Friday, November 28, 2008
Thursday, November 27, 2008
Check out Endotext
The main page reads We offer the only complete, authoritative, constantly updated, down-loadable source on clinical endocrinology, without registration or cost. Almost seems too good to be true, but what I’ve checked out so far is very good. (H/T to Robert J. Rushakoff speaking at Bob Wachters’ 12th Annual Hospital Medicine course).
Antiarrhythmic effects of statins
In this study they decreased atrial fib/flutter by 53% and inappropriate AICD discharges by 39%.
Wednesday, November 26, 2008
Hepatic encephalopathy
Ammonia is instrumental in the pathogenesis. It’s not just a marker.
Ammonia causes astrocyte swelling and alterations in neurotransmitter metabolism.
Cytokines cause astrocyte swelling, explaining the role of infection in precipitating HE.
Those are some of the interesting points in a review published in Seminars in Liver Disease, one of the better reviews I’ve seen on the subject.
Ammonia causes astrocyte swelling and alterations in neurotransmitter metabolism.
Cytokines cause astrocyte swelling, explaining the role of infection in precipitating HE.
Those are some of the interesting points in a review published in Seminars in Liver Disease, one of the better reviews I’ve seen on the subject.
Tuesday, November 25, 2008
T wave abnormality: cardiac or cerebral?
In 1954 George Burch described T wave abnormalities as myocardial ischemia mimics in patients with a variety of acute cerebral insults. His classic paper, which popularized the term cerebral T waves, is available as free full text here. (Note the nine lead electrocardiograms recorded from the string galvanometer on photographic paper).
Fifty four years later we’re just beginning to understand the neurocardiac mechanisms. Those mechanisms, along with a few ECG examples, were recently reviewed in the American Journal of Emergency Medicine. An algorithm to help differentiate cardiac from cerebral T wave abnormalities is presented. However, considerable overlap between the patterns exists.
Fifty four years later we’re just beginning to understand the neurocardiac mechanisms. Those mechanisms, along with a few ECG examples, were recently reviewed in the American Journal of Emergency Medicine. An algorithm to help differentiate cardiac from cerebral T wave abnormalities is presented. However, considerable overlap between the patterns exists.
Monday, November 24, 2008
Web based diabetes management tutorials
General management
Inpatient management
H/T to Robert J. Rushakoff, from his talk at Bob Wachter’s Hospital Medicine course.
Inpatient management
H/T to Robert J. Rushakoff, from his talk at Bob Wachter’s Hospital Medicine course.
Sunday, November 23, 2008
Hospitalists and the economy
I can already hear the buzz at SHM 2009. How will the recession affect the hospitalist movement? How should hospitalists be compensated in tough economic times? And, one more time, How can we measure and demonstrate our value?
The past few weeks have seen some interesting and provocative posts on this subject. Adam Singer, author of The Hospitalist Blog, thinks the economic woes of hospitals will trickle down to hospitalists. His solution? If I read him correctly, he thinks hospitalist programs should become “self sufficient” and subsist entirely (or almost entirely) from their billing revenues:
I’m skeptical as to how that can be done. I think he plans to explain in installment three.
Bob Wachter’s prognosis, though not quite so pessimistic, is guarded:
(Do ya think hospital CEOs should participate too, Bob?) ;)
What disturbs me just a wee bit in both posts is the characterization of hospitalist compensation. Referring to the difference between what programs are paid and the fees they produce, Adam uses the term “subsidy” and Bob talks about “support payments.” It implies most programs don’t really “earn their keep.” The usual workaround for that uncomfortable notion invokes all the mental gymnastics about hospitalists’ “value.”
Sure, hospitalist programs bring a great deal more to health care systems than the fees they generate. Much of that value, though, is intangible. It can’t be measured. Here’s the value test: imagine waking up some morning to find that your hospital’s hospitalist program has imploded.
