Sunday, March 30, 2014

Schnitzler syndrome

Considered rare, but probably under diagnosed.

Platelet transfusions in critically ill patients: a review

A systematic review in the journal Blood concluded:
Recommendation: For critically ill adults with severe thrombocytopenia and no evidence of bleeding, there is insufficient evidence to make a recommendation for or against platelet transfusion.

However, the authors cite the Surviving Sepsis guidelines which made a weak recommendation for prophylactic platelet transfusion in patients with platelet counts below 20,000 who have significant bleeding risk.

Saturday, March 29, 2014

Sideroblastic anemia induced by linezolid

This report makes a pretty convincing case that it's a real entity. I was a bit surprised the article didn't mention vitamin B6, which has a connection. Rare cases of B6 responsive sideroblastic anemia (of a variety of causes) were reported in the 1950s and 60s but soon fell off the radar screen. In more recent years reports have surfaced of B6 responsive anemia (but not other cytopenias) in patients taking linezolid. Those reports, at least the ones I have seen, do not mention sideroblasts.  

ProfRoofs lectures

Videos for students in the medical sciences.

Friday, March 28, 2014

Elevated troponin and abnormal ECG: is it ACS or could it be PE?

Clinical circumstances and the electrocardiogram can provide powerful clues but they are widely ignored. Mistaking PE for ACS or heart failure are well known examples of misdiagnosis. Today's environment of core measures, care pathways and rapid throughput pressures physicians more than ever before to jump to the most superficially apparent cause (troponin positive, thinking stops).

When PE presents with an abnormal ECG and an elevated troponin it is massive or submassive. Nevertheless it tends to be missed. Here is a great post from Dr. Smith which discusses some of the nuances.

Thursday, March 27, 2014

AV block occurring when it shouldn't: the paradoxical critical rate phenomenon

When we think of rate related AV block we almost always assume it occurs at faster supraventricular rates, especially type 2 AV block and bundle branch block. Occasionally, rarely in fact, it's the reverse: block occurs only during bradycardia or following a longer RR interval. If a vagal mechanism is excluded (which can usually be done by careful examination of the strips and clinical circumstances) the best known mechanism is phase 4 block which is the topic of the linked article.

Other causes of related electrocardiographic curiosities are supernormal conduction and the Wedensky effect.

Hospital Medicine 2014, Las Vegas

I'm here attending the national meeting of the Society of Hospital Medicine. The clinical sessions have charged my batteries and the organizational/political ones have stoked the fire. I'll have much to say about all that later---maybe in a week or two (there's no way I could do the meeting justice by live blogging or tweeting). In the meantime auto-posting will keep the blog alive until I get home.

Wednesday, March 26, 2014

Relative hyperlactatemia

---meaning elevated lactate levels within the reference range, was associated with increased mortality in this study of ICU patients. A value of 1.35 mmol/L was found to be the best cutoff.  

Which patients admitted with pneumonia should get blood cultures?

This topic has been a little controversial. Core measures have just now caught up with the more selective culture recommendations from guidelines. A nice topic update is posted at Academic Life in Emergency Medicine.

Tuesday, March 25, 2014

What are the factors that determine professional satisfaction among physicians?

A recent RAND corporation study addressing this question came up with several interesting findings. As expected, time pressures, externally imposed regulations and threats to the stability of income were negatives. No definitive patterns emerged about the impact of the Affordable Care Act (ACA) perhaps, according to the authors, because it's too early in the game. Intrusive regulation has been increasing steadily for decades and the ACA may prove to be just another point along that continuum. But concerning the impact of proposed new models of health care organization (e.g. the ACO) in the ACA the authors were able to draw upon data from analogous models brought by the wave of managed care in the 1990s. Findings from that era pointed to a negative impact on professional satisfaction.

The report did cite a lot of frustration among physicians about the meaningful use requirements for EMRs (not a part of Obamacare). In general, data from the report indicate that physicians like the idea of the EMR in the abstract (think it has promise) but perceive many aspects of present day use to be impediments to professional satisfaction. Chief among these are poor communication of clinical information (downsides of templates and other automated EMR functions) and the loading on of clerical duties out of the scope of physician training inherent in the way the EMR is used. As such the EMR is perceived as a time consumer rather than a time saver.

For more on the negative impact of the EMR on professional satisfaction see this post at Health Care Renewal.

Patient harm during nursing home stay

From a BMJ news report:
A third of Medicare patients who are discharged to a skilled nursing facility for post-acute care are harmed during their stay at the nursing home, says a new report.1
In the study by the Office of Inspector General at the US Department of Health and Human Services, investigators reviewed the records of 653 randomly selected Medicare beneficiaries whose stay at a skilled nursing facility had lasted a maximum of 35 days and had ended in August 2011.

Here is the link to the original report. According to the report 22% of patients experienced serious harm and 59% of the episodes were preventable.

A close look at the methods of the study suggests several cautions in interpreting the findings. The 59% figure is open to question. The determination of preventability was often based on weak circumstantial evidence and unwarranted assumptions. Many of the events that were truly preventable reflected a need for greater vigilance but not error.

Pharmacy involvement in patient education and discharge medication instructions

---reduced 30 day all cause readmissions in heart failure patients in this study. Via Hospital Medicine Virtual Journal Club.

Monday, March 24, 2014

Unrecognized pheochromocytoma

A case report and mini review.

