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.