Via Hospital Medicine Quick Hits, with a link to info from the FDA.
Wednesday, August 31, 2011
According to this new systematic review the evidence consistently points to improved neurologic outcomes attributable to the intervention, though there are some problems with the data.
A free full text update was published in the Texas Heart Institute Journal. Several causal genes have been identified with over 100 mutations. Approximately 10% of cases represent phenocopy, clinically indistinguishable from the genetic cases. Read the rest.
Tuesday, August 30, 2011
Surprising findings presented at ATS 2011, summarized in this Medscape report, suggest that many hospitalized patients who die of pneumonia do not follow the expected trajectory of hypoxia and organ failure. Rather, they die suddenly on the general wards of arrhythmia not preceded by hemodynamic deterioration. From the report:
"Our study found a compelling signal that a significant portion of pneumonia patients who suffer a cardiac arrest in the hospital do so abruptly," he said. "We found that 56% of cases of cardiac arrest among these patients were not caused or preceded by hypotension, and almost 40% happened outside of the ICU...”
"This does raise the possibility that we are not triaging patients appropriately at the time of admission. It also raises the possibility that there is a confounding issue or set of issues. For example, is there a significant rate of previously undetected heart disease in this group? Is this the result of certain antibiotics causing heart rhythm issues? Were low oxygen levels not treated aggressively enough on a general medical unit? Hopefully, this large dataset will allow for future retrospective analyses of these issues," Dr. Fenster said.
The fact that arrhythmia was the leading cause of cardiac arrest among the patients is also notable, he said.
"If arrhythmia is indeed the most common cause of arrest, perhaps there is a role for more aggressive oxygen supplementation, electrolyte repletion, and avoidance of proarrhythmic drugs in an at-risk population."
Hypokalemia and hypomagnesemia are common in hospitalized patients. I have to wonder if these conditions combined with hypoxemia and the use of fluoroquinolone antibiotics which prolong the QT interval might predispose patients to arrhythmias.
This is not the first paper that failed to show overall superiority of linezolid.
Friday, August 26, 2011
There are symptoms and there are signs. They are separate categories. Pain is a symptom, not a sign. It cannot be the fifth vital sign. Pain as the “fifth vital sign” was nothing more than a publicity stunt. More from Lucy Hornstein guest blogging at Kevin MD.
Thursday, August 25, 2011
For several years soldiers returning from Iraq and Afghanistan have been investigated at Vanderbilt Medical Center (referred from Fort Campbell Kentucky) for exertional dyspnea. This was regarded as a mysterious syndrome for several years. Imaging and physiologic studies were normal or non-specific. Biopsies revealed constrictive bronchiolitis in most. Exposure to sulfur fires may have been the culprit.
Wednesday, August 24, 2011
|Mountain view from lobby of conference center|
Dr. Gordon Ewy, Professor of Cardiology at the University of Arizona and pioneer in CPR and emergency cardiac care, presented an update. As I have noted from past attendance at this course Dr. Ewy has been years---about a decade in fact---ahead of the American Heart Association. I also said when blogging last year's conference:
I'm usually a strong advocate for guideline based care. Almost all the studies I've examined on the effects of guideline adherence show outcomes to be improved. There's one notable exception: the AHA guidelines for CPR and emergency cardiac care.
Dr. Ewy made many of the same points this year as last. The new emphasis this year was a solidification of data showing improved outcomes with his method compared to guideline based BLS and ACLS as well as expanded discussion of the post resuscitation bundle. By the way, several years ago Dr. Ewy gave the method a new name: cardiocerebral resuscitation (CCR), reflecting the de-emphasis on rescue breathing and the improved brain outcomes.
When I blogged this conference last year the 2010 ACLS guidelines were not out. Those guidelines, published a few months later, were influenced by Ewy's work and incorporated some needed changes but didn't go far enough.
So let's see how Ewy's CCR compares with AHA's BLS and ACLS.
