ITP

An update on evaluation and management.

Constrictive bronchiolitis

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.

Research article.

NEJM blog post.

Background.

Wiggle waves, small spike waves and smooth potential waves: variations in epsilon waves and other ECG criteria for right ventricular cardiomyopathy

Review here.

Tutorials in the Tetons 2011---ACLS update

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.

BLS

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.

Quick reference: generalized convulsive status epilepticus

From the Paucis Verbis series at Academic Life in Emergency Medicine.

New FDA regs on Zocor

I know I'm late with this. Here's a post at Clinical Correlations. Along with an FDA link.

Gram negative bacteria which produce carbapenem-hydrolyzing enzymes---treatment options

Here is an update from Future Microbiology. Free full text from Medscape here.

Tutorials in the Tetons 2011---what's new in the epidemiology of atrial fibrillation?

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:

Body mass index associated with new a fib risk.

BMI correlates positively with age adjusted a fib risk.

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.

Tutorials in the Tetons 2011---noninvasive cardiovascular imaging

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.

Management of accidental hypothermia

A quick reference card from the Paucis Verbis series at Academic Life in Emergency Medicine.

Nuclear power plant accidents

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.

Review of the innate immune system

---with some material on the adaptive system, posted at Allergy Cases.

HT to Nephron Power.

Tattoos---are they safe?

You’d think so now that the procedure is more refined and mainstream. Well---

Update on TTP

The information in this review is derived from the vast Oklahoma TTP-HUS registry.

Inhaled corticosteroids raise the risk of diabetes onset and progression

---in this study of patients treated with ICS for respiratory disease.

In the young patient with DVT

---don't forget about iliac vein compression syndrome. A different diagnostic and treatment strategy is important for a good outcome.

IgG-4 associated disease---not just autoimmune pancreatitis

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.

Reversing coagulation defects in patients presenting with intracranial hemorrhage

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.

CME in Wyoming

I arrived in Grand Teton National Park today to attend this conference. I'll try and blog the conference to the extent Internet access will allow (not the fastest out here). Sessions begin Saturday.

Angioedema

A wonderful repository of links here.

Early goal directed therapy in the ER is cost effective

From a study published in Critical Care Medicine.

Adult Still's disease

I recently had occasion to review this topic and found a number of articles. I chose this one to link here because it is available as free full text.

Jane: the Journal/Author Name Estimator

An interesting tool for authors. Via Academic Life in Emergency Medicine.

Update on cutaneous fungal infections in Joplin tornado victims

MMWR article here.

Medscape commentary here.

Background here.

Management of cardiac arrest in pregnancy

A free full text review. The review is helpful but as you would expect there's not a lot of good science to guide us.

Point of care echo to evaluate for pericardial tampanade

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.

ADH and pain

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.

Global Kidney Academy

An on line nephrology learning resource.

Via Nephron Power.

Giant call arteritis: did you know?

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.

Chronic HT in pregnancy

A review in NEJM and commentary in the NEJM blog.

Check out Blitter

It's a search engine that preferentially retrieves content linked by clinical bloggers and tweeters. A new idea from the folks at the TRIP database. Via Live in the Fast Lane.

Hospital acquired anemia due to repeated lab draws

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.

NHS scraps plans for centralized electronic medical record

Doomed after years in development.

Via Health Care Renewal.

Are electronic medical records really electronic data dumps?

An interesting post from Health Care Renewal.

Reactions to the Annals article on costs attributable to the hospitalist model

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?

More from Hospitalist.net and Kevin MD.

New COPD guidelines

From ACP, ACCP, ATS and ERS.

The hospitalist model: value neutral!

At least according to the latest study. Savings in inpatient costs were more than counterbalbnced by increased costs related to bounce-backs and nursing home utilization.

Differential diagnosis of wide complex tachycardia

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.

Reduction of central-line infections

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.

ERCAST

Podcasts in emergency medicine.

Does clinical decision support in the electronic medical record increase guideline adherence?

Not in this large study.

Cystic disease of the kidney

Cystic disease of the kidney

View more presentations from Nephrology, NSLIJ

A presentation from Slideshare via Nephron Power.

Acquired von Willebrand syndrome

A review of associated disorders, clinical features, diagnosis and management.

Ceftaroline (Teflaro)---what's its role?

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.

A clinical image collection

From Life in the Fast Lane.

A clinical prediction rule may obviate the need for TEE in patients with nosocomial Staph aureus bacteremia

Here is the abstract of the recent paper. The complete rule is not covered in the abstract but is outlined in this post from Hospital Medicine Quick Hits.