Phaeochromocytoma is a rare catecholamine-producing tumour with an annual incidence rate of 2 cases per 1 million per year in the general population [1]. The incidence of phaeochromocytoma in autopsy studies is under 0.1% and autopsy studies have also shown that up to 50% of phaeochromocytomas are unrecognized [2]. The tumour has protean manifestations, mimicking a variety of conditions, earning the title “great mimic” and often resulting in erroneous and delayed diagnosis, which if missed or not properly treated, will almost invariably prove fatal [3]

Early discharge planning and outcomes

Here's an interesting systematic review finding that while early discharge planning didn't affect outcomes of the index (current) admission it did extend the readmission interval and reduced the LOS of the readmission. From the paper:

The findings suggest that by implementing early discharge planning focused on functional needs’ assessment for discharge home, patient and caregiver education and follow-up, medication review and information transmittal, clinicians may anticipate reductions in older adults’ hospital readmissions by 22% and readmission lengths of hospital stay by almost two and a half days, compared with usual care.


Brief videos on various medical topics.

Sunday, March 23, 2014

The hospital pharmacist as part of the multidisciplinary ICU team

From an article in Chest:
Critical care pharmacy services in the ICU have expanded from traditional dispensing responsibilities to being recognized as an essential component of multidisciplinary care for critically ill patients. Augmented by technology and resource utilization, this shift in roles has allowed pharmacists to provide valuable services in the form of assisting physicians and clinicians with pharmacotherapy decision-making, reducing medication errors, and improving medication safety systems to optimize patient outcomes. Documented improvements in the management of infections, anticoagulation therapy, sedation, and analgesia for patients receiving mechanical ventilation and in emergency response help to justify the need for clinical pharmacy services for critically ill patients. Contributions to quality improvement initiatives, scholarly and research activities, and the education and training of interdisciplinary personnel are also valued services offered by clinical pharmacists.

Minute Physics

Physics concepts explained in seconds.

Aerosolized colistin as an adjunct to IV colistin

It appeared to be helpful in this study of patients with VAP due to colistin-only sensitive organisms.

Saturday, March 22, 2014

Stethoscope contamination after patient contact

This study looked at stethoscope bacterial contamination and compared it with hand contamination after a single patient contact.

Stethoscope diaphragm contamination was found to exceed contamination of all parts of the hand except for the fingertips.

The authors recommend cleaning the stethoscope after every patient exam. This should be common sense, but system improvements (like hand washing, as important as that is) tend to become substitutes for common sense. As a result we've all but ignored stethoscope cleaning.

I have another suggestion. By all means use the stethoscope (and clean it after you use it) if you intend, and have the skill, to use it as a meaningful clinical tool. Do not use it merely as a coding enhancer.

Via Hospital Medicine Virtual Journal Club.

Preventing hypokalemia in hospitalized patients

From a recent study:
Objectives To determine if administering potassium preemptively in maintenance intravenous fluid would prevent episodes of hypokalemia and reduce the need for potassium boluses.
Methods Medical records of 267 patients with normal potassium and creatinine levels at admission who did not receive total parenteral nutrition were reviewed. The 156 patients who met the study criteria were categorized by group: those who received potassium via maintenance intravenous fluid (treatment; n = 76) and those who did not (control; n = 80). The treatment group had potassium chloride or acetate added to intravenous fluid delivered at 36 to 72 mmol/d...
The patients given maintenance potassium preemptively received significantly fewer (P less than .001) potassium boluses (0.8) than did the control group (2.73), for a mean savings of $231 per patient for the treatment group.
Conclusions Patients with normal potassium and creatinine levels at admission benefitted from a maintenance intravenous dose of potassium of 72 to 144 mmol/L per day. Compared with control patients, patients receiving this dose avoided detrimental hypokalemic events, had fewer invasive procedures and lower costs, and required less nursing care.

Hang normal saline as the maintenance IV fluid on patients with good kidneys and no potassium supplement or potassium sparing drugs on board and they are likely to be hypokalmemic the next morning. If straight normal saline with no additives is the default IV fluid these days it may be driven by CPOE. Customizing IV fluids is more difficult if you don't have a unit secretary to enter it for you.

Via Hospital Medicine Virtual Journal Club.

CPOE and medication prescribing errors

For some time now computerized physician order entry (CPOE) has been credited with “intercepting” medical errors. How many of these “error interceptions” are clinically meaningful is not known. Here is a study demonstrating errors attributable to CPOE. There is a trade off, and the overall impact on patient safety is not known. Via Hospital Medicine Virtual Journal Club.

Friday, March 21, 2014

When do poison control centers recommend lipid rescue therapy?

Here is a report from a survey of medical directors of poison control centers:
The majority of PCC medical directors completed the survey (45 out of 57; 79 %). Of the 45 respondents, all felt that IFE therapy played a role in the acute overdose setting. Most PCCs (30 out of 45; 67 %) have a protocol for IFE therapy. In a scenario with “cardiac arrest” due to a single xenobiotic, directors stated that their center would “always” or “often” recommend IFE after overdose of bupivacaine (43 out of 45; 96 %), verapamil (36 out of 45; 80 %), amitriptyline (31 out of 45; 69 %), or an unknown xenobiotic (12 out of 45; 27 %). In a scenario with “shock” due to a single xenobiotic, directors stated that their PCC would “always” or “often” recommend IFE after overdose of bupivacaine (40 out of 45; 89 %), verapamil (28 out of 45; 62 %), amitriptyline (25 out of 45; 56 %), or an unknown xenobiotic (8 out of 45; 18 %). IFE therapy is being recommended by US PCCs; protocols and dosing regimens are nearly uniform. Most directors feel that IFE is safe but are more likely to recommend IFE in patients with cardiac arrest than in patients with severe hemodynamic compromise.