AHA 2010: Rescue breathing remains in the guidelines for trained rescuers but with a change in sequence (CAB instead of ABC) with hands-only CPR “encouraged” but for lay rescuers only.
CCR: Rescue breathing considered harmful and eliminated for all rescuers.
ACLS (in the field)
AHA 2010: Rescue breathing (CAB, 30:2 ratio) continues until advanced airway; “consider” advanced airway early on but timing of such airway open to clinical judgment.
CCR: Passive O2 administration via NRB mask and oral airway; no rescue breathing; no advanced airway unless failure of ROSC after at least three cycles of 200 compressions.
AHA 2010: Analyze rhythm and shock if indicated, as soon as device connected.
CCR: Analyze and shock only after 200 compressions (circulatory phase, see below).
Caveats: This method applies only to adult victims of suspected primary cardiac arrest. Children and those whose arrest is suspected clinically to be of respiratory etiology would undergo guideline based resuscitation. Delay in the use of the AED applies mainly to emergency medical personnel responding in the field, as these are patients in the circulatory phase of arrest (5 minutes down time or greater). Early use of the defibrillator, according to the guidelines, would still apply to patients believed to be in the electrical phase, e.g. those arresting in the hospital or whose arrest is witnessed in a public place where an AED is on site and immediately available.
For a discussion of the three phases of arrest see here.
For a nice summary of CCR the full text of this article is worth obtaining.
CCR has been made the official protocol in four regions of the country: greater Phoenix, greater Tucson, a region in Wisconsin and greater Kansas City. These four areas have demonstrated striking improvements in neurologically intact survival over multiple other communities that use guideline based protocols.
From the Paucis Verbis series at Academic Life in Emergency Medicine.
Tuesday, August 23, 2011
|Teton view from the terrace behind the conference center|
Atrial fibrillation is never been a mundane topic at this conference. So what could possibly be exciting about a fib? Dr. Bernard Gersh from Mayo Clinic presented this year's update.
There are some fascinating new insights about its changing epidemiology, based on pathogenesis. It's no surprise that the incidence is increasing. But there's a substantial component of this rise that's not accounted for by aging of the population. The short version is that it's the epidemic of obesity. Here are some primary sources which explain the association:
The mechanisms? In addition to the obvious associations with sleep apnea and hypertension, obesity is associated with neurohormonal disturbances, inflammation, LVH and diastolic dysfunction. The latter lead to increased LA size.
Finally, pericardial fat deposition, which is associated with obesity and has proinflammatory properties, is associated with atrial fibrillation independent of the usual risk factors.
LV diastolic dysfunction showed a powerful association with incident AF in this study.
Obesity's association with AF operates in part via the correlation between weight gain and vascular stiffness. Vascular stiffness, a consequence of atherosclerosis, over time leads to increased LA size. LA size, according to the speaker, is the “hemoglobin A1C” of many aspects of cardiovascular disease. (For more about the importance of LA size and its assessment via electrocardiography see here).
What about lone atrial fibrillation? This paper has a wealth of information on its natural history and demonstrates event free survival similar to that of the general population over many years, until vascular risk factors supervene (at which time it is no longer “lone” AF).
What does this all mean? It appears that two diseases, with some overlap, are represented in the spectrum of AF. Lone AF, purely an electrical disorder, has a benign course. The stroke risk is similar to the general population until years later when vascular risk factors and/or structural heart disease develop. The more ordinary atrial fibrillation, which hospitalists more often see, appears to be a marker of vascular and structural heart disease. The correlation with atherosclerosis explains why aspirin has a modest effect in stroke prevention---it doesn't prevent cardioembolism but does prevent some of those strokes that come from the vascular disease that underlies the more common type of AF.
Dr. George Beller, Professor of Cardiology at the University of Virginia, spoke on noninvasive imaging with a focus on CT calcium scoring. He was one of the authors of the 2010 ACCF/AHA guidelines on screening of asymptomatic persons, which cover calcium scoring and other noninvasive techniques.