Note that the rule applies only to nosocomial Staph aureus bacteremia.

Delirium guidelines from NICE

Available here. HT to Hospital Medicine Quick Hits.

Clot Connect MD

A resource on thrombosis and thrombophilia.

Dealing with bleeding in patients on Pradaxa

Very little has been published on this, but some folks have worked it out. Here's a very helpful post on the topic from the EMCrit blog.

The anticoagulation forum

This is an educational resource on topics related to antithrombotic therapy. Archived webcasts of the 11th National Conference on Anticoagulant Therapy are posted.

Pure quackery invades a critical care nursing journal

You've got to see it to believe it. Via Respectful Insolence.

Appreciating hospitalists for (gasp!) their clinical skills

Since its origins the hospitalist movement has been redefined. According to our founding documents a hospitalist was a generalist physician, usually an internist, who brought exceptional clinical skills to the care of hospitalized patients. Emphasis on the word clinical. Things devolved considerably since then. Clinical expertise gradually took a back seat to clerical skills, coding and performance measures. Today our thought leaders, or many of them, seem to devalue clinical expertise.

I'm not generally impressed by promotional items about hospitalists, but a recent post by Dr. John M got my attention because it focused on hospitalists as excellent clinicians:

But for good patient care, the details are important too. Hospitalists are good at details. In fact, an internists’ area of expertise is in using, considering and synthesizing such specifics. They mesh together a patient’s history, exam, laboratory values, X-rays, and other specialists’ opinions. I feel strongly that having thinkers on the case is a good thing.

What's wrong with performance measures?

In large part they are substitutes for thought. That's why they are so faulty and so many docs resist them.

CT angiography is not the diagnostic modality of choice for PE

A recent study published in Chest evaluated the sequence of clinical scoring, D-dimer testing, compression ultrasonography, V/Q scanning and CT (MDCT) in that order for the diagnosis and rule-out of PE. CT was only needed in 11% of the patients:

Results: Detection of DVT by ultrasonography established the diagnosis of PE in 43 (13%). Lung scan associated with clinical probability was diagnostic in 243 (76%) of the remaining patients. MDCT scan was required in only 35 (11%) of the patients. The 3-month thromboembolic risk in patients not given anticoagulants, based on the results of the diagnostic protocol, was 0.53% (95% CI, 0.09-2.94).

Conclusions: A diagnostic strategy combining clinical assessment, d-dimer, ultrasonography, and lung scan gave a noninvasive diagnosis in the majority of outpatients with suspected PE and appeared to be safe.

A related editorial was titled Retro Is the Rage!: Ventilation-Perfusion Scanning Is Alive and Well in the Diagnosis of Pulmonary Embolism.

Well, I'm going to savor this moment for a little self aggrandizement. I told you so. I've been hammering this point for the last six years on this blog. The evidence has never favored CT over V/Q for PE. Minimizing the use of CT in the evaluation of patients for PE will save costs, radiation risk and kidneys.

Review of therapeutic hypothermia after cardiac arrest

Here's a nice update from CCJM with free full text and CME available.

Points of interest:

For neurologically appropriate patients (GCS less than 8) the intervention carries a class I recommendation in the 2010 ACLS guidelines when the cardiac arrest was out of hospital and the initial rhythm was VF or pulseless VT and spontaneous circulation was restored in less than 60 minutes.

For all other rhythms and for in hospital arrest of any rhythm the intervention is given a class IIb recommendation.

Patients without obvious extracardiac cause for their arrest need prompt coronary angiography. Therapeutic hypothermia can be implemented in parallel with cardiac catheterization, with the protocol started before or during the procedure.

All bets are off for estimating neurologic prognosis until 72 hours after rewarming.

Trends in elective PCI post-COURAGE

It looks like cardiologists are following the evidence according to this new study:

Conclusions—Publication of results from the COURAGE trial was temporally associated with a significant and sustained decline in the use of PCI to treat patients with stable angina. The long-term impact of this change in practice on patient outcomes remains to be determined.

Unexplained AV block in younger patients: think beyond the pacemaker!

In this recent paper investigators found a surprisingly high prevalence of cardiac sarcoidosis and giant cell myocarditis among patients aged 18-55 with unexplained AV block requiring pacing:

Conclusions—CS and GCM explain greater than or equal to 25% of initially unexplained AVB in young and middle-aged adults. These patients are at high risk for adverse cardiac events.