Early goal directed therapy: unbundling the resuscitation bundle

Recall that a few days ago I gave you a heads up that results of three new sepsis trials evaluating EGDT were about to be released. The first of those, the ProCESS trial, was just published, on line ahead of print in NEJM. You can access the full text here. Let's get straight to the findings:

We enrolled 1341 patients, of whom 439 were randomly assigned to protocol-based EGDT, 446 to protocol-based standard therapy, and 456 to usual care. Resuscitation strategies differed significantly with respect to the monitoring of central venous pressure and oxygen and the use of intravenous fluids, vasopressors, inotropes, and blood transfusions. By 60 days, there were 92 deaths in the protocol-based EGDT group (21.0%), 81 in the protocol-based standard-therapy group (18.2%), and 86 in the usual-care group (18.9%) (relative risk with protocol-based therapy vs. usual care, 1.04; 95% confidence interval [CI], 0.82 to 1.31; P=0.83; relative risk with protocol-based EGDT vs. protocol-based standard therapy, 1.15; 95% CI, 0.88 to 1.51; P=0.31). There were no significant differences in 90-day mortality, 1-year mortality, or the need for organ support.

The social media are full of comments like “EGDT is dead” and “EGDT is of no benefit.” Before reaching such a simplistic conclusion consider the following:

The original Rivers study in 2001 showed---

In-hospital mortality was 30.5 percent in the group assigned to early goal-directed therapy, as compared with 46.5 percent in the group assigned to standard therapy (P=0.009).

That means a 35% relative risk mortality reduction, 16% absolute risk reduction and NNT of 6 attributable to EGDT.

The mortality was much lower in all three groups in the ProCESS trial, on the order of 18-20%.

That reflects an overall trend of reduced mortality in severe sepsis as illustrated by this recent paper:

Retrospective, observational study from 2000 to 2012 including 101 064 patients with severe sepsis from 171 ICUs with various patient case mix in Australia and New Zealand.

Hospital outcome (mortality and discharge to home, to other hospital, or to rehabilitation).

Absolute mortality in severe sepsis decreased from 35.0% (95% CI, 33.2%-36.8%; 949/2708) to 18.4% (95% CI, 17.8%-19.0%; 2300/12 512; P less than .001), representing an overall decrease of 16.7% (95% CI, 14.8%-18.6%), an annual rate of absolute decrease of 1.3%, and a relative risk reduction of 47.5% (95% CI, 44.1%-50.8%). After adjusted analysis mortality decreased throughout the study period with an odds ratio (OR) of 0.49 (95% CI, 0.46-0.52) in 2012, using the year 2000 as the reference (P less than .001).

Although differences in the use of various resuscitation modalities reached statistical significance among the treatment groups in ProCESS, these differences were not large with the exception of transfusion and dobutamine administration, which were much more frequent in the EGDT group.

Patients in the protocolized non-EGDT group had to undergo a clinical hemodynamic assessment at least once an hour.

What does this all mean?

“Usual care” for sepsis has, over the past decade, incorporated evidence based process improvements, including the principles of EGDT. This is attributable in large part to the Surviving SepsisCampaign, which was once criticized as a marketing campaign disguised as evidencebased medicine.

“Usual care” has now improved to the point where system improvements in the form of bundles may no longer be important. This comment form one of the other blogs says it well:

Lastly, we need to be cautious about contamination here. The principles of EGDT are well known and widely applied even if they are not part of a strict protocol. The differences between a strict regime and what has now become common knowledge and practice since 2001 are unlikely to be as dramatic as they were back in 2001. We must ask ourselves whether this is a failure of a protocol to be different or rather the success of it’s dissemination to a wider clinical practice.

The real questions addressed by this study concerned which specific components of the resuscitation bundle (EGDT) need to be preserved and which can be dispensed with. It appears now that dobutamine and aggressive transfusion will take a back seat.

That leaves us with the question of the central line. From the ProCESS trial we can conclude that clinical volume assessment is an acceptable alternative to CVP monitoring in many patients. Central venous oxygen saturation is not essential (lactate measurements and clinical parameters are reasonable surrogates).

What about the need for a central line (or IO access) for administration of pressors? Is the use of norepinephrine via a peripheral IV contraindicated? According to this post and literaturereview at the EM Crit blog that may be an urban legend, but you can read the post and go to the primary sources and decide for yourself.

How wide is too wide for paced QRS?

If it's acutely wider than expected think of hyperkalemia and drug (sodium channel blocker) toxicity. Dr. Smith discusses here.

(Similar thinking would apply to LBBB).

Viral etiology of nosocomial pneumonia

From a recent paper in Current Opinion in Infectious Diseases:

Respiratory viruses may be responsible for healthcare-associated pneumonia, because affected patients and those with CAP have the same risk factors for viral disease. In mechanically ventilated patients, viruses belonging to the Herpesviridae family, namely herpes simplex virus (HSV) and cytomegalovirus, can be reactivated and cause bronchopneumonitis or ventilator-associated pneumonia, respectively. Recent results confirmed the high rate of HSV reactivation in the distal airways of mechanically ventilated patients, and that patients with high virus loads (greater than 10 copies/ml of bronchoalveolar lavage fluid) have poorer outcomes than those with low or no virus load. However, the responsibility of mimivirus, initially described as a possible cause of pneumonia, was not confirmed for nosocomial pneumonia.