What did I take away from the talk? Despite the fact that the test characteristics, radiation safety and cost have improved dramatically since the early days of screening via electron beam CT the test remains widely over promoted.
Who should have CT calcium scoring? Let's start with this: there is weakness in the supporting evidence and no slam dunk (level I) recommendation that anyone should have CT calcium scoring.
The highest level of recommendation in the guideline is IIa. For the general population the IIa recommendation is for any patient with an intermediate Framingham risk score (because it misses a substantial number of patients who are at high risk). For diabetics the IIa recommendation applies to all (because, despite the popular notion that all asymptomatic patients with DM-2 have CAD whether it has been officially diagnosed or not there is a significant subset with zero calcium scores whose cardiac prognosis is as good as that of the general population). There are nuances of clinical judgment, of course, as to age cutoffs beyond which screening is not appropriate even in these populations.
A zero calcium score offers reassurance. Would a positive score lead to a stress imaging test or cardiac catheterization? That's a difficult question to answer in the present era, post COURAGE and BARI 2b. A high score would lead to more intensive medical management of risk factors than would otherwise be indicated.
What is the pathophysiologic rationale for calcium scoring? Early in the preclinical stage of the atherosclerotic process intramural plaques form. When they rupture it is an asymptomatic event because they do not compromise the lumen. Calcium soon deposits in these asymptomatic ruptured plaques, thus providing an early marker of the atherosclerotic process.
Carotid IMT measurement for screening of asymptomatic individuals is backed by similar evidence and recommendations in the guidelines. It has the disadvantage of being more operator dependent.
Here is a NEJM review which explains things nicely and puts the history of plant accidents in perspective:
In the partial meltdown at Three Mile Island, the plant's containment structure fulfilled its purpose, and a minimal amount of radiation was released.2 However, there was no such containment structure in place at the Chernobyl reactor — the explosions and the subsequent fire sent a giant plume of radioactive material into the atmosphere. Although the Three Mile Island accident has not yet led to identifiable health effects,3-5 the Chernobyl accident resulted in 28 deaths related to radiation exposure in the year after the accident.6,7 The long-term effects of the Chernobyl accident are still being characterized, as we discuss in more detail below. The situation at Fukushima, though still in daily flux, will probably end up ranking between these two historical accidents in terms of radiation releases and health consequences.
More from the NEJM blog.
Monday, August 22, 2011
---in this study of patients treated with ICS for respiratory disease.
Friday, August 19, 2011
It can be a systemic disease affecting multiple other organs including the kidneys, where it usually presents as tubulointerstitial nephritis. The pathology is infiltration with IgG-4 producing plasma cells and T lymphocytes. Via Renal Fellow Network.
In a an issue of Emergency Medicine News Dr. James Roberts comments on the section of the new ICH guidelines concerning coagulation and platelet defect reversal. Sometimes guidelines are little more than an acknowledgement that we don't really know what to do for the clinical problem in question but, given limited evidence, here's the authors' best shot. As Roberts points out that's particularly true in the case of ICH and accompanying hemostatic defects.
The 2010 guidelines offer few changes in this area. They are nicely summarized in the article. For coumadin reversal, alongside vitamin K IV, the guidelines recommend FFP or consideration for PCC as an alternative, and shy away form rFVIIa, saying it is “not routinely recommended.” Non-recommendation of rFVIIa for unselected patients in this setting is a change from the old guidelines. The guidelines do not recommend giving platelets to reverse the effects of antiplatelet agents in patients with normal counts, a new recommendation. Platelet transfusions for patients with severe thrombocytopenia are recommended, although the appropriate platelet count threshold is not defined. Dr. Roberts suggests maybe 50-100K, although this is certainly not defined by high level research evidence.
The article contains a lot of practical pearls on the nuances of giving plasma, IV vitamin K, and other issues.
Thursday, August 18, 2011
From a study published in Critical Care Medicine.
Wednesday, August 17, 2011
This is emerging as an important procedure for critically ill hemodynamically unstable patients. Here's an article on the topic in a recent issue of Resuscitation.
It's been known for a long time that a variety of acute situations lead to elevated levels. In fact, save for perhaps the overnight chest pain or TIA obs you can just about take elevated vasopressin levels for granted in hospitalized patients. But is there anything specific about the association with pain? Here's a post with links to the literature at Nephron Power.
Thursday, August 11, 2011
Wednesday, August 10, 2011
From the NEJM blog:
The classic manifestations are headache, jaw claudication, PMR, and visual symptoms. However, 40% of patients present with less typical manifestations, such as breast or ovarian masses, peripheral neuropathy, SIADH, or mesenteric ischemia.
Let's not forget aortic aneurysm and/or dissection, which can show up years after remission of GCA.
Regarding treatment, steroid sparing immunosupression seems popular in practice. However, the blog author pointed out that such agents have not been validated by high level evidence.
What the post left out about treatment is that low dose aspirin reduces vascular events and is now a recommended adjunct, along side steroids, in the treatment of GCA.
The primary NEJM article is here.
Tuesday, August 09, 2011
From a recent study:
Results Moderate to severe HAA developed in 3551 patients (20%). The mean (SD) phlebotomy volume was higher in patients with HAA (173.8 [139.3] mL) vs those without HAA (83.5 [52.0 mL]; P less than .001). There was significant variation in the mean diagnostic blood loss across hospitals (moderate to severe HAA: range, 119.1-246.0 mL; mild HAA or no HAA: 53.0-110.1 mL). For every 50 mL of blood drawn, the risk of moderate to severe HAA increased by 18% (relative risk [RR], 1.18; 95% confidence interval [CI], 1.13-1.22), which was only modestly attenuated after multivariable adjustment (RR, 1.15; 95% CI, 1.12-1.18).
Conclusions Blood loss from greater use of phlebotomy is independently associated with the development of HAA. These findings suggest that HAA may be preventable by implementing strategies to limit blood loss from laboratory testing.
HT to Hospital Medicine Quick Hits.
An interesting post from Health Care Renewal.
Monday, August 08, 2011
My recent post about the new Annals study showing hospitalist care to be associated with reductions in inpatient costs counterbalanced by increased costs 30 days post discharge was, due to time constraints this week, quite pithy. Now I have a little more time to reflect on the findings and comment on some of the other blog reactions. (Such is the life of a 7 on, 7 off hospitalist).
My short version: if you discharge patients quicker and sicker you'll have more bounce-backs and more utilization of post hospital services. Research comparing the pre- and post-DRG eras strongly suggests that financial incentives beginning with the advent of DRGs cause patient instability at discharge (quicker and sicker) which contributes to bad outcomes.
Now to briefly review the research findings, prior to the Annals paper, on utilization attributable to the model. As I said here and elsewhere, the data are mixed. Analysis of research findings was compromised because one of the largest and best quality studies ever done, presented at HM 2005, finding no improvement in efficiency attributable to the hospitalist model, was buried, the apparent victim of publication bias. Then a study last year, I thought, tipped the balance of evidence in favor of the hospitalist model. But none of this research looked at the cost of the entire 30 day episode of care as the Annals study did.
Happy Hospitalist wrote:
Let's just assume that hospitalist patients are equal in all ways to patients cared for by primary care physicians. It's also possible that primary care physicians shift cost into the hospital where DRG payments don't account for or fund for additional service. In an environment where hospital Medicare profit margins have been negative for almost a decade, doctors who try and get everything done in the hospital aren't doing their community hospital any service. A hospital that goes under will provide no care for anyone.
