately come to mind. Bayesian analysis of claims such as these is a formal and quantitative method of establishing what common sense has always told us concerning those occasional weakly positive, methodologically questionable studies of implausible claims. They’re what I call evidence based woo. Consider the miniscule value of P(A) in Bayes’ theorem for such claims as the woo factor, a factor which evidence based medicine leaves out of its analysis.
We need a balanced view. EBM proponents are correct in saying that pathophysiologic rationale alone is not sufficient. (They’re fond of trotting out the CAST study to make that point). But they are wrong to ignore and devalue such knowledge. In order to evaluate the claims of CAM we need clinical evidence taken in the light of fundamental biologic principles.
Finally, and somewhat paradoxically, the rise in unfounded CAM modalities may be an unintended consequence of the EBM movement. EBM advocates devalue scientific rationale and physiologic plausibility.
The problem may be a form of extreme empiricism applied to clinical questions. Empiricism, according to the dictionary, regards direct experience and observation as the only source of knowledge. In medicine, according to the definition, empiricism “disregards scientific theory and relies solely on practical experience.” That is not a core principle of EBM as I understand it, but it is a popular and pervasive distortion.
How many times, for example, have you heard the old saw “there is no alternative medicine; there is only medicine which has been shown to work and medicine which has not been shown to work?” That may be appealing at first glance, but EBM’s obsession with finding out what treatments “work”, with total disregard for biologic plausibility and prior knowledge, has spawned an explosion of dubious “clinical studies” on all sorts of woo, from acupuncture to those wooiest forms of woo such as homeopathy and Reiki. Seldom is anything solved by such studies. No claims are ever proven, nor are they totally dismissed. The lingering doubt perpetually fuels more inconclusive “research.” The track record of the National Center for Complementary and Alternative Medicine speaks for itself in this regard.
I examined some of the failings of EBM in a post last year. Methodologic flaws in CAM research, chance variation combined with positive publication bias and biased Medline indexing are just a few of the reasons. But I’m afraid I didn’t make these points nearly as well as Kimball Atwood recently did in two wonderful posts in the Science Based Medicine blog.
He points out that treatments must pass not only the evidentiary test but also the test of scientific plausibility. Because EBM devalues the latter it is inadequate for the evaluation of implausible claims even though it may perform well in evaluating plausible ones. This fundamental error is built into EBM’s system of analysis as illustrated by its evidence hierarchy, which places physiologic rationale and scientific principles at the bottom of the heap. Atwood illustrates the consequences of such faulty analysis in the first of his two posts:
Thus a “positive” clinical trial is given more weight than “physiology, bench research or ‘first principles’,” even when the latter definitively refute the claim.
Using the example of homeopathy, the focus of the first of his two posts, Atwood goes through a long list of fundamental scientific principles in opposition to the claims of homeopathy and then asks:
Is it realistic to assume that this “level” of evidence, when brought to bear on a claim that has no explanatory power in nature, can be overthrown by ambiguous clinical trials of dubious design? EBM tacitly makes that assumption.
In the second post Atwood gives the issue a more quantitative treatment by contrasting EBM’s use of popular frequentist statistics with Bayesian statistical analysis which seeks to determine how new evidence modifies prior knowledge (such as basic science principles, physiologic rationale, etc.). Most of us are familiar with the use of Bayesian analysis in evaluating laboratory test results in individual patients because it is widely advocated and taught as a tool for diagnosis. Although equally valid (and superior in many ways to the popular frequentist approach) for analysis of clinical trial data for evaluation of treatments, it is not a tool of EBM.
Atwood issues a plea for incorporation of Bayesian thinking in the evaluation of clinical claims because it takes into account scientific plausibility. According to Bayes’ theorem, whether you’re evaluating the probability of disease in a patient or the probability that a health claim is true the prior probability, P(A), based on what was known before, occupies the numerator of the equation. Thus if P(A) is zero no amount of observational data could establish the hypothesis as true. If P(A) is infinitesimally small nothing short of overwhelming experimental evidence could establish the hypothesis as true.
Homeopathy, Reiki and Therapeutic Touch immediately come to mind. Bayesian analysis of claims such as these is a formal and quantitative method of establishing what common sense has always told us concerning those occasional weakly positive, methodologically questionable studies of implausible claims. They’re what I call evidence based woo. Consider the miniscule value of P(A) in Bayes’ theorem for such claims as the woo factor, a factor which evidence based medicine leaves out of its analysis.
We need a balanced view. EBM proponents are correct in saying that pathophysiologic rationale alone is not sufficient. (They’re fond of trotting out the CAST study to make that point). But they are wrong to ignore and devalue such knowledge. In order to evaluate the claims of CAM we need clinical evidence taken in the light of fundamental biologic principles.
Saturday, February 16, 2008
More on the Surviving Sepsis Guidelines 2004-2008
Last Tuesday I began a review of the changes in the Surviving Sepsis Guidelines (SSG) as reflected in the 2008 revisions, recently made available in full text via Medscape. In that post I focused on the controversial recommendations concerning activated protein C, noting that the guideline authors had taken into account the best and most current evidence. Their decision to downgrade the recommendation for activated protein C should put to rest concerns about commercial influence corrupting the guidelines.
What else is new and of interest? I’ll present a summary here of other significant changes from 2004, along with points of special interest.