Respiratory viruses are mainly responsible for CAP, but they may also cause healthcare-associated pneumonia. HSV bronchopneumonitis and cytomegalovirus pneumonia are not rare diseases..

Via Hospital Medicine Virtual Journal Club.

Thursday, March 20, 2014

Hospital readmissions: not necessarily the fault of poor care transition

CMS has penalties for hospital readmissions. These are based on the premise that inadequate hospital care, poor discharge planning and poor transitions care are to blame. That premise, for a large number of today's hospitalized patients, is false according to a recent NEJM Perspective piece. These patients, referred to in the article as hospital-dependent, belong in a separate category. We don't have data from systematic studies but in clinical experience hospital-dependent patients account for a large portion of readmissions. So we have two categories of readmission (these overlap somewhat but it is useful to think of it in this way): (a) preventable and (b) inevitable due to inherent patient attributes. The hospital-dependent patient is category (b).

An example from category (a) might be the heart failure patient who is otherwise healthy (translate: doesn't have a problem list a mile long) discharged with inadequate education or without timely clinic access.

Category (b) patients have these characteristics:


Multiple complex problems each of which, despite optimal management, is precariously close to decompensation at any moment.

Little physiologic reserve.

Not terminal and desiring to live.

Live from one exacerbation to another, discharged from inpatient care each time they are, however tenuously, patched together. Again.

We like to think patients are ultimately better off at home because the hospital can be an unsafe place in many ways. But it's different, say the authors, for hospital-dependent patients. The hospital may be the safest environment for them. They are in continual need, even in the post-acute phase, of rapidly accessible technology and high level care teams. Despite all of today's systems improvements that environment doesn't exist outside the hospital.

The first principle of evidence based medicine is respect for patient preferences and values. Hospital-dependent patients, despite being made aware of the availability of hospice care, want to live even if much of that life is spent in the confines of a hospital. Our health care system does not have good options for them. The authors might not admit it but in my reading of the article they come just short of saying that what these patients really need is to spend the rest of their lives in acute care hospitals.

Early in my career frail patients with multiple complex problems were kept in hospitals for extended periods of time. The Prospective Payment System came along in 1984 and no longer allowed that. The “bounce-back” became the norm as a result.

If there is a systems approach to accommodate this large population of patients it will be very expensive, say the authors. Maybe darn near as expensive as life long acute care hospitalization.

Presenting ECG findings and outcomes in NSTEMI patients

From a recent paper in the American Journal of Cardiology:

The angiogram revealed that patients with ST-segment depression had more left main, proximal left anterior descending, and 3-vessel coronary artery disease and underwent coronary artery bypass grafting most often. In contrast, patients with transient ST-segment elevation had 1-vessel CAD and underwent percutaneous coronary intervention the most. The unadjusted mortality was highest in the ST-segment depression group, followed by the no ischemic changes, transient ST-segment elevation, and T-wave inversion group. Adjusted mortality using the ACTION Registry-GWTG in-hospital mortality model with the no ischemic changes group as the reference showed that in-hospital mortality was similar in the transient ST-segment elevation (odds ratio 1.15, 95% confidence interval 0.97 to 1.37; p = 0.10), higher in the ST-segment depression group (odds ratio 1.46, 95% confidence interval 1.37 to 1.54; p less than 0.0001), and lower in the T-wave inversion group (odds ratio 0.91, 95% confidence interval 0.83 to 0.99; p = 0.026). In conclusion, the clinical and angiographic characteristics and treatment and outcomes of patients with NSTEMI differed substantially according to the presenting ECG findings. Patients with ST-segment depression have a greater burden of co-morbidities and coronary atherosclerosis and have a greater risk of adjusted in-hospital mortality compared with the other groups.

Of note, a subset of this “NSTEMI” population actually had transient ST elevation further highlighting the confusion around the distinction of STEMI versus NSTEMI.

Review of noninvasive ventilation in the treatment of hypercapnic respiratory failure

This review is from the journal Breathe.

Acute exacerbation of COPD is the best established indication for NIV in the category of hypercapnic respiratory failure. But as evident from the review these indications are expanding and contraindications (particularly depressed level of consciousness) are shrinking, or becoming relative as opposed to absolute. One concern I had in this otherwise excellent review was mention of neuromuscular respiratory disease (without specification any given type and without mention of Guillain-Barre) as an indication for NIV. While I suppose, as more and more experience is gained with NIV in neuromuscular respiratory disease it will emerge as an alternative in some situations my last read on GB was that early invasive ventilation was the modality of choice for certain respiratory situations even before the onset of hypercapnia.

Wednesday, March 19, 2014

Results reporting after PE imaging

When a CTA demonstrated PE, delays in reporting results were associated with increased mortality in this study. It should go without saying that timely results reporting might improve outcome and that's not the reason I posted this. I found this paper interesting because it is another one of many studies showing that treatment of VTE matters. Shouldn't that go without saying too? Not necessarily these days. There's a rising chorus of voices coming from certain EBM purists, mainly in academic emergency medicine, saying that the treatment of VTE is not evidence based. There's a long story behind that which will be the topic of future posts.  

Chronic critical illness: a modern day purgatory?

That's a term used in a recent NEJM piece concerning the topic.