A high rate of adverse events was noted in follow up of the CS and GCM patients. In contrast, those patients whose heart block remained idiopathic after investigation had a benign course.

The Clinical Perspective piece related to this article stated:

These data suggest that CS and GCM are not uncommon causes of AVB in young and middle-aged adults and that the prognosis of CS and GCM is poor even when the first manifestation is AVB. We encourage a policy of active and systematic screening for CS and GCM in all adults aged less than 55 presenting with unexplained high-degree AVB.

Benign versus malignant early repolarization---can they be distinguished?

The early repolarization pattern on the electrocardiogram was long considered a benign variant. Recent evidence suggests a subset of patients in whom it signifies an increased risk of sudden cardiac death. I blogged on that topic here and here.

A recent study addressed electrocardiographic distinctions:

Conclusions—ST-segment morphology variants associated with ER separates subjects with and without an increased risk of arrhythmic death in middle-aged subjects. Rapidly ascending ST segments after the J-point, the dominant ST pattern in healthy athletes, seems to be a benign variant of ER.

On the other hand, horizontal or descending ST segments signify an increased risk of death.

Quick reference card, asthma classification

The asthma classification is important to an understanding of the treatment guidelines. I’ve always found it difficult to keep straight, so this quick reference from the Paucis Verbis series at the Academic Life in Emergency Medicine blog should be useful.

CT pulmonary angiography and overdiagnosis of PE

A new study published in Archives of Internal Medicine looked at changing trends in diagnosis and outcomes for pulmonary embolism since introduction of CT pulmonary angiography:

We compared age-adjusted incidence, mortality, and treatment complications (in-hospital gastrointestinal tract or intracranial hemorrhage or secondary thrombocytopenia) of PE among US adults before (1993-1998) and after (1998-2006) CTPA was introduced. 

Results Pulmonary embolism incidence was unchanged before CTPA (P = .64) but increased substantially after CTPA (81% increase, from 62.1 to 112.3 per 100 000; P less than .001). Pulmonary embolism mortality decreased during both periods: more so before CTPA (8% reduction, from 13.4 to 12.3 per 100 000; P less than .001) than after (3% reduction, from 12.3 to 11.9 per 100 000; P = .02). Case fatality improved slightly before (8% decrease, from 13.2% to 12.1%; P = .02) and substantially after CTPA (36% decrease, from 12.1% to 7.8%; P less than .001). Meanwhile, CTPA was associated with an increase in presumed complications of anticoagulation for PE: before CTPA, the complication rate was stable (P = .24), but after it increased by 71% (from 3.1 to 5.3 per 100 000; P less than .001).

The authors note that these findings suggest overdiagnosis attributable to CTPA due to detection of isolated inconsequential filling defects. As the data show, this has significant clinical consequences. In that sense CTPA may be considered by some to be more sensitive than V/Q scanning. However, when long term clinical outcomes are used as the standard V/Q scanning has demonstrated superior sensitivity so long as a normal perfusion scan (note that’s normal, not “low prob”) is used to rule out PE.

The changing profile of bacterial meningitis

From an NEJM study:

The incidence of meningitis changed by −31% (95% confidence interval [CI], −33 to −29) during the surveillance period, from 2.00 cases per 100,000 population (95% CI, 1.85 to 2.15) in 1998–1999 to 1.38 cases per 100,000 population (95% CI 1.27 to 1.50) in 2006–2007. The median age of patients increased from 30.3 years in 1998–1999 to 41.9 years in 2006–2007..

Of the 1670 cases reported during 2003–2007, S. pneumoniae was the predominant infective species (58.0%), followed by GBS (18.1%), N. meningitidis (13.9%), H. influenzae (6.7%), and L. monocytogenes (3.4%). An estimated 4100 cases and 500 deaths from bacterial meningitis occurred annually in the United States during 2003–2007.

Parenteral iron therapy

---is enjoying expanded use. Newer products are safer and no longer carry black box warnings.

Brugada pattern quick reference card

From the Paucis Verbis series at the Academic Life in Emergency Medicine blog.

ACLS and the use of antiarrhythmic agents

Here's a new systematic review published in the journal Resuscitation. The conclusions were in line with the current recommendations:

Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.

Post thrombotic syndrome

A review.

Anticoagulation after VTE---indefinite or time limited?

Here's another review on the topic.

Points of interest:

Although thrombophilia testing predicts initial VTE it is not reliable for predicting recurrance.

Thrombophilia testing does not have a primary role in decision making regarding the duration of anticoagulation.

Thrombophilia testing has a limited role in individual circumstances and must take into account patient preference.

D-dimer testing after a course of anticoagulation is predictive of recurrent VTE and has a role in decision making about the duration of anticoagulation.

The duration of anticoagulation is largely a clinical decision, based on current guidelines and modified by the clinician's judgment in individual circumstances and the preference of an informed patient.

The recommendations in this review are similar to those of another review I linked here.

Diagnosis and treatment of VTE in pregnancy

A free full text review.

What's the appropriate cancer work up for patients presenting with unprovoked VTE?

A recently published evidence based review concluded:

Based on the available studies, we recommend that clinicians maintain a low threshold of suspicion for malignancy in patients who present with an unprovoked VTE. Moreover, patients with unprovoked VTE should provide a thorough medical history, undergo a physical examination, chest X-ray, and routine laboratory tests (including complete blood count, basic chemistries, liver function, and lactate dehydrogenase), and be up to date with age- and gender-specific cancer screening (Grade 1C). Additional diagnostic testing should be guided by any abnormal findings gleaned from the initial clinical or laboratory data.

Off-label use of recombinant factor VIIa---evidence based review of efficacy and safety

Despite the fact that recombinant factor VIIa is physiologically appealing for a variety of bleeding scenarios its approved indications are extremely limited. It is estimated that over 90% of its use is off -label. Here is a review of the evidence regarding VIIa for various off-label uses. The evidence of benefit in terms of hard clinical endpoints is scant, and in the off-label population the VTE risk is higher. Recommendations vary from guideline to guideline. The authors conclude:

In the absence of clearly supportive data, and with much data suggesting an increased risk of TAEs, we recommend that practicing hematologists exercise restraint in the use of rFVIIa in off-label settings. Until better quality and more statistically significant data regarding the use of rFVIIa in different off-label scenarios become available, we believe it is useful for professional organizations to develop conservative evidence-based guidelines for use of rFVIIa in off-label settings that should be updated frequently to reflect findings from new trials. We hope that patient safety will be appropriately guarded by this mechanism, while encouraging physicians to adapt their clinical practice to fresh evidence.

VTE in cancer patients

Here's a nice free full text review.

Thrombocytopenia in the ICU

Should you stop certain drugs? Modify your anticoagulant strategy? Delay important procedures? Transfuse platelets? This review may help.

Points of special interest:

Thrombocytopenia in the critically ill patient portends a worse outcome.

The most valuable clue as to the etiology of thrombocytopenia is often the time course of its development and recovery. Typical patterns are illustrated in the article.

Pocket mobile echocardiography---ready for prime time?

Should all hospitalists be carrying these things around? This Annals study suggests that more study is needed before they are ready for widespread use.

Chronic thromboembolic pulmonary hypertension

No longer an autopsy curiosity or an untreatable disease according to this review.

Claims of rapid response systems still unsupported

Yet another study, this one recently published in Chest, has failed to show an impact. RRTs are widely used in hospitals and widely claimed to be patient safety tools. Although the RRT may have a niche in your hospital or be a driver of education and process improvement the patient safety claim remains unfounded. Via Hospital Medicine Quick Hits.

Nesiritide---debate settled?

The long awaited nesiritide trial was just published in NEJM. Not really all that new, as it had been presented in part at American Heart last November. The long and the short: no difference in the big outcomes, with a modest improvement in dyspnea at the price of more hypotension. If nesiritide has a niche I don't know what it is. It's certainly not a front line agent for acute decompensated heart failure in hospitalized patients.


HT to Hospital Medicine Quick Hits.

Which hospitalized patients should receive GI bleeding prophylaxis with acid-suppressive medication?

According to this report acid-suppressive medications may be over utilized. The practice is widespread throughout hospitals. However, the evidence only supports use in critically ill patients.

Outpatient management of PE---when is it safe?

A recently published study in the Lancet examined this question:

We undertook an open-label, randomised non-inferiority trial at 19 emergency departments in Switzerland, France, Belgium, and the USA. We randomly assigned patients with acute, symptomatic pulmonary embolism and a low risk of death (pulmonary embolism severity index risk classes I or II) with a computer-generated randomisation sequence (blocks of 2–4) in a 1:1 ratio to initial outpatient (ie, discharged from hospital greater than or equal to 24 h after randomisation) or inpatient treatment with subcutaneous enoxaparin (greater than or equal to 5 days)...

So in the outpatient arm the entirety of treatment was not really outpatient. Evidently patients remained in the ER or in an observation unit for up to 24 hours. More from the article:

...one (0·6%) of 171 outpatients developed recurrent venous thromboembolism within 90 days compared with none of 168 inpatients (95% upper confidence limit [UCL] 2·7%; p=0·011). Only one (0·6%) patient in each treatment group died within 90 days (95% UCL 2·1%; p=0·005), and two (1·2%) of 171 outpatients and no inpatients had major bleeding within 14 days (95% UCL 3·6%; p=0·031). By 90 days, three (1·8%) outpatients but no inpatients had developed major bleeding (95% UCL 4·5%; p=0·086).

So while there was no difference in mortality there was a small increase in recurrent VTE and bleeding with outpatient treatment. Despite this the authors concluded that outpatient treatment was safe in selected low risk patients. How did they define low risk? Using the the pulmonary embolism severity index (PESI). I discussed the PESI previously here. As I cited in that post, an older study had suggested that the PESI could help select patients for outpatient treatment. The original study on the PESI is here.


Biomarkers and echocardiography are the traditional tools for acute risk assessment in PE, but clinical scores like the PESI are emerging as comparable means.


HT to Hospital Medicine Quick Hits.

ABCD 2---too easy to be true?

Clinicians have long relied on the ABCD 2 score to help determine which patients who present to the ER with TIA can be sent home for completion of their work up as an out patient. But the tool had never been prospectively validated. A new study in CMAJ tried to do just that. The result? If you use the traditional cut off of a score of 5 the sensitivity is lousy. If you use AHA's recommended score of 2 the sensitivity improves considerably but the specificity is poor.


A related Medscape piece offers some insightful comments from one of the study authors and new perspectives on today's stroke care:

The investigators found that an ABCD2 score of more than 5 had low sensitivity (31.6%; 95% confidence interval [CI], 19.1% – 47.5%) for predicting subsequent stroke at 7 days. For predicting stroke at 90 days, its sensitivity was 29.2% (95% CI, 19.6% – 41.2%). "These sensitivities are too low to be clinically acceptable," Dr. Perry said...

"The proposed threshold by the American Heart Association, which is a score greater than 2 to indicate high risk, was very sensitive; however, it classified all but a few patients as high risk, so it is not very discriminating for early stroke," Dr. Perry noted.

Which means you might as well admit just about everybody, if not to the hospital to a stroke obs unit, if you have one, or hold them in the ER long enough to do more extensive imaging, more than just a CT scan.


How would the score perform if integrated with aggressive imaging in the ER? That's a question for further study.

Serum potassium levels after cardiac arrest

Here's a really interesting study that looked at serum potassium levels after cardiac arrest:

The mean potassium level was 3.9±0.9mmol/l and thus within the reference range of 3.5–5.0mmol/l, but the overall prevalence of hypokalaemia was high (31.0%). Moderate rather than severe hypokalaemia was typically observed..

Among those six patients with extreme hypokalaemia defined as a potassium levels below the 2.5 percentile, two adult females were identified to suffer from previously untreated body scheme disorder with furosemide abuse (potassium 1.1 and 1.4mmol/l). Another patient (potassium 2.1mmol/l) suffered from poorly controlled bulimia nervosa and acute diarrhoea due to GI infection and one (potassium 2.4mmol/l) from untreated bulimic anorexia...

Conclusions

In contrast to moderately reduced potassium which is a frequent finding in adult patients at the time of admission for non-traumatic cardiac arrest, severe hypokalaemia is uncommon. The high prevalence of patients with body dysmorphophobic eating disorders in this group underscores accidental self-induced hypokalaemia may evolve as an important differential diagnosis in cardiac arrest in young female patients.

Mild to moderate hypokalemia after cardiac arrest may be redistributional, due either to endogenous catecholamines associated with the cardiac event or to administered epinephrine and therefore may not reflect pre-arrest potassium levels. In this study severe hypokalemia was associated with eating disorders and extreme dieting.


That, you may recall, is what caused Terri Schiavo's cardiac arrest:

Upon admission to the hospital, her serum potassium level was noted to be very low, at 2.0 mEq/L...

Her medical chart contained a note that "she apparently has been trying to keep her weight down with dieting by herself, drinking liquids most of the time during the day and drinking about 10–15 glasses of iced tea”...

Terri's husband, Michael, later filed and won a malpractice suit against her obstetrician, Dr. Stephen Igel, who was treating her for infertility, on the basis that he failed to diagnose bulimia as the cause of her infertility.

Postmortem examination, including a molecular autopsy, found no evidence of structural heart disease or channelopathy.