Correct. The findings of the Annals paper suggest that hospitalists shift utilization from single inpatient stays to other services. In some cases that might mean a shift from Medicare part A (non fee for service) to part B (generally fee for service). For the hospital bounce-back it means the hospital gets a whole new DRG payment for the same episode of care. Not good for the medical commons but hospital administrators love it under today's incentives (those incentives may change soon).
Happy adds this note of caution:
The data is from 2001-2006. A lot has happened, especially in IT, in the last 10 years. The discharge process has improved in many ways, and we know that a healthy discharge process helps prevent readmissions more than any other aspect of care. It is quite possible that the 2011 discharge process has eliminated or reduced many readmissions that would have otherwise occurred in 2001, when resume home meds was the most common acceptable discharge process.
But “med rec” as we now know it has been a failure. Sound in concept but inscrutably hard to implement in the real world and there's no convincing evidence that it improves outcomes over the old way. But I digress. Yes, things have changed in the last few years. There have been major efforts to improve the discharge process. It would be reasonable to assume this has helped improve outcomes but we don't know from research data. It's equally plausible that the collapse of primary care that has occurred over the same period has driven outcomes in the other direction.
Happy's post offers a lot of speculation that the patients cared for by hospitalists were more ill and complex. Be that as it may the conclusions of the Annals paper reflect the best evidence we have to date on overall costs.
Over at Med Rants DB cited lack of continuity, both at admission and discharge. I believe I recall Bob Wachter saying on more than one occasion that this discontinuity is deliberate. It's built into the model. There's been a lot of stewing about how to compensate for it. DB had this common sense advice:
We need to develop a better system for communication. We must (and I use that verb purposely) learn how to communicate better between primary care physicians and hospitalists. We must spend time on the phone – paper and email are insufficient, because we need questions and answers; we need to stress the important observations – on both sides of the communication.
A phone call at admission and again at discharge would be helpful but how does one find time? Say you admit 4 and discharge 4 complex patients on an average day. 8 phone calls. At 15 minutes per call (taking into account the time you spend on hold and playing phone-tag) that's 2 hours carved out of your day.
DB's point is backed up by evidence that just making the PCP aware the patient is being hospitalized reduces adverse events. There are guidelines which address this. They place much of the onus for communication on the ED physician and the PCP. That's as it should be. All involved should do their part. Hospitalists can't do it alone. They are not the grand integrators of health care.
DB made this interesting point:
I have written many times that the best care in a hospital comes from a physician who does both inpatient and outpatient care.
All other things being equal that would be true. The original notion of hospital medicine was that physicians who spent 100% of their clinical time caring for hospitalized patients developed exceptional skills in inpatient medicine which would exceed those of traditional doctors. That's where the educational emphasis was: the latest on sepsis, pneumonia, thromboembolism, cardiac emergencies, metabolic and toxic emergencies and the like. Research over the past decade has shown no difference in clinical outcomes between the hospitalist and the traditional model of care, suggesting that any harm attributable to the discontinuity was counterbalanced by the special expertise. That may not be true much longer, though, as the educational focus of hospital medicine shifts increasingly to the organizational and business issues (coding, clin doc, performance measures) while clinical skills are devalued.
Bob Wachter, generally a booster of the hospitalist model, made no attempt to spin the results:
Like the Annals editorialists, Lena Chen and Sanjay Saint of the University of Michigan, I find myself unable to dispute the main findings. The sample size is huge, the definitions and assumptions are reasonable, and the analysis is strong.
Although he disagrees with me on the “quicker and sicker” notion he correctly cites multiple factors that are inherent in the hospitalist model:
More likely, the findings represent the cumulative effects of influences on all the players. Hospitalists – highly motivated to cut hospital days – were more likely to send patients to skilled nursing facilities when they were ready to leave and less able to hook the patients back up with their primary care doctors at the time of discharge. Primary care docs who were uninvolved in the hospitalization may have been less comfortable that they understood the ins-and-outs of the hospital stay and more likely to favor readmission for the post-discharge patient who wasn’t doing well. Patients may have believed that, since their PCP didn’t see them in the hospital, the best thing for them to do if they were wobbly was to return to the ED or the hospital.
Here's where I disagree with Bob (and a lot of other people):
Today’s study tells us that hospitalists have done their jobs well, but the job has been defined too narrowly...
As hospitals’ lenses widen..their willingness to help support their hospitalist programs will be predicated on the latter’s prove ability to improve quality, safety, patient experience, and efficiency over that entire period, not just the hospital stay.
Indeed the founding notion of hospital medicine was narrow, as reflected in the original name of our professional society, the National Association of Inpatient Physicians. So a fundamental question becomes is special clinical expertise in the acute care of inpatients really too narrow? Who do you want caring for your hospitalized patients? A clinician whose total focus is on their clinical problems or a part time clinician, part time business consultant whose skills are spread a mile wide and an inch deep?
Thursday, August 04, 2011
Wednesday, August 03, 2011
Over at the EMS 12-Lead blog there is a series of posts on this topic. The first post, available here, contains the links to the other five. These are not like the discussions you'll find in formal review articles or textbooks. They deal with real world situations encountered in the emergency setting. The author deemphasizes morphologic criteria and reminds readers of the adage “a wide complex tachycardia is VT until proven otherwise.” You'll make fewer mistakes if you start there. When you're under the gun in the emergency setting you don't want to waste too much precious time trying to make a fancy morphologic diagnosis. Later on when you have time to scratch your head, or in stable patients, you can do a detailed morphologic analysis. The most widely used criteria nowadays are the Brugada criteria. Those criteria are easily misunderstood. The original Brugada paper explains the nuances and limitations of the method. It also reviews and references the older more traditional morphologic criteria. The latter have serious limitations but may warrant consideration if the Brugada criteria fail to yield a definitive diagnosis.
Finally, it is increasingly being recognized that extracardiac causes, particularly hyperkalemia and drug overdose, can lead to some bizarre wide complex tachycardias. Although these do not fulfill criteria for SVT with aberrancy many are not VT.
The Medscape title is deceptive: ICUs Cut Central-Line Bloodstream Infections to Zero.
The research letter published recently in the Archives of Internal Medicine, referenced in the Medscape report, claimed nothing of the kind. That's not to diminish the importance of the study. What it did show some ICUs have been able to go from 1 to 2 years without any infections, attributable to the use of a bundle of evidence based interventions.
Clearly central-line infections can be reduced and as use of the interventions becomes more widely adopted will asymptotically approach zero.
Tuesday, August 02, 2011
Monday, August 01, 2011
I'm not sure at this point but here are some reviews I found.
From the Journal of Antimicrobial Chemotherapy:
..exhibits antibacterial activity against typical respiratory pathogens such as Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus and common Gram-negative pathogens. In particular, ceftaroline has activity against resistant Gram-positive cocci, including penicillin- and multidrug-resistant S. pneumoniae, as well as methicillin-resistant S. aureus. The activity of ceftaroline against these phenotypes is attributed to its ability to bind to modified penicillin-binding proteins with high affinity when compared with other β-lactams.
Here's another one from the same journal available as free full text:
..approved in the USA for the treatment of acute bacterial skin and skin structure infections (ABSSSIs) and community-acquired bacterial pneumonia (CABP).
The spectrum of activity is shown in this table and deserves comment. This spectrum includes organisms outside the approved indications. Of note, on the gram positive side VISA, VRSA, coag negative staph, Listeria and enterococcus (but not VRE) are included. That represents a significant increase in the gram positive spectrum for cephalosporins. On the gram negative side Pseudomonas and ESBL producing organisms are NOT covered, so this is not a big gun for empiric gram negative coverage.
This free full text review contains more detailed pharmacokinetic and pharmacodynamic information which may be helpful in predicting activity against various pathogens in off label clinical situations.