Chronic critical illness (CCI) was originally administratively defined. Patients who survived their critical illness yet had the need for long term labor intensive care, often with continued mechanical ventilation, were eligible for transfer to a different category of hospital (oxymoronically called a long term acute care or LTAC hospital) under a different reimbursement and regulatory environment. But according to the article it's more than an administrative designation. It's a real clinical entity. The piece emphasizes a need for more training in the field of CCI and points to the generally poor prognosis of such patients.

A new disease?

From the paper:

..says Judith Nelson, a palliative care and critical care specialist at New York City's Mount Sinai Hospital who has conducted seminal research in this population. “This is a disease. It's sometimes or even often worse than some cancers in terms of its mortality and effect on quality of life. People know what cancer means. They've heard of it. But they've not heard of this.”

Better training and education needed

And why? According to the author:

Indeed, numerous studies reveal that we are, quite simply, bad at talking to families about prolonged illness...A survey of patients or surrogate decision makers for 100 chronically critically ill patients who had recently undergone tracheotomy revealed that the majority had made key decisions without any information about expected 1-year survival, functional status, cognitive status, or alternatives to continuing mechanical ventilation...
House officers increasingly receive formal training before leading conversations about the goals of a patient's care. Discussing the pros, cons, and long-term sequelae of a tracheotomy and of subsequent transfer to an LTAC hospital is another area in which we could benefit from further formalized training..

Yes, we could use more education in how to better inform patients and their families. That's part of the value of excellent palliative care. But is that the only reason? Education in advance care planning was the dominant focus of the article, with little or no mention on how we might do a better job of getting some of these patients well and on their feet. That's the concerning thread in the article. While making no declarative statement to this effect the author implies that CCI patients belong in a hospice rather than an LTAC.

The Cochrane Collaboration 20 years later

Here is an editorial in BMJ on the history of the Cochrane Collaboration. It is not appropriately critical (overlooking a couple of the CC's huge blind spots) though it pretends to be. It ignores the fact that through the years the CC has been accommodating, even promotional, towards unscientific ideas like homeopathy and therapeutic touch. I documented that problem, with examples of reviews favorable, or neutral, to homeopathy and acupuncture as treatments for a variety of conditions, in this post. Unfortunately the links to the Cochrane reviews provided in that post are no longer active. But here is a Cochrane review stating that the only methodologically suitable trial showed a benefit of acupuncture in the treatment of mumps, and recommending that more trials be done. This review from the CC cited studies purporting to show a mortality and function benefit derived from acupuncture in the treatment of acute stroke, but said that methodologically stronger studies are needed. The list of these sorts of Cochrane “evidence based” reviews goes on and on. Apparently, in the philosophy of the CC, the biologic plausibility of a study doesn't matter in the least in critical appraisal of the results. Moreover, the nuttiness of an idea does not disqualify it as the topic for a review. What does qualify a topic for Cochrane review is popularity. If a modality of treatment is popular in some part of the world, no matter how implausible, it seems to warrant a review.

CC's other big blind spot is one I've commented on before and which has been termed by others as “methodolatry.” Definition:

the profane worship of the randomized clinical trial as the only valid method of investigation.

This is illustrated by a CC review of anticoagulation for acute venous thromboembolism (VTE):

Authors' conclusions
The limited evidence from RCTs of anticoagulants versus NSAIDs or placebo is inconclusive regarding the efficacy and safety of anticoagulants in VTE treatment. The use of anticoagulants is widely accepted in clinical practice, so a further RCT comparing anticoagulants to placebo could not ethically be carried out.

The authors' statements are a little weaselly. They're saying there's no good evidence to support anticoagulants but come short of recommending for or against them. And while saying it would not be ethical to do a RCT they come short of saying there is no equipoise. In fact, given their presentation of the evidence as showing unknown benefit they imply that there is equipoise.

These statements carry the potential for harm as illustrated by their citation on a web site purporting to advance the cause of evidence based medicine (EBM), the NNT, a popular open access site that encourages clinicians and patients to evaluate evidence for claims of popular treatments. The NNT's piece on anticoagulants for the treatment of VTE, using the Cochrane review as its only source material, states regarding the treatment of VTE with anticoagulants:

100% saw no benefit
0% were helped by being saved from death

Only through the lens of methodolatry could such a conclusion be reached. In fact there is evidence in favor of the treatment of VTE with anticoagulants. Though not from high quality placebo controlled RCTs the evidence is, in the aggregate, compelling.

Tuesday, March 18, 2014

What are the key attributes of an effective hospitalist group?

This is what the Society of Hospital Medicine has come up with and it is available as free full text. A lot of it is pretty nebulous to me and raises as many questions as it does answers. I may try and unpack some of that in a future post but I can only read the word “stakeholder” so many times in one sitting.

An oral history of evidence based medicine

JAMA and BMJ have posted a series of video interviews and a panel discussion with some of the founders of evidence based medicine (EBM). This is a must see if you're interested in a better understanding of EBM and its origins.

I'll open my discussion of the series with a quote from one of the panelists, Kay Dickersin, Director of the Johns Hopkins Center for Clinical Trials: “It is curious, even shocking, that the adjective 'evidence based' is needed. The public must wonder on what basis medical decisions are made otherwise. Is it intuition? Magic?” When I first encountered the term a couple of decades ago I wondered the same thing. What else had I been basing my practice on all that time if not on evidence?