Early goal directed therapy (EGDT)
The recommendation for EGDT remains strong and has not significantly changed from the 2004 guidelines. The authors again emphasize that the protocol should begin immediately upon recognition of hypoperfusion and not be delayed until ICU admission. The assessment of a patient’s candidacy for EGDT, which can be rapidly and simply done in the ER, includes establishing that SIRS is present, infection is clinically suspected, hypotension or lactate elevation is present and that the patient does not have an advanced decision documented which would preclude hemodynamic resuscitation.
Antibiotic selection
The guidelines contain stronger language than in 2004 concerning the importance of a broad spectrum of initial antibiotic therapy and add a discussion of the importance of anti-MRSA coverage. Noteworthy is this new statement:
They go on to stress that antibiotics can be narrowed later after microbiologic date are available.
Choice of vasopressor
Data in recent years from observational studies, including the SOAP study which came out since the 2004 guidelines, have suggested inferior outcomes with dopamine. Nevertheless, the guideline authors recommend norepinephrine and dopamine as equal alternatives for initial pressor therapy, noting that high level direct comparison studies have not been done.
Corticosteroids
The corticosteroid recommendation, as I predicted late last year, was made more restrictive in keeping with evidence from the CORTICUS study. The 2004 recommendations called for “stress doses” of hydrocortisone in patients requiring pressors after fluid resuscitation. The 2008 guidelines restrict the use of steroids to patients who demonstrate refractoriness to pressor therapy. The guidelines do not recommend cortrosyn stimulation testing to diagnose critical illness related corticosteroid insufficiency (CIRCI). CIRCI, however, is to be distinguished from classical adrenal insufficiency, which may warrant testing in critically ill patients.
Glycemic control
The 2008 SSGs provide a strong recommendation for glycemic control utilizing an insulin drip protocol. However, the recommendation for a specific target (150 mg/dl) is a weak one, reflecting controversy and uncertainty that has prevailed about the appropriate target since publication of the 2004 guidelines.
This summary of the 2008 SSG recommendations is not comprehensive. The document should be read in the original and maintained for reference.
What else is new and of interest? I’ll present a summary here of other significant changes from 2004, along with points of special interest.
Early goal directed therapy (EGDT)
The recommendation for EGDT remains strong and has not significantly changed from the 2004 guidelines. The authors again emphasize that the protocol should begin immediately upon recognition of hypoperfusion and not be delayed until ICU admission. The assessment of a patient’s candidacy for EGDT, which can be rapidly and simply done in the ER, includes establishing that SIRS is present, infection is clinically suspected, hypotension or lactate elevation is present and that the patient does not have an advanced decision documented which would preclude hemodynamic resuscitation.
Antibiotic selection
The guidelines contain stronger language than in 2004 concerning the importance of a broad spectrum of initial antibiotic therapy and add a discussion of the importance of anti-MRSA coverage. Noteworthy is this new statement:
Patients with severe sepsis or septic shock warrant broad-spectrum therapy until the causative organism and its antibiotic susceptibilities are defined. Restriction of antibiotics as a strategy to reduce the development of antimicrobial resistance or to reduce cost is not an appropriate initial strategy in this patient population.
They go on to stress that antibiotics can be narrowed later after microbiologic date are available.
Choice of vasopressor
Data in recent years from observational studies, including the SOAP study which came out since the 2004 guidelines, have suggested inferior outcomes with dopamine. Nevertheless, the guideline authors recommend norepinephrine and dopamine as equal alternatives for initial pressor therapy, noting that high level direct comparison studies have not been done.
Corticosteroids
The corticosteroid recommendation, as I predicted late last year, was made more restrictive in keeping with evidence from the CORTICUS study. The 2004 recommendations called for “stress doses” of hydrocortisone in patients requiring pressors after fluid resuscitation. The 2008 guidelines restrict the use of steroids to patients who demonstrate refractoriness to pressor therapy. The guidelines do not recommend cortrosyn stimulation testing to diagnose critical illness related corticosteroid insufficiency (CIRCI). CIRCI, however, is to be distinguished from classical adrenal insufficiency, which may warrant testing in critically ill patients.
Glycemic control
The 2008 SSGs provide a strong recommendation for glycemic control utilizing an insulin drip protocol. However, the recommendation for a specific target (150 mg/dl) is a weak one, reflecting controversy and uncertainty that has prevailed about the appropriate target since publication of the 2004 guidelines.
This summary of the 2008 SSG recommendations is not comprehensive. The document should be read in the original and maintained for reference.
Thursday, February 14, 2008
The John Ritter malpractice trial
---is underway and a spate of news reports offers some glimpses. I may comment and link from some of them later. For now I’ll just present excerpts from one of my commenters on an earlier post. It speaks well to the issue and requires little elaboration:
Av overweight appearance would be deceptive in that it is not the body habitus one would typically see in patients at risk for dissection.
The commenter goes on:
Read the rest.
To the attorneys who commented with “measured responses” urging us to temper judgment, I would ask at what point you say “enough’s enough.” Is there any amount of damages that should trigger outrage?
What we do know from the AP, is that the Defense attorneys will provide evidence that Ritter had failed an insurance exam 3 years prior to the incident for "incredibly abnormal" blood levels. Triglycerides were 7 times normal. He had evidence of plaque build-up. He was advised to see a cardiologist. He never did.For three years, Ritter repeatedly missed follow-up visits, did not get a cardiologist, worked long hours on the set and was decidedly overweight. When he became ill, he went to the ER.
Av overweight appearance would be deceptive in that it is not the body habitus one would typically see in patients at risk for dissection.
The commenter goes on:
In court yesterday, according to ABC news, the plaintiff's Cardiac Surgeon
(supposed unbiased expert)………
Upon cross examination, things became heated when it was revealed that the Expert had a conflict of interest. In fact, Ritter's wife, Amy Yasbeck, had spent time speaking at the Expert's symposium recently.The Cardiologist's Defense Attorney also quoted from this Expert's OWN book that stated, finding an aortic dissection was like looking for a "needle in a haystack" and that (essentially) in malpractice situations, physicians should be given the benefit of the doubt because they are so difficult to find and so easily mistaken for a heart attack.
Read the rest.
To the attorneys who commented with “measured responses” urging us to temper judgment, I would ask at what point you say “enough’s enough.” Is there any amount of damages that should trigger outrage?
Saturday, February 09, 2008
Maharishi Mahesh Yogi passed away Tuesday
Maharishi Mahesh Yogi, developer and promoter of Transcendental Meditation (TM), died February 5, 2008. TM is a topic of interest to me for two reasons. Caught up in the Beatles generation when it was all the rage, I was fascinated by its claims. I have since come to believe that it is the best example (one of many) of Eastern religion cloaked in pseudoscientific and self-help jargon and repackaged for Western consumption (Yoga, anyone?).
To further sanitize it in order to introduce it into the public schools it was, for a time, renamed “The Science of Creative Intelligence.” However, its claims that it required no religious accommodation did not stand up to close scrutiny. It failed an establishment clause challenge in 1977 and the New Jersey public schools were enjoined from teaching it.
To further sanitize it in order to introduce it into the public schools it was, for a time, renamed “The Science of Creative Intelligence.” However, its claims that it required no religious accommodation did not stand up to close scrutiny. It failed an establishment clause challenge in 1977 and the New Jersey public schools were enjoined from teaching it.
Interesting acid-base case posted at Medrants
DB posted a case from morning report and put me on the spot with a challenge! I posted my best guess in his comments.
Friday, February 08, 2008
The ACCORD study: what does it mean?
A safety analysis and early halt to the intensive glycemic control arm of the ACCORD study was reported yesterday in an NIH press release. It says intensive glycemic control (it was really what I’d call ultra-intensive glycemic control, more stringent than what current guidelines call for) was associated with increased cardiovascular mortality (essentially macrovascular) in patients with type 2 diabetes.
That’s the main, plain message I want to put forth at the beginning of this post before I dismantle the New York Times distortion of the study. The Times article not only over hypes the results but fails to mention the primary source anywhere in the article. That would at least have pointed readers to reliable information.
The opening sentence, patently absurd to anyone who understands epidemiologic issues related to type 2 diabetes, might be a bit confusing to the lay public:
That might have been the popular hype but it is absolutely not what researchers believed for decades (or at any time, for that matter). Although a decade or so ago we learned that intensive glycemic control reduces microvascular complications in DM-1 (DCCT) and in DM-2 (UKPDS) there’s been nary a shred of evidence that it helps macrovascular disease (heart attacks and strokes) at least in DM-2. (A very long follow up of DCCT suggested late macrovascular benefit in DM-1 but that’s a different disease entirely from DM-2, and not the focus of this discussion).
Although evidence of macrovascular benefit in DM-2 with intensive control was lacking, as early as 1998 an analysis of UKPDS hinted at macrovascular benefits (stroke only) attributable to a unique drug (metformin) though not to intensive control, and only in a very narrowly defined population (patients with DM-2 who were obese and on metformin as initial monotherapy, not as add on). Hardly clean and convincing evidence, but it was a hint.
A stronger hint that any drug treatment might improve macrovascular outcomes in DM-2 did not come until quite recently with the release of the PROACTIVE study. So, not until late 2005 did we begin to see evidence that treatment might offer macrovascular benefits. That was unprecedented, and I blogged about it at the time as something of a breakthrough. But it was not evidence, nor in my opinion was it even hypothesis generating, that the benefits were a result of glycemic control. Far more plausible was a unique effect of pioglitazone via non-glycemic mechanisms such as favorable lipid effects, improvement in insulin resistance and improvement in endothelial function. (For a more detailed analysis on the non-evidence for the glycemic control-macrovascular notion see my posts here, here and here).
The New York Times article quoted several medical experts who expressed concern and disappointment in the results, over characterizing their reaction (in a one sentence paragraph, as if to add to the dramatic effect) as “stunned.”
There was nothing stunning or even surprising about it. So what was going on? Ironically, the clue might be found in a quote from the NYT article itself, although the article missed the significance of the clue entirely:
Therein may lie the answer. Patients with type 2 diabetes, many of whom were no doubt obese, were given intensive insulin treatment. Some of then were even pumping! I suspect most of the patients were on insulin, given the aggressive glycemic targets that were achieved. Insulin resistant to start with, the patients treated intensively with insulin likely required high doses which promoted weight gain, sure to beget worsened resistance followed by up-ramping of the dose as they drifted out of control, and on the vicious cycle went.
Anyone who treats obese type-2 diabetics with insulin has seen the cycle. The patient is out of control, so up goes the insulin dose. After transient improvement the inevitable weight gain leads to worsened insulin resistance and worsened hyperglycemia. Up goes the dose again and the cycle repeats. That can’t be good for one’s macrovascular health because insulin resistance is in and of itself a potent macrovascular risk factor. Moreover, it fuels the metabolic syndrome, the principal dyslipidemia of type 2 diabetes.
The suggestion that intensive insulin treatment drove macrovascular disease should surprise no one. It adds to our understanding of the treatment of DM-2 by confirming what we already suspected: 1) that intensive glycemic control does not prevent macrovascular disease and 2) pharmacologic agents for DM-2, including insulin, with the possible exception of those with unique vascular protective actions, have the potential for macrovascular harm.
Other blog reactions to the study came from Med Rants and Health Care Renewal, which I may comment on in future posts as time permits. Their posts cover issues relating to the appropriateness of current guidelines and whether guideline concordant glycemic control for DM-2 really produces meaningful microvascular ourcomes.
That’s the main, plain message I want to put forth at the beginning of this post before I dismantle the New York Times distortion of the study. The Times article not only over hypes the results but fails to mention the primary source anywhere in the article. That would at least have pointed readers to reliable information.
The opening sentence, patently absurd to anyone who understands epidemiologic issues related to type 2 diabetes, might be a bit confusing to the lay public:
For decades, researchers believed that if people with diabetes lowered their blood sugar to normal levels, they would no longer be at high risk of dying from heart disease.
That might have been the popular hype but it is absolutely not what researchers believed for decades (or at any time, for that matter). Although a decade or so ago we learned that intensive glycemic control reduces microvascular complications in DM-1 (DCCT) and in DM-2 (UKPDS) there’s been nary a shred of evidence that it helps macrovascular disease (heart attacks and strokes) at least in DM-2. (A very long follow up of DCCT suggested late macrovascular benefit in DM-1 but that’s a different disease entirely from DM-2, and not the focus of this discussion).
Although evidence of macrovascular benefit in DM-2 with intensive control was lacking, as early as 1998 an analysis of UKPDS hinted at macrovascular benefits (stroke only) attributable to a unique drug (metformin) though not to intensive control, and only in a very narrowly defined population (patients with DM-2 who were obese and on metformin as initial monotherapy, not as add on). Hardly clean and convincing evidence, but it was a hint.
A stronger hint that any drug treatment might improve macrovascular outcomes in DM-2 did not come until quite recently with the release of the PROACTIVE study. So, not until late 2005 did we begin to see evidence that treatment might offer macrovascular benefits. That was unprecedented, and I blogged about it at the time as something of a breakthrough. But it was not evidence, nor in my opinion was it even hypothesis generating, that the benefits were a result of glycemic control. Far more plausible was a unique effect of pioglitazone via non-glycemic mechanisms such as favorable lipid effects, improvement in insulin resistance and improvement in endothelial function. (For a more detailed analysis on the non-evidence for the glycemic control-macrovascular notion see my posts here, here and here).
The New York Times article quoted several medical experts who expressed concern and disappointment in the results, over characterizing their reaction (in a one sentence paragraph, as if to add to the dramatic effect) as “stunned.”
There was nothing stunning or even surprising about it. So what was going on? Ironically, the clue might be found in a quote from the NYT article itself, although the article missed the significance of the clue entirely:
Dr. John Buse, the vice-chairman of the study’s steering committee and the president of medicine and science at the American Diabetes Association, described what was required to get blood sugar levels low, as measured by a protein, hemoglobin A1C, which was supposed to be at 6 percent or less.
“Many were taking four or five shots of insulin a day,” he said. “Some were using insulin pumps. Some were monitoring their blood sugar seven or eight times a day.”
Therein may lie the answer. Patients with type 2 diabetes, many of whom were no doubt obese, were given intensive insulin treatment. Some of then were even pumping! I suspect most of the patients were on insulin, given the aggressive glycemic targets that were achieved. Insulin resistant to start with, the patients treated intensively with insulin likely required high doses which promoted weight gain, sure to beget worsened resistance followed by up-ramping of the dose as they drifted out of control, and on the vicious cycle went.
Anyone who treats obese type-2 diabetics with insulin has seen the cycle. The patient is out of control, so up goes the insulin dose. After transient improvement the inevitable weight gain leads to worsened insulin resistance and worsened hyperglycemia. Up goes the dose again and the cycle repeats. That can’t be good for one’s macrovascular health because insulin resistance is in and of itself a potent macrovascular risk factor. Moreover, it fuels the metabolic syndrome, the principal dyslipidemia of type 2 diabetes.
The suggestion that intensive insulin treatment drove macrovascular disease should surprise no one. It adds to our understanding of the treatment of DM-2 by confirming what we already suspected: 1) that intensive glycemic control does not prevent macrovascular disease and 2) pharmacologic agents for DM-2, including insulin, with the possible exception of those with unique vascular protective actions, have the potential for macrovascular harm.
Other blog reactions to the study came from Med Rants and Health Care Renewal, which I may comment on in future posts as time permits. Their posts cover issues relating to the appropriateness of current guidelines and whether guideline concordant glycemic control for DM-2 really produces meaningful microvascular ourcomes.
Thursday, February 07, 2008
Medical school professors react to criticism and defend the CAMbrian explosion. Is Flexner really smiling down?
Our recent Medscape Roundtable discussion on the controversies surrounding integrative medicine in the med school curriculum must have hit a home run. It got the attention of the leadership of the Consortium of Academic Health Centers for Integrative Medicine (CAHCIM), arguably (with the possible exception of the AMSA) the most influential and best organized group supporting the infusion of, to put it kindly and gently, questionable teachings into the mainstream curriculum.
Members of the Consortium posted a letter to the editor in which they defended the “CAMbrian explosion”, concluding that instead of turning over in his grave, Abraham Flexner may in fact be “smiling down.” Although defects in their arguments are easy enough to spot two of the Roundtable authors, Dr. Roy Poses and I, posted a reply that can be accessed on the same page.
Members of the Consortium posted a letter to the editor in which they defended the “CAMbrian explosion”, concluding that instead of turning over in his grave, Abraham Flexner may in fact be “smiling down.” Although defects in their arguments are easy enough to spot two of the Roundtable authors, Dr. Roy Poses and I, posted a reply that can be accessed on the same page.
From the other side of the sheets
As my readers know, I generally don’t blog about local issues or patients. I’m going to take exception today and blog about a patient. I recently became one.
A week ago Sunday at about 3 AM, my on call shift nearing completion, things were finally “quiet” enough for me to head for the hospitalist sleeping quarters to crash for an hour or two. Settling into the arms of Morpheus and thinking “I’ve survived another call night” I began to notice an uneasy but familiar sensation in my left flank. I had had kidney stones before, several of which I had passed easily. But as the sensation intensified to actual pain I was reminded of my episode of a few years ago, a very large stone stuck in my left ureteropelvic junction (UPJ) that ultimately required lithotripsy. Initial thoughts of “I don’t have time for this” soon gave way to “wow, this really hurts, I hope I can make it through the rest of my shift.” I paced the floor wondering what to do. An entrance to the ER was just across the hall. It would be easy enough to walk over there and get help of some sort, but no. I had to finish my shift. I was about to have a week off; then I could do something. The pain waxed and waned in typical colicky fashion before dulling down to a merely annoying level and I finished my shift.
Denial began to take over once I arrived home feeling much better. Maybe the stone had dropped into my bladder. Spirits lifted, I resolved then and there not to ruin my week off fiddling with this problem and (so I rationalized) consuming those precious medical resources. I made it through the week fairly well, subsisting on nothing more than a few Tylenol, but with just enough pain to convince me, toward the end of the week, to call my PCP (yes, I actually have one) who ordered a CT scan. This revealed a 5mm stone just below the UPJ (hmmm, UpToDate says that’s almost small enough to pass with the help of forced fluids and a little Flomax, I thought).
A KUB several days later showing no signs of passage convinced the urologist it was time to intervene, so I went in for extracorporeal shock wave lithotripsy (ESWL) yesterday. By that time, though virtually pain free, constitutional symptoms, gradual dehydration and fatigue had taken their toll. I was glad to be doing something, finally.
The nursing and anesthesia staff (even those I had occasionally snapped at in past moments of frustration) were professional and courteous, and I tried my best not to fall into the VIP syndrome. Despite my repeated protestations that I was pain free I was asked multiple times to “rate my pain” on a scale of 1 to 10.
All went well. The procedure was successful and, as a bonus, there were no laboratory surprises. The malaise was gone and I returned home yesterday afternoon feeling rejuvenated, expansive and inspired to write this post. I think there are lessons here for me to ponder---lessons about being a better steward of my health and being a better doctor.
Disclaimer and disclosure: the use of Flomax described in this posting is off-label. I would have posted an image of my stone fragments, but the dog ate them.
A week ago Sunday at about 3 AM, my on call shift nearing completion, things were finally “quiet” enough for me to head for the hospitalist sleeping quarters to crash for an hour or two. Settling into the arms of Morpheus and thinking “I’ve survived another call night” I began to notice an uneasy but familiar sensation in my left flank. I had had kidney stones before, several of which I had passed easily. But as the sensation intensified to actual pain I was reminded of my episode of a few years ago, a very large stone stuck in my left ureteropelvic junction (UPJ) that ultimately required lithotripsy. Initial thoughts of “I don’t have time for this” soon gave way to “wow, this really hurts, I hope I can make it through the rest of my shift.” I paced the floor wondering what to do. An entrance to the ER was just across the hall. It would be easy enough to walk over there and get help of some sort, but no. I had to finish my shift. I was about to have a week off; then I could do something. The pain waxed and waned in typical colicky fashion before dulling down to a merely annoying level and I finished my shift.
Denial began to take over once I arrived home feeling much better. Maybe the stone had dropped into my bladder. Spirits lifted, I resolved then and there not to ruin my week off fiddling with this problem and (so I rationalized) consuming those precious medical resources. I made it through the week fairly well, subsisting on nothing more than a few Tylenol, but with just enough pain to convince me, toward the end of the week, to call my PCP (yes, I actually have one) who ordered a CT scan. This revealed a 5mm stone just below the UPJ (hmmm, UpToDate says that’s almost small enough to pass with the help of forced fluids and a little Flomax, I thought).
A KUB several days later showing no signs of passage convinced the urologist it was time to intervene, so I went in for extracorporeal shock wave lithotripsy (ESWL) yesterday. By that time, though virtually pain free, constitutional symptoms, gradual dehydration and fatigue had taken their toll. I was glad to be doing something, finally.
The nursing and anesthesia staff (even those I had occasionally snapped at in past moments of frustration) were professional and courteous, and I tried my best not to fall into the VIP syndrome. Despite my repeated protestations that I was pain free I was asked multiple times to “rate my pain” on a scale of 1 to 10.
All went well. The procedure was successful and, as a bonus, there were no laboratory surprises. The malaise was gone and I returned home yesterday afternoon feeling rejuvenated, expansive and inspired to write this post. I think there are lessons here for me to ponder---lessons about being a better steward of my health and being a better doctor.
Disclaimer and disclosure: the use of Flomax described in this posting is off-label. I would have posted an image of my stone fragments, but the dog ate them.
Wednesday, February 06, 2008
Reactions to the John Ritter malpractice suit
Blog reactions to the Ritter suit are trickling in. Here are some I found noteworthy.
A post from the New York Personal Injury Law Blog (one I find enjoyable to read, as law blogs go) says, somewhat to my surprise, that:
Well, that’s news to me. I hope he’s (Eric Turkewitz) right. He reports that jury selection started yesterday. Pretty darn important, that. Unless the media reports are profoundly misleading (and that’s a big “if”) it will be difficult for the plaintiffs to sustain their burden of proof in the eyes of an objective jury. That’s why, in this high stakes legal battle, you can bet, the plaintiff attorneys will be scrambling for passionate, emotion driven, star struck jurors.
Dr. Wes, blogging over at Med Page Today, cites inflated public expectations of medicine:
Society expects a zero defect medical system with diagnostic and therapeutic perfection. Dr. Wes notes another lesson from this lawsuit: it is an example of why defensive over testing is done and why medical costs are so high.
Finally, read the comment by The Happy Hospitalist on my February 4 post. He correctly points out that this isn’t malpractice; it’s a matter of differential diagnosis. No matter how strongly the signs, symptoms and test results point to a particular diagnosis the patient could always have something else. Occasional misdiagnosis is inevitable, even by the best, brightest and most careful clinicians. Such misdiagnosis is considered medical error these days, and that’s just plain wrong. It inflates published estimates of medical mistakes and drives unreasonable public expectations.
A post from the New York Personal Injury Law Blog (one I find enjoyable to read, as law blogs go) says, somewhat to my surprise, that:
Suits against emergency departments are very difficult, though not impossible. Jurors will, if given half a chance, give the benefit of the doubt to emergency room physicians, often times even if their own protocols are violated.
Well, that’s news to me. I hope he’s (Eric Turkewitz) right. He reports that jury selection started yesterday. Pretty darn important, that. Unless the media reports are profoundly misleading (and that’s a big “if”) it will be difficult for the plaintiffs to sustain their burden of proof in the eyes of an objective jury. That’s why, in this high stakes legal battle, you can bet, the plaintiff attorneys will be scrambling for passionate, emotion driven, star struck jurors.
Dr. Wes, blogging over at Med Page Today, cites inflated public expectations of medicine:
Unfortunately, our profession has hyped its tools, instruments and outcomes so excessively through magazines, TV advertisements, miraculous TV shows (take "ER" or "House, MD" for instance) and hospital "Top 100" ratings, that the general public has forgotten that we cannot always fix everything or cure everything. To miss a diagnosis of a relatively rare disease (relative to more common disorders) is no longer acceptable in America.
Society expects a zero defect medical system with diagnostic and therapeutic perfection. Dr. Wes notes another lesson from this lawsuit: it is an example of why defensive over testing is done and why medical costs are so high.
Finally, read the comment by The Happy Hospitalist on my February 4 post. He correctly points out that this isn’t malpractice; it’s a matter of differential diagnosis. No matter how strongly the signs, symptoms and test results point to a particular diagnosis the patient could always have something else. Occasional misdiagnosis is inevitable, even by the best, brightest and most careful clinicians. Such misdiagnosis is considered medical error these days, and that’s just plain wrong. It inflates published estimates of medical mistakes and drives unreasonable public expectations.
Aortic dissection and related syndromes
---including intramural hematoma, penetrating atherosclerotic ulcer, unstable aneurysm, localized intimal tears and post traumatic dissections are frequently lumped under the heading of acute aortic syndrome. A review and editorial in the Cleveland Clinic Journal of Medicine discuss classifications, clinical manifestations, management and the role of CT.
Tuesday, February 05, 2008
Love those ‘lanches
In that greatest and most elaborate of all computer games, blogging, there are numerous ways to score points. One, sort of analogous to baseball’s grand slam home run, is the proverbial ‘lanche. The term is usually combined with a blogger’s name and refers to a spike in traffic that results when said blogger links to one of your posts. It originally referred to the coveted Instalanche, meaning, of course, the huge increase in traffic following a link from the widely read Instapundit blog. I’ve never had an Instalanche but I’ve had my share of Kevinlanches and Oraclanches which always make for a good blogging day.
Today I experienced one of the more significant ‘lanches in my blogging carreer---an Overlawyeredlanche. The folks at Overlawyered included my latest John Ritter Lawsuit post in their February 5 roundup. Many thanks for the link!
I knew something was up when I checked my blog stats:
For my humble little blog that's a lot of hits!
Today I experienced one of the more significant ‘lanches in my blogging carreer---an Overlawyeredlanche. The folks at Overlawyered included my latest John Ritter Lawsuit post in their February 5 roundup. Many thanks for the link!
I knew something was up when I checked my blog stats:
For my humble little blog that's a lot of hits!
NCCAM: $1 billion and counting, and nothing to show for it
When DC’s Improbable Science declared that the NCCAM had denounced homeopathy I was stunned. Could this be true? After years and years and millions of tax dollars had the National Center for Complementary and Alternative Medicine (NCCAM, which I think would be more appropriately named NCPP for National Center for the Promotion of Pseudoscience) finally settled something by debunking homeopathy, one of the wooiest forms of woo? The link was to this Newsweek article on CAM which quoted the acting director of NCCAM thusly:
My encouragement was short lived thanks to a post by Dr. David Gorski, writing for the Science Based Medicine blog. He trotted out examples to show that the NCCAM, in fact, continues to fund “research” on homeopathy right along with all the other woo. How about this one: Dilution and Succussion in Homepathic Remedy Dose-Response Patterns. Here’s how Gorski describes the study:
In reading the proposal had I not known this was funded by a grant from NCCAM I would have thought it was a parody---something right out of Q Fever, perhaps.
Gorski’s post is not just about homeopathy. The piece, one of the most comprehensive analyses of the NCCAM I’ve ever seen and well worth reading in its entirety, drives home three important points:
Throughout its history and at multiple levels of organization the NCCAM is rife with conflicts of interest.
After spending about a billion dollars over many years the NCCAM has validated nothing and debunked nothing (of any scientific importance, anyway) in the world of complementary and alternative medicine.
Much of the activity of NCCAM (and money spent) is promotional.
I’ve had a few things to say about NCCAM in prior posts:
NCCAM’s Trial to Assess Chelation Therapy (TACT) is not only unnecessary but was doomed from the get-go by design flaws and conflicts of interest.
They keep hammering away in support of the same old woo despite implausibility and lack of supporting evidence.
Dr. Jack Killen, acting deputy director of the National Center for Complementary and Alternative Medicine, says homeopathy "goes beyond current understanding of chemistry and physics." He adds: "There is, to my knowledge, no condition for which homeopathy has been proven to be an effective treatment."
My encouragement was short lived thanks to a post by Dr. David Gorski, writing for the Science Based Medicine blog. He trotted out examples to show that the NCCAM, in fact, continues to fund “research” on homeopathy right along with all the other woo. How about this one: Dilution and Succussion in Homepathic Remedy Dose-Response Patterns. Here’s how Gorski describes the study:
This latter grant actually proposes to study whether succussion (the vigorous shaking done with each homeopathic dilution) that, claim homeopaths, is necessary to “potentize” their remedies affects the dose-response characteristics of homeopathic remedies up to 30C dilution (30 times 100-fold, or a dilution factor of 1 x 10-60). This is a dilution factor many orders of magnitude larger than Avagaddro’s number, which is makes a 30C homeopathic remedy nothing but water. Period. In fact, the investigators are actually going to compare stirring with succussion to see whether succussion, as homepaths claim, improves the dose-response curve. It beggars the imagination that such a project was actually seriously considered and then scored highly by a study section.
In reading the proposal had I not known this was funded by a grant from NCCAM I would have thought it was a parody---something right out of Q Fever, perhaps.
Gorski’s post is not just about homeopathy. The piece, one of the most comprehensive analyses of the NCCAM I’ve ever seen and well worth reading in its entirety, drives home three important points:
Throughout its history and at multiple levels of organization the NCCAM is rife with conflicts of interest.
After spending about a billion dollars over many years the NCCAM has validated nothing and debunked nothing (of any scientific importance, anyway) in the world of complementary and alternative medicine.
Much of the activity of NCCAM (and money spent) is promotional.
I’ve had a few things to say about NCCAM in prior posts:
NCCAM’s Trial to Assess Chelation Therapy (TACT) is not only unnecessary but was doomed from the get-go by design flaws and conflicts of interest.
They keep hammering away in support of the same old woo despite implausibility and lack of supporting evidence.
Retired Doc observes his blog birthday
---and reflects on things he’s observed in three years of blogging. (Some great content, by the way).
A strong, declarative statement against CAM
---came from a medical student, no less. In a recent post Jake Young said: Complementary and alternative medicine has no business participating in mainstream science or medicine. He went on to dismantle some of the tired arguments for incorporating woo into mainstream medicine. Medical students, read this post before you decide to suspend disbelief and check your brains at the door to the classroom. Via Orac.
Monday, February 04, 2008
I’ll take $67 million to go with that, please!
To go with what? To go with the $14 million John Ritter’s family has already received in settlements following his death, according to the Los Angeles Times. In the upcoming malpractice suit, $67 million is the amount being sought from two doctors involved in Ritter’s care, one who read a CT scan in 2001 and another who treated Ritter the night of his death in 2003.
But, you ask, what about California’s $250,000 damage cap? That’s for damages related to pain and suffering. The $67 million, according to Ritter’s family and their lawyers, represents “actual” damages---money they say Ritter likely would have made over the next several years given the projected success of his acting career.
I blogged about this a couple of years ago. At that time I maintained (based on what I could glean from news reports) that Ritter’s presentation was more suggestive of myocardial ischemia or infarction than aortic dissection, that he did not exhibit risk factors for dissection and that his doctors acted appropriately on the clinical information they had. Although new reports from the past couple of weeks suggest some twists and turns in the story I still maintain (to the extent that one can believe newspaper reports) that Ritter’s doctors acted appropriately.
Let’s look at some of the clinical issues. According to the Los Angeles Times report the chest x-ray Ritter’s doctors ordered in the ER was not done in a timely manner (or not done at all). By the time the doctors realized this, apparently, Ritter had destabilized and they, acutely aware that time to reperfusion means less opportunity to salvage heart muscle and save the patient (one study suggests a mortality increase of 0.9% per minute of delay), were scrambling to get him off to the cardiac catheterization laboratory. That seems reasonable from where I sit, but important issues to be hammered out include the value of plain chest radiography (a portable chest x-ray done under less than optimal conditions, at that) in the initial evaluation of patients with aortic dissection. What are the positive and negative predictive values? Are they good enough to have averted Ritter’s trip to the cath lab? At the rate Ritter was deteriorating, would there have been time for a CT? Would the CT have diagnosed Ritter’s dissection any more rapidly than his doctors were able to do during cardiac catheterization? Aortic angiography, a part of cardiac catheterization, is a test used to diagnose acute aortic disease and, according to the LA Times report, revealed the dissection:
The article also notes:
What were those abnormalities? Were they biomarkers? Electrocardiographic signs? How specific were they? Did they suggest the “acute coronary syndrome” pathway (aspirin, anticoagulation, cath lab) as an appropriate course of action?
And what about the CT scan Ritter received 2 years earlier? The plaintiffs contend Ritter’s aorta was enlarged then; the defense experts say it wasn’t. What was the diameter of the aortic annulus? Did it exceed a threshold for follow up imaging or even elective surgery?
Do the answers to these difficult and complex questions satisfy the burden of proof that a different course of action, according to a reasonable standard of care, should have been taken and that such action would have saved Ritter’s life? It seems a real stretch to me provided the issues are given an objective analysis. But comments from Ritter’s widow suggests she’s hoping for an emotional verdict:
If anything near that amount of money is awarded it will send some not so healthy messages, one of which concerns how we should treat VIPs. As the LA Times article points out concerning the case:
Ritter’s wife goes on to suggest her motivation is to help others:
And if she should decide to donate the proceeds of this legal action to the American Heart Association it would trump a great deal of cynicism that’s bound to follow any claim that it’s “not about the money.”
But, you ask, what about California’s $250,000 damage cap? That’s for damages related to pain and suffering. The $67 million, according to Ritter’s family and their lawyers, represents “actual” damages---money they say Ritter likely would have made over the next several years given the projected success of his acting career.
I blogged about this a couple of years ago. At that time I maintained (based on what I could glean from news reports) that Ritter’s presentation was more suggestive of myocardial ischemia or infarction than aortic dissection, that he did not exhibit risk factors for dissection and that his doctors acted appropriately on the clinical information they had. Although new reports from the past couple of weeks suggest some twists and turns in the story I still maintain (to the extent that one can believe newspaper reports) that Ritter’s doctors acted appropriately.
Let’s look at some of the clinical issues. According to the Los Angeles Times report the chest x-ray Ritter’s doctors ordered in the ER was not done in a timely manner (or not done at all). By the time the doctors realized this, apparently, Ritter had destabilized and they, acutely aware that time to reperfusion means less opportunity to salvage heart muscle and save the patient (one study suggests a mortality increase of 0.9% per minute of delay), were scrambling to get him off to the cardiac catheterization laboratory. That seems reasonable from where I sit, but important issues to be hammered out include the value of plain chest radiography (a portable chest x-ray done under less than optimal conditions, at that) in the initial evaluation of patients with aortic dissection. What are the positive and negative predictive values? Are they good enough to have averted Ritter’s trip to the cath lab? At the rate Ritter was deteriorating, would there have been time for a CT? Would the CT have diagnosed Ritter’s dissection any more rapidly than his doctors were able to do during cardiac catheterization? Aortic angiography, a part of cardiac catheterization, is a test used to diagnose acute aortic disease and, according to the LA Times report, revealed the dissection:
He also quickly planned a cardiac catheterization. During the procedure, Ritter's condition worsened and a large aortic dissection was found.
The article also notes:
Around 7:15 p.m., a test showed abnormalities that the doctor thought were consistent with a heart attack. Lee, who was on call, was at Ritter's bedside at 7:25 p.m.
What were those abnormalities? Were they biomarkers? Electrocardiographic signs? How specific were they? Did they suggest the “acute coronary syndrome” pathway (aspirin, anticoagulation, cath lab) as an appropriate course of action?
And what about the CT scan Ritter received 2 years earlier? The plaintiffs contend Ritter’s aorta was enlarged then; the defense experts say it wasn’t. What was the diameter of the aortic annulus? Did it exceed a threshold for follow up imaging or even elective surgery?
Do the answers to these difficult and complex questions satisfy the burden of proof that a different course of action, according to a reasonable standard of care, should have been taken and that such action would have saved Ritter’s life? It seems a real stretch to me provided the issues are given an objective analysis. But comments from Ritter’s widow suggests she’s hoping for an emotional verdict:
"You can't treat my kid's dad for something and kill him in the process," she said."I think the money will show how angry the jury will be about what happened to John and what could happen to them."
If anything near that amount of money is awarded it will send some not so healthy messages, one of which concerns how we should treat VIPs. As the LA Times article points out concerning the case:
It also will highlight how differently malpractice lawsuits play out when the alleged victim is wealthy. Ritter, best known for his starring role as Jack Tripper on "Three's Company," was an actor with tremendous earning potential, the plaintiffs' lawyers say. Because of his subsequent success on the series "8 Simple Rules for Dating My Teenage Daughter," his family is asking for more than $67 million in damages -- a stratospheric sum compared with most such claims.
Ritter’s wife goes on to suggest her motivation is to help others:
Yasbeck said she knows the trial will provide a public airing of Ritter's health and potential wealth and attract plenty of media attention. She said she hopes it also will bring awareness to aortic diseases."It's never comfortable, but the idea of the awareness that this brings to the issue trumps that," she said. "My discomfort is nothing compared to people who are losing their family to aortic dissection. I can be uncomfortable for however long the trial goes. I'm ready."
And if she should decide to donate the proceeds of this legal action to the American Heart Association it would trump a great deal of cynicism that’s bound to follow any claim that it’s “not about the money.”
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