The past few weeks have seen some interesting and provocative posts on this subject. Adam Singer, author of The Hospitalist Blog, thinks the economic woes of hospitals will trickle down to hospitalists. His solution? If I read him correctly, he thinks hospitalist programs should become “self sufficient” and subsist entirely (or almost entirely) from their billing revenues:
Herein lays the opportunity for hospitalist groups of all types to seize this moment and reevaluate their business models with the goal of reducing their dependency on hospital subsidy dollars to sustain their practices. There are some situations where obtaining hospital stipends are totally appropriate, such as providing on-site night coverage or caring for a disproportionate share of indigent patients, but these situations are more the exception than the rule. Focus on finding opportunities and staffing models for your practice that will generate enough profit so that your practice is self-sustaining. Better to view your hospital subsidy as a luxury that your practice could live without if you had to, rather than as a necessity that you need in order to survive. It can be done.
I’m skeptical as to how that can be done. I think he plans to explain in installment three.
Bob Wachter’s prognosis, though not quite so pessimistic, is guarded:
My own feeling is that we should accept our share of any shared pain. If budgets are being cut across our institution, we should participate in reasonable belt tightening.
(Do ya think hospital CEOs should participate too, Bob?) ;)
What disturbs me just a wee bit in both posts is the characterization of hospitalist compensation. Referring to the difference between what programs are paid and the fees they produce, Adam uses the term “subsidy” and Bob talks about “support payments.” It implies most programs don’t really “earn their keep.” The usual workaround for that uncomfortable notion invokes all the mental gymnastics about hospitalists’ “value.”
Sure, hospitalist programs bring a great deal more to health care systems than the fees they generate. Much of that value, though, is intangible. It can’t be measured. Here’s the value test: imagine waking up some morning to find that your hospital’s hospitalist program has imploded.
Another new clinical blog
Well, not so new---it’s been up and running since April---but I just found out about it from the Clinical Cases and Images blog. The masthead for Renal Fellow Network reads: A website written for renal fellows by renal fellows with one new "Nephrology Teaching Point" posted on a daily basis. Hard core clinical content. No fluff. I like it.
Saturday, November 22, 2008
AHA 2008 roundup
I’m late with this and it’s all been posted elsewhere, so why here and now?
Very seldom do medical research findings warrant coverage as breaking news. Rare findings which are really earth shattering are often not appreciated as such until months or years later. Many media reports from the AHA sessions were little more than sound bites and many were over hyped. When those reports came out I was too busy and tired to blog. Now, after an opportunity to check primary sources and think about the findings, I offer my own take on some of the ones that interested me.
JUPITER The NEJM abstract concludes with:
So---statin treatment works for primary prevention in patients with “normal” cholesterol levels. Earthshaking? Hardly. We knew this a decade ago. Remember AFCAPS/TexCAPS?
This study helps confirm the findings of AFCAPS/TexCAPS and (I think) extends them to even healthier patients. The study was hyped and probably won’t (or shouldn’t) change practice much. For a thoughtful and nuanced view of JUPITER see the accompanying NEJM editorial.
When considering the use of statins for primary prevention in low risk patients one must weigh in absolute risk reduction (the NNT in JUPITER was 120 patients treated for 1.9 years), cost effectiveness (Dr. Wes does the math for Crestor here) and the risks of years and years of statin use.
What’s the significance of the hs-CRP test? Although statins (at least some) lower CRP levels, the main significance is that CRP, like diabetes, smoking and hypertension, is a risk factor and the higher the patient’s risk the bigger the bang for the buck with LDL reduction. This was shown several years ago for hs-CRP in a subgroup analysis of AFCAPS/TexCAPS. The statin used in that study, lovastatin (Mevacor) is now on Walmart’s $4 generic list. Do the math again and it looks a good deal better from a cost effectiveness standpoint.
Negative Thinking Predicts Depression in Heart-Failure Patients. Did we really need a study to figure that out?
LDL particle concentration versus LDL cholesterol concentration Via Reuters Health:
We’ve known this for years. Although the guidelines have not emphasized it enough the concept of residual risk after statin therapy (RRAST) is emerging. LDL reduction is important and, in the aggregate, the lower the better. In many individual patients, though, it’s not enough. The fact that statin trials show RRR’s of 25-30% begs the question “why not 80%, why not 100%?” (Bob Superko addressed this in his classic paper here, and, along with Spencer King, provided an update here).
From the Reuters piece:
High LDL particle concentration relative to LDLC concentration reflects the atherogenic lipoprotein profile (ALP) characterized by abnormally small LDL particle diameter. This is a phenotypic expression of the metabolic syndrome and for practical purposes many regard it as synonymous (this is not invariably so---the ALP is nicely explained in the Superko papers linked above). The ALP and the associated metabolic syndrome represent the most common genetic causes of CAD and are certainly the most important contributors to RRAST.
Perhaps most concerning from the AHA presentation was this:
This is a finding that needs better understanding. Do statins somehow turn on genes that cause metabolic syndrome? What’s the solution? When the patient is at goal with statin therapy the RRAST must be assessed. The determination of triglycerides, HDLC and the total/HDL ratio are helpful. If the metabolic syndrome is evident diet and exercise are the best treatments, and drug therapy options include niacins and fibrates.
It has been suggested that lowering LDLC to extremely low concentrations with statins may offset this residual---lower the cholesterol concentration enough with statins and eventually the particle concentration will go down, perhaps. In that connection note a little mentioned aspect of JUPITER---LDLC was lowered to a median of 55 and RRR’s were on the order of an unprecedented 50% in contrast to the 25-30% reductions cited for other statin trials. Maybe there’s something to it.
Vitamins C and E Here we go again. No benefit. Vitamin E may even be harmful. There’s never been any favorable evidence for vitamin C and vitamin E was blown out of the water years ago. That hasn’t stopped some from promoting it, though.
Irbesartan and heart failure with preserved EF
Again, this result for irbesartan (Avapro) is not new regarding ARB’s and heart failure with preserved ejection fraction (HFPEF). The CHARM-preserved study reached a similar conclusion years ago with candesartan (Atacand). There is little in the way of evidence from clinical trials to guide clinicians in the long term treatment of HFPEF. The best we can do now is to do a better job of treating their co-morbidities, of which they have many. If those co-morbidities include hypertension irbesartan as well as other antihypertensive agents might be reasonable choices. To say that irbesartan is of no value in the treatment of patients with HFPEF is simplistic. (Patients to be included in the irbesartan study could not have uncontrolled hypertension).
Perioperative beta blockers---another negative meta-analysis. From the Lancet paper:
Well, they already have, quite some time ago. Now, the only strong guideline recommendation, for practical purposes, is that if the patient is already on a beta blocker for cardiovascular indications it should be continued perioperatively.
Statin dose-response relationships: Search Me This one’s a little complicated. Simvastatin (Zocor) was only marginally better at 80 mg in comparison to 20 mg daily in terms of reducing events in a secondary prevention study. But when this study is taken into account with multiple other statin trials the notion that lower LDLC is better still holds. Most disturbing was the markedly increased incidence of myopathy at the 80 mg dose. According to expert commentary about this study, if it’s desirable to seek very low LDLC targets in your patient it may be better to switch to a safer statin as opposed to increasing simvastatin to 80 mg. Simvastatin is safe when used according to the product safety labeling. This labeling, however, particularly the section on drug interactions, has become so complicated that simvastatin is getting a little tricky to prescribe. One has to review the patient’s entire med list and, unless one has a photographic memory, look up the labeling each time.
Very seldom do medical research findings warrant coverage as breaking news. Rare findings which are really earth shattering are often not appreciated as such until months or years later. Many media reports from the AHA sessions were little more than sound bites and many were over hyped. When those reports came out I was too busy and tired to blog. Now, after an opportunity to check primary sources and think about the findings, I offer my own take on some of the ones that interested me.
JUPITER The NEJM abstract concludes with:
In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events.
So---statin treatment works for primary prevention in patients with “normal” cholesterol levels. Earthshaking? Hardly. We knew this a decade ago. Remember AFCAPS/TexCAPS?
This study helps confirm the findings of AFCAPS/TexCAPS and (I think) extends them to even healthier patients. The study was hyped and probably won’t (or shouldn’t) change practice much. For a thoughtful and nuanced view of JUPITER see the accompanying NEJM editorial.
When considering the use of statins for primary prevention in low risk patients one must weigh in absolute risk reduction (the NNT in JUPITER was 120 patients treated for 1.9 years), cost effectiveness (Dr. Wes does the math for Crestor here) and the risks of years and years of statin use.
What’s the significance of the hs-CRP test? Although statins (at least some) lower CRP levels, the main significance is that CRP, like diabetes, smoking and hypertension, is a risk factor and the higher the patient’s risk the bigger the bang for the buck with LDL reduction. This was shown several years ago for hs-CRP in a subgroup analysis of AFCAPS/TexCAPS. The statin used in that study, lovastatin (Mevacor) is now on Walmart’s $4 generic list. Do the math again and it looks a good deal better from a cost effectiveness standpoint.
Negative Thinking Predicts Depression in Heart-Failure Patients. Did we really need a study to figure that out?
LDL particle concentration versus LDL cholesterol concentration Via Reuters Health:
Risk of cardiovascular disease can remain high even after low-density lipoprotein (LDL) cholesterol target levels have been reached in patients with the metabolic syndrome.
We’ve known this for years. Although the guidelines have not emphasized it enough the concept of residual risk after statin therapy (RRAST) is emerging. LDL reduction is important and, in the aggregate, the lower the better. In many individual patients, though, it’s not enough. The fact that statin trials show RRR’s of 25-30% begs the question “why not 80%, why not 100%?” (Bob Superko addressed this in his classic paper here, and, along with Spencer King, provided an update here).
From the Reuters piece:
Risk may be better gauged with low-density lipoprotein particle concentration, investigators announced here at the American Heart Association's Scientific Sessions 2008.
High LDL particle concentration relative to LDLC concentration reflects the atherogenic lipoprotein profile (ALP) characterized by abnormally small LDL particle diameter. This is a phenotypic expression of the metabolic syndrome and for practical purposes many regard it as synonymous (this is not invariably so---the ALP is nicely explained in the Superko papers linked above). The ALP and the associated metabolic syndrome represent the most common genetic causes of CAD and are certainly the most important contributors to RRAST.
Perhaps most concerning from the AHA presentation was this:
"Lipoprotein particle concentration may go up as LDL cholesterol levels are lowered with treatment," Dr. Robert Rosenson of the University of Michigan at Ann Arbor told Reuters Health after he presented his team's findings regarding 401 patients with metabolic syndrome and a 10-year risk of coronary heart disease greater than10%.
This is a finding that needs better understanding. Do statins somehow turn on genes that cause metabolic syndrome? What’s the solution? When the patient is at goal with statin therapy the RRAST must be assessed. The determination of triglycerides, HDLC and the total/HDL ratio are helpful. If the metabolic syndrome is evident diet and exercise are the best treatments, and drug therapy options include niacins and fibrates.
It has been suggested that lowering LDLC to extremely low concentrations with statins may offset this residual---lower the cholesterol concentration enough with statins and eventually the particle concentration will go down, perhaps. In that connection note a little mentioned aspect of JUPITER---LDLC was lowered to a median of 55 and RRR’s were on the order of an unprecedented 50% in contrast to the 25-30% reductions cited for other statin trials. Maybe there’s something to it.
Vitamins C and E Here we go again. No benefit. Vitamin E may even be harmful. There’s never been any favorable evidence for vitamin C and vitamin E was blown out of the water years ago. That hasn’t stopped some from promoting it, though.
Irbesartan and heart failure with preserved EF
During a mean follow-up of 49.5 months, the primary outcome occurred in 742 patients in the irbesartan group and 763 in the placebo group. Primary event rates in the irbesartan and placebo groups were 100.4 and 105.4 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% confidence interval [CI], 0.86 to 1.05; P=0.35). Overall rates of death were 52.6 and 52.3 per 1000 patient-years, respectively (hazard ratio, 1.00; 95% CI, 0.88 to 1.14; P=0.98). Rates of hospitalization for cardiovascular causes that contributed to the primary outcome were 70.6 and 74.3 per 1000 patient-years, respectively (hazard ratio, 0.95; 95% CI, 0.85 to 1.08; P=0.44). There were no significant differences in the other prespecified outcomes.
Again, this result for irbesartan (Avapro) is not new regarding ARB’s and heart failure with preserved ejection fraction (HFPEF). The CHARM-preserved study reached a similar conclusion years ago with candesartan (Atacand). There is little in the way of evidence from clinical trials to guide clinicians in the long term treatment of HFPEF. The best we can do now is to do a better job of treating their co-morbidities, of which they have many. If those co-morbidities include hypertension irbesartan as well as other antihypertensive agents might be reasonable choices. To say that irbesartan is of no value in the treatment of patients with HFPEF is simplistic. (Patients to be included in the irbesartan study could not have uncontrolled hypertension).
Perioperative beta blockers---another negative meta-analysis. From the Lancet paper:
The ACC/AHA guidelines committee should soften their advocacy for this intervention until conclusive evidence is available.
Well, they already have, quite some time ago. Now, the only strong guideline recommendation, for practical purposes, is that if the patient is already on a beta blocker for cardiovascular indications it should be continued perioperatively.
Statin dose-response relationships: Search Me This one’s a little complicated. Simvastatin (Zocor) was only marginally better at 80 mg in comparison to 20 mg daily in terms of reducing events in a secondary prevention study. But when this study is taken into account with multiple other statin trials the notion that lower LDLC is better still holds. Most disturbing was the markedly increased incidence of myopathy at the 80 mg dose. According to expert commentary about this study, if it’s desirable to seek very low LDLC targets in your patient it may be better to switch to a safer statin as opposed to increasing simvastatin to 80 mg. Simvastatin is safe when used according to the product safety labeling. This labeling, however, particularly the section on drug interactions, has become so complicated that simvastatin is getting a little tricky to prescribe. One has to review the patient’s entire med list and, unless one has a photographic memory, look up the labeling each time.
Classic paper: An unusual electrocardiographic pattern predicts dilated cardiomypoathy
Uncomplicated left bundle branch block is associated with a normal axis. Left bundle branch block with right axis deviation is a rare electrocardiographic pattern. In a classic paper Nicolic and Marriott described this pattern and noted a high predictive value for dilated cardiomypoathy. Subsequent observations have confirmed the association.
Friday, November 21, 2008
Point of care lactate levels for early identification of sepsis patients at high risk of death
It’s widely accepted that sepsis treatment should be regarded with the same urgency as trauma or acute STEMI. However early recognition of sepsis is notoriously poor. Is there a solution? How about a fingerstick lactate in the triage area? Better yet, in the ambulance? Here’s a study examining the issue.
Idiopathic pulmonary fibrosis
---was recently reviewed in the Orphanet Journal of Rare Diseases.
Key points:
While idiopathic pulmonary fibrosis (IPF) is often a wastebasket term for many patients with lung fibrosis it is actually a rare disease with specific diagnostic criteria. Because of its rarity and dismal prognosis (survival and quality of life worse than many forms of cancer) patients should not be given this label unless specific diagnostic criteria are met.
Terminology has been confusing, as the term IPF has been used interchangeably with usual interstitial pneumonia (UIP) and cryptogenic fibrosing alveolitis (CFA). UIP refers to the histologic pattern characteristic of IPF, not a particular disease. CFA is the former European term for IPF.
IPF is one of a large family of diseases popularly referred to as interstitial lung disease (ILD). ILD is an inaccurate choice of terms because these diseases usually have a phase or component of alveolitis. The preferred term is diffuse parenchymal lung disease (DPLD).
Pharmacologic options, covered in the review, are poor. Transplantation is appropriate in a select group of patients.
Key points:
While idiopathic pulmonary fibrosis (IPF) is often a wastebasket term for many patients with lung fibrosis it is actually a rare disease with specific diagnostic criteria. Because of its rarity and dismal prognosis (survival and quality of life worse than many forms of cancer) patients should not be given this label unless specific diagnostic criteria are met.
Terminology has been confusing, as the term IPF has been used interchangeably with usual interstitial pneumonia (UIP) and cryptogenic fibrosing alveolitis (CFA). UIP refers to the histologic pattern characteristic of IPF, not a particular disease. CFA is the former European term for IPF.
IPF is one of a large family of diseases popularly referred to as interstitial lung disease (ILD). ILD is an inaccurate choice of terms because these diseases usually have a phase or component of alveolitis. The preferred term is diffuse parenchymal lung disease (DPLD).
Pharmacologic options, covered in the review, are poor. Transplantation is appropriate in a select group of patients.
What’s ahead in gram negative infections?
An article from Expert Review of Anti-Infective Therapy examines the emerging threats of resistant gram negative organisms and what we have now, or in the pipeline, to deal with them. In general there are few gram negative agents in late stages of development.
At present, Tygecycline is a consideration for Acinetobacter baumannii infections although its role is uncertain. A. baumannii frequently causes pulmonary infections. In that connection the recently reported failure of Tygecycline in the phase III HAP/VAP trial is concerning.
At present, Tygecycline is a consideration for Acinetobacter baumannii infections although its role is uncertain. A. baumannii frequently causes pulmonary infections. In that connection the recently reported failure of Tygecycline in the phase III HAP/VAP trial is concerning.
Is it woo or is it real?
Maybe a little of both?
This demonstration took place on I've Got a Secret, a popular CBS game show from the early 60’s
Neurologists, psychiatrists, skeptics, what’s going on?
(Don’t try this at home).
This demonstration took place on I've Got a Secret, a popular CBS game show from the early 60’s
Neurologists, psychiatrists, skeptics, what’s going on?
(Don’t try this at home).
Thursday, November 20, 2008
Discharge planning after glycemic control in hospitalized patients
So you’ve done a good job controlling your critically ill patient’s blood sugar with an insulin drip. The patient has recovered and discharge is approaching. Now what? This CME approved Medscape article provides some tips for the transition to out patient care.
A while back, after an exchange with Dr. Daniel Carlat, author of the Carlat Psychiatry Blog (really more of a pharma-critical site than a psychiatry blog) I vowed to asses all Medscape CME offerings I post for bias, imbalance and non-evidence based content. This has gotten to be a competition between collections of anecdotes (which, mind you, do not equal evidence).
The activity in question is based entirely on an article from the Medscape Journal of Medicine. Editorial assistance for the article was provided by the makers of Lantus. (Does that mean it is one of those dreaded ghost written articles?). The author received no financial support from industry. The CME activity itself is non-industry supported.
Ghost written or not, the article can easily be critically appraised by examination of primary sources of evidence. The only thing I found that was non-evidence based and unbalanced was the discussion of glycemic control via insulin drips in the initial phase of critical illness and acute coronary syndrome. Specifically, the article selectively cites evidence in favor of tight glycemic targets while tending to ignore negative studies and the prevailing controversy surrounding in patient glucose control.
The principal focus of the article is on the transitions from insulin drip to sub q insulin to discharge. Those sections contain helpful tables and text on basal bolus regimens. Although they mention the pharmacokinetic advantages of the newer insulins none are mentioned by brand name and no clear recommendation for one over others is made.
My final take? The only unbalanced portion of this presentation was the promotion of plain old regular insulin and had nothing to do with the company which was in a position to influence content.
A while back, after an exchange with Dr. Daniel Carlat, author of the Carlat Psychiatry Blog (really more of a pharma-critical site than a psychiatry blog) I vowed to asses all Medscape CME offerings I post for bias, imbalance and non-evidence based content. This has gotten to be a competition between collections of anecdotes (which, mind you, do not equal evidence).
The activity in question is based entirely on an article from the Medscape Journal of Medicine. Editorial assistance for the article was provided by the makers of Lantus. (Does that mean it is one of those dreaded ghost written articles?). The author received no financial support from industry. The CME activity itself is non-industry supported.
Ghost written or not, the article can easily be critically appraised by examination of primary sources of evidence. The only thing I found that was non-evidence based and unbalanced was the discussion of glycemic control via insulin drips in the initial phase of critical illness and acute coronary syndrome. Specifically, the article selectively cites evidence in favor of tight glycemic targets while tending to ignore negative studies and the prevailing controversy surrounding in patient glucose control.
The principal focus of the article is on the transitions from insulin drip to sub q insulin to discharge. Those sections contain helpful tables and text on basal bolus regimens. Although they mention the pharmacokinetic advantages of the newer insulins none are mentioned by brand name and no clear recommendation for one over others is made.
My final take? The only unbalanced portion of this presentation was the promotion of plain old regular insulin and had nothing to do with the company which was in a position to influence content.
Injectable second generation antipsychotics and benzodiazepines in combination: safety considerations
For years we’ve combined or alternated injectable benzodiazepines (e.g. Ativan) with injectable first generation antipsychotics (e.g. Haldol) to manage delirium and agitation in hospitalized patients based on the rationale that the pharmacologic properties of one may complement and help minimize adverse effects of the other. The use of second generation antipsychotics in such combinations has become somewhat popular as these agents became available in parenteral form. However, such use has brought to light unanticipated cardiovascular and respiratory safety concerns particularly with Olanzapine (Zyprexa). This has led at least one institution to implement restrictions which are explained, along with a brief review of pertinent literature, in an article in the American Journal of Health-System Pharmacy. The full text is provided via Medscape.
Wednesday, November 19, 2008
Exciting developments in the medical blogosphere
Just as I endeavor to increase the readability and usability of Notes from Dr. RW as a hospitalist (primarily clinical) blog two other developments are noteworthy. First, Docnotes (formerly known as Family Medicine Notes) plans to rev things up after a period of dormancy. Jacob Reider, the blog author, put it this way in a recent post:
Those not long in the blogging world will under appreciate this development. Jacob (who also maintains the aggregator Medlogs) is a medical blogging pioneer. Family Medicine Notes started in 1999 and as far as I know is the oldest medical blog extant. It, along with Medrants, Medpundit and RangleMD got me interested in blogging. For its first several years it was a place for lively discussions of clinical medicine, healthcare informatics and the state of blogging in general. Then, as a result of competing interests and responsibilities, things began to slow down. For the past couple of years it has functioned mainly as a listing of links, largely on informatics topics of narrow interest, with just enough content to avoid Grunt Doc’s obituary listing. I didn’t always agree with Jacob but I enjoyed reading his clinical discussions and valued his expertise on blogging.
Then, just today, I discovered Hospital medicine Quick Hits written by academic hospitalist Danielle Schuerer. This is another SHM sponsored blog and it’s purely clinical---a nice complement to Bob Wachter’s blog which emphasizes the administrative side. Judging from the content posted so far it looks to be another valuable clinical resource for hospital medicine. I’ll be lurking and linking often.
The past two years - this blog has been stale - due to my professional role mirroring my personal interests in a way that makes my thoughts potentially company secrets that can't be shared.
I'm working on ways to change that so that this blog once again becomes the valuable asset that it once was. Stay tuned.
Those not long in the blogging world will under appreciate this development. Jacob (who also maintains the aggregator Medlogs) is a medical blogging pioneer. Family Medicine Notes started in 1999 and as far as I know is the oldest medical blog extant. It, along with Medrants, Medpundit and RangleMD got me interested in blogging. For its first several years it was a place for lively discussions of clinical medicine, healthcare informatics and the state of blogging in general. Then, as a result of competing interests and responsibilities, things began to slow down. For the past couple of years it has functioned mainly as a listing of links, largely on informatics topics of narrow interest, with just enough content to avoid Grunt Doc’s obituary listing. I didn’t always agree with Jacob but I enjoyed reading his clinical discussions and valued his expertise on blogging.
Then, just today, I discovered Hospital medicine Quick Hits written by academic hospitalist Danielle Schuerer. This is another SHM sponsored blog and it’s purely clinical---a nice complement to Bob Wachter’s blog which emphasizes the administrative side. Judging from the content posted so far it looks to be another valuable clinical resource for hospital medicine. I’ll be lurking and linking often.
I’ve gone green
---with a new blog design that readers may find a little easier on the eyes. Better yet, the search engine up top actually works now. Long overdue category archive and blog roll updates, along with other tweaks, are coming soon.
Liberation from mechanical ventilation
In the resources linked here the term “weaning” is often misused in reference to the process of liberating patients from ventilators. “Weaning” harks back to the days when we used sequential reductions of SIMV or pressure support levels to get patients off ventilators, methods which became obsolete more than a decade ago. Rather than weaning most patients need daily assessment for readiness for extubation. The patients who need weaning are the exceptions. If your patient truly needs weaning you might want to get help from a pulmonologist.
With that clarification out of the way it’s time for me to update an old post which summarized recommendations on this topic. That post presented an evidence based method for daily extubation assessment of mechanically ventilated patients, focusing on the spontaneous breathing trial (SBT). Although I stand by the premise of that post it needs updating in light of this study which looked at integrating the daily SBT with a daily spontaneous awakening trial (SAT) as a protocol. Given that daily SATs (sedation interruptions) and SBTs are commonplace (or should be) in mechanically ventilated patients what’s so new and different about this? I don’t know for sure, but when those two procedures were organized in the form of an explicit protocol they out performed usual care in several metrics including mortality (NNT=7!). So what was usual care? Surprisingly it looked pretty evidence based---it employed the daily spontaneous breathing trial. But, apparently, in the usual care group, given that the SATs were not coordinated with the SBTs as part of an explicit protocol patients tended to be over sedated at the time of their SBT. So more patients flunked their SBT or were judged too sleepy for extubation and thus experienced more days of mechanical ventilation.
In a subsequent review the authors explained their protocol and elaborated on issues surrounding it. For those without full text access here is a graphic of the protocol.
With that clarification out of the way it’s time for me to update an old post which summarized recommendations on this topic. That post presented an evidence based method for daily extubation assessment of mechanically ventilated patients, focusing on the spontaneous breathing trial (SBT). Although I stand by the premise of that post it needs updating in light of this study which looked at integrating the daily SBT with a daily spontaneous awakening trial (SAT) as a protocol. Given that daily SATs (sedation interruptions) and SBTs are commonplace (or should be) in mechanically ventilated patients what’s so new and different about this? I don’t know for sure, but when those two procedures were organized in the form of an explicit protocol they out performed usual care in several metrics including mortality (NNT=7!). So what was usual care? Surprisingly it looked pretty evidence based---it employed the daily spontaneous breathing trial. But, apparently, in the usual care group, given that the SATs were not coordinated with the SBTs as part of an explicit protocol patients tended to be over sedated at the time of their SBT. So more patients flunked their SBT or were judged too sleepy for extubation and thus experienced more days of mechanical ventilation.
In a subsequent review the authors explained their protocol and elaborated on issues surrounding it. For those without full text access here is a graphic of the protocol.
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