Two of the interviews are with David Sackett, widely known as one of EBM's main apologists. He talked about the beginnings of the movement and emphasized that it is not merely a collection and critical appraisal (a term the EBM founders coined) of evidence. Rather, it goes beyond that to encompass the judgment of the individual clinician and the preferences and values of the individual patient. Those two elements often get left out of the discussion. Because the individual patient is a key element of EBM, proponents of medicine done by central planning can never claim to advocate for evidence based medicine. Along the same lines Dr. Gordon Guyatt remarked that there is no clinical decision that doesn't have the individual patient's preferences and values attached to it. As a corollary, evidence alone cannot inform a clinical decision.

Originally the founders were going to name the new movement “scientific medicine” but the basic science people at the table cringed. “We are scientific,” they protested. Hence the name EBM was created. The irony is that while the founders intended to be scientific the movement over time has played out as unscientific in many ways as I and others have documented. (Recognition of these unscientific aspects of EBM has given birth to another movement, Science Based Medicine, or SBM).

A good deal of the discussion centered around the Cochrane Collaboration. Regarded as a centerpiece of EBM the Cochrane Collaboration has become a platform for some unsound ideas (see here).

One of the discussants, Drummond Rennie, recalls the rise to prominence of meta-analysis. The rediscovery of meta-analysis in the 1970s, according to Rennie, was one of the antecedents of EBM. Meta-analysis offered a cohesive and logical way to synthesize seemingly disparate research studies. Without meta-analysis one was left only to select among contradictory lines of evidence. In an exaggeration Rennie says rather than do that one might as well have thrown out all old research.

Dr. Brian Haynes was asked whether EBM was too much work for the busy clinician. When one considers the steps involved in searching, critical appraisal and application it does seem a daunting task. Certainly it would have been too time consuming before the era of computer searching. On line searching was available in the 1980s (you had to go to considerable trouble to set it up) but had not yet reached prime time even by the time EBM was announced to the world in 1992.

Haynes said that he and his colleagues were working from the beginning to make the process user friendly in everyday practice. They have been exploring ways to put best evidence into secondary sources, including even textbooks (some EBM purists decry the use of textbooks) so that doctors will not have to do primary literature searches and critical appraisal. Currently available secondary resources, said Haynes, may not be where they need to be yet but are improving.

As Guyatt pointed out the leaders realized early on that getting all clinicians to search and critically appraise the literature individually was an unattainable ideal. The best that could be done was to educate clinicians in the principles of EBM so they could then make more intelligent and effective use of secondary sources. Evidence derived from such sources has already been critically appraised and has been referred to as “pre-processed” evidence. Some EBM purists, taking a negative view of this approach, consider it an unfortunate compromise and have called it “evidence based capitulation.”

There was an irritating tone throughout the series: the implication that before the launch of the movement known as EBM medical practice was not based on evidence, or even science, at all. That is simply not true. As I said in my post marking the 20th anniversary of EBM the movement did not bring us anything fundamentally new. The idea that evidence is necessary goes back as far as the scientific revolution of the 17th century. Over 100 years ago the Flexner Report emphasized the need for evidence to prevail over dogma. Clinical trials, even comparative effectiveness research, go back to at least the 1960s. All EBM really did was to give us a more systematic and rigorous way to apply the best evidence to patient care.

There were huge gaps between evidence and practice before the launch of the movement but there still are. These gaps, which are somewhat inscrutable, will narrow over time but never completely close.

Angiotensin receptor blockers: are they protective against dementia?

There is low level evidence to suggest they are. From a recent review:
Purpose of review: The recent advances in our understanding of Alzheimer's disease pathophysiology and the renin angiotensin system pathways suggest that angiotensin receptor blockers (ARBs) are ideal drugs to explore for Alzheimer's disease therapy...
Studies in animal models suggest that ARBs have cognitive protective effects that are related to their ability to decrease production and oligomerization and increase degradation of Aβ and their vascular effects (improve blood–brain barrier, restore endothelial function, decrease inflammation, and increase cerebral blood flow). Human observational studies have further suggested that ARB use is associated with decreased risk of Alzheimer's disease and protection against future cognitive decline. Our work has suggested that ARB use is associated with decreased amyloid deposition in the brain in Alzheimer's disease and can provide cognitive protection in those with mild cognitive impairment, a prodromal state for Alzheimer's disease, and dementia.
Summary: To date, no robust clinical trial of ARBs in Alzheimer's disease has been performed. All things being equal, it is reasonable to consider ARBs in those with cognitive risks.

Monday, March 17, 2014

Takotsubo cardiomyopathy versus STEMI

Typically patients with Takotsubo cardiomyopathy (now better referred to as stress cardiomyopathy, SC) have a relatively small troponin elevation in comparison to the degree of left ventricular systolic dysfunction, so the findings of this paper make perfect sense:

All patients underwent acute echocardiography, and the peak troponin I level was determined. The troponin-ejection fraction product (TEFP) was derived by multiplying the peak troponin I level and the echocardiographically derived left ventricular ejection fraction. Comparing the SC and STEMI groups, the mean left ventricular ejection fraction at the time of presentation was 30 ± 9% versus 44 ± 11%, respectively (p less than 0.001), and the peak troponin I was 7.6 ± 18 versus 102.2 ± 110.3 ng/dl, respectively (p less than 0.001). The mean TEFP was thus 182 ± 380 and 4,088 ± 4,244 for the SC and STEMI groups, respectively (p less than 0.001). Receiver operating characteristic curve analysis showed that a TEFP value greater than or equal to 250 had a sensitivity of 95%, a specificity of 87%, a negative predictive value of 94%, a positive predictive value of 88%, and an overall accuracy of 91% to differentiate a true STEMI from SC (C-statistic 0.91 ± 0.02, p less than 0.001). In conclusion, for patients not undergoing emergent angiography, the TEFP may be used with high accuracy to differentiate SC with nonobstructive coronary artery disease from true STEMI due to coronary occlusion.

For information on the electrocardiographic differentiation see here.

Acute warfarin overdose

From a recent review:

While guidelines exist for management of a supratherapeutic international normalized ratio following therapeutic warfarin use, these guidelines are not designed for management of the acute warfarin overdose. There is a paucity of literature describing the latter..Twenty-three patients were admitted during the time period; males accounted for 15/23 (62.5 %) subjects. The median (interquartile range (IQR)) age was 43 (32–48.5) years. Seventeen subjects received vitamin K, with a median (IQR) dose of 15 (10–50) mg. The maximal total amount of vitamin K administered to a single patient during the index hospitalization was 110 mg. Three bleeding events occurred; one classified as major, and two as minor. All patients made a full recovery. In this case series of acute warfarin overdose, nearly all patients developed a coagulopathy, and nearly three-quarters of patients received vitamin K. Bleeding events occurred in a minority of patients.

Don't confuse this relatively benign situation with superwarfarin overdose, which is much more serious in terms of a higher incidence of bleeding, higher doses of vitamin K for reversal and a more prolonged course of toxicity.

Asystole following lipid rescue therapy

A couple of case reports were recently published in a toxicology journal:

Use of intravenous fat emulsion (IFE) for the treatment of poisoned patients in extremis is increasing. Little literature exists describing failures and complications of IFE. We describe two cardiac arrests temporally associated with IFE. A 50-year-old woman presented after ingesting 80 total tablets of metoprolol 25 mg and bupropion 150 mg. Bradycardia and hypotension were refractory to calcium salts, catecholamines, and high dose insulin (HDI). With a pulse of 40/min and mean arterial pressure (MAP) of 30 mmHg, 100 mL of 20 % IFE was given; within 30 s, brady-asystolic arrest occurred. Pulses returned after 3 min of CPR. The patient died on hospital day 4 of multisystem organ failure (MSOF). A 53-year-old man presented after ingesting of 3,600 mg of diltiazem and 1,200 mg of propranolol. Bradycardia and hypotension were refractory to calcium salts, catecholamines, HDI, bicarbonate, and atropine. With a pulse of 30/min and a MAP of 40 mmHg, 150 mL of 20 % IFE was given; within 1 min, a brady-asystolic arrest occurred. Pulses returned after 6 min of CPR. The patient died on hospital day 7 of MSOF. Reported cases of IFE failures or potential complications are sparse. This report adds only case experience, not clarity.

That last sentence is important. All we can say for sure is that we have two examples of lipid rescue failure. As for the cause of the asystole let's not lose sight of the obvious fact that both patients had overdosed on drugs that suppress the conduction system and could themselves cause asystole.

There's a good perspective on the article over at The Poison Review.

Sunday, March 16, 2014

Sticky platelet syndrome

Here are a couple of reviews on this syndrome. [1] [2] Here is a case report and mini review. [3]

From the mini review:

Sticky platelets syndrome (SPS) is an inherited thrombophilia characterized by platelet hyperaggregability, which can lead to the higher risk of thrombosis. The etiology of SPS remains unclear, but several gene polymorphisms have been recently studied and autosomal dominant heredity is suspected. Although SPS is traditionally connected with arterial thrombosis, several cases of SPS as a cause of venous thromboembolism have been described.

VTE is being increasingly recognized, so the syndrome is now considered to be one of both venous and arterial hypercoagulability. Moreover, low dose aspirin controls the clinical manifestations. That is a little counterintuitive alongside the notion that platelets cause thrombi in arteries whereas the coagulation proteins do so in veins and heart chambers, exclusively. That notion is simplistic and has been challenged by accumulating evidence that antiplatelet agents may have some effectiveness in preventing VTE and cardiac thrombi.

There is apparently some controversy regarding its importance in the field of hypercoagulability. According to the articles cited above it is a common underlying cause of thromboembolic disease. If true it is underappreciated. UpToDate devotes only a very brief section to it and questions whether it is a real clinical entity.

STEMI versus NSTEMI: misunderstood, misapplied

The terminology and classification of myocardial infarction has gone through several twists and turns through the years. As far back as I can remember my folks talking about it (my father was a physician) they called it acute coronary thrombosis. The years that followed saw changes in terminology which relied on either mistaken assumptions or poor electrocardiographic surrogates. One by one they've been proven wrong. When I started my training MIs were classified as transmural or subendocardial. That later gave way to transmural versus nontransmural. These terms were based on questionable assumptions about cardiac pathology and later transitioned to descriptive electrocardiographic terminology so that in the 1980s we had Q wave versus non Q wave infarction. In recent years of course this has been replaced by the present day designation of STEMI versus NSTEMI.

Branden Phibbs, MD, professor of cardiology at the University of Arizona, began challenging these distinctions in the early 1980s with this paper in which he made the case that the electrocardiographic distinction between transmural and subendocardial MI was a myth, useless clinically and prognostically. His arguments won the day and the designation was abandoned in favor of the more descriptive terms “Q wave” and “non Q wave” infarction. But in 1999 Phibbs and several other notables in the field struck again with the publication of this paper asserting that the distinction between Q wave and non Q wave infarction was clinically meaningless. Following that publication Phibbs continued relentlessly to hammer away, appealing to the evidence and ultimately won out, putting to rest once and for all the notion of Q wave infarction.

And so arose the categories of STEMI and NSTEMI. This designation was appealing in its descriptive simplicity. But in 2010 Phibbs weighed in again with the publication of another paper, a review of the pathologic changes and outcomes associated with the designations of STEMI and NSTEMI and concluded, just as was the case with Q wave versus non Q wave or with transmural versus subendocardial infarctions, that the STEMI/NSTEMI classification was useless. I blogged the paper a short time later and noted:

So here's what he's saying: In his review of the world's literature, clinical and pathological correlations do not support a meaningful electrocardiographic distinction between STEMI and NSTEMI. At first that seems counterintuitive but as I think about it I can think of several explanations for why the distinction would be artificial. He's not arguing that there's no such thing as a STEMI or a NSTEMI (after all, some MI patients have ST elevations and some don't), but that the distinction is not clinically or pathologically meaningful. There might be a number of reasons.

I went on to say that I was convinced from the paper that the distinctions were of questionable value but added that if the patient presented with obvious ischemic ST segment elevations it made the diagnosis of acute MI easier.

The paper was important because it questioned the validity of STEMI as a surrogate for acute coronary occlusion. But by that time STEMI had become embedded in performance measures for early reperfusion of patients presenting with MI.

Since 2010 much has been written demonstrating that ST segment elevation is a poor surrogate for acute coronary occlusion, further explaining the findings in the 2010 paper by Phibbs.

That brings me to this recent post at Dr. Smith's ECG blog which demonstrates the point nicely in a case of acute inferior infarction. Note that in his discussion Dr. Smith uses the term “STEMI” even though the patient doesn't meet the traditional ST segment criteria to denote that the patient has acute coronary occlusion. The patient in question, despite having been found in the catheterization laboratory to have acute occlusion of the right coronary artery, had only trace inferior ST elevations, certainly well below the threshold for any traditional or performance driven criteria. Yet, as Dr. Smith points out, this pattern is pathognomonic of acute coronary occlusion and inferior infarction. The telltale signs are: high amplitude (relative to the magnitude of the QRS complex) and broad based inferior T waves and reciprocal change in AVL. For inferior infarction due to acute coronary occlusion the reciprocal change in AVL is much more reliable than the “indicative” inferior ST elevations according to Dr. Smith, whose research findings on this topic are the basis for a manuscript in preparation.

The ECG remains a valuable tool for the diagnosis of acute ischemic syndromes. But for the diagnosis of acute coronary occlusion the electrocardiographic findings go beyond the ST segment. I agree with Dr. Phibbs that we need to replace STEMI with a better designation for acute coronary occlusion.

Tall R wave in V1: an exercise in differential diagnosis

For some electrocardiographic findings the diagnosis is apparent at a glance. It can't be anything else. For other presentations there is a list of causes and diagnosis based on your first hunch may be misleading. This is true of the tall R in V1 (usually seen as R wave amplitude larger than the S wave amplitude) where, if you jump to the more obvious causes such as RVH or posterior infarction and don't make a list you are likely to overlook less commonly appreciated entities such as hypertrophic cardiomyopathy and WPW. The pattern is nicely explained, along with a discussion of the concept of differential diagnosis (listing the causes) at the ECG Interpretation blog.

I cited an article on this topic awhile back and came up with a slightly different list but you get the idea.

Saturday, March 15, 2014

Systematic review of the effects of EMRs

This review in the Annals of Internal Medicine looked at decision support and CPOE.

From the review:

Conclusion: Strong evidence supports the use of clinical decision support and computerized provider order entry. However, insufficient reporting of implementation and context of use makes it impossible to determine why some health IT implementations are successful and others are not. The most important improvement that can be made in health IT evaluations is increased reporting of the effects of implementation and context.

However, the report addressed process metrics rather than meaningful outcomes.

The choosing wisely list in nephrology

Here are a couple of points from the list I found interesting:
Avoid nonsteroidal anti-inflammatory drugs (NSAIDS) in individuals with hypertension or heart failure or CKD of all causes, including diabetes.
The use of NSAIDS, including cyclo-oxygenase type 2 (COX-2) inhibitors, for the pharmacological treatment of musculoskeletal pain can elevate blood pressure, make antihypertensive drugs less effective, cause fluid retention and worsen kidney function in these individuals. Other agents such as acetaminophen, tramadol or short-term use of narcotic analgesics may be safer than and as effective as NSAIDs.

Don’t place peripherally inserted central catheters (PICC) in stage III–V CKD patients without consulting nephrology.
Venous preservation is critical for stage III–V CKD patients. Arteriovenous fistulas (AVF) are the best hemodialysis access, with fewer complications and lower patient mortality, versus grafts or catheters. Excessive venous puncture damages veins, destroying potential AVF sites. PICC lines and subclavian vein puncture can cause venous thrombosis and central vein stenosis. Early nephrology consultation increases AVF use at hemodialysis initiation and may avoid unnecessary PICC lines or central/peripheral vein puncture.

Friday, March 14, 2014

MDMA (ecstasy): what the hospitalist needs to know

Here's a nice run down at Clinical Correlations.

Another hyperkalemia ECG

With practice the likely diagnosis on tracings like this will come to mind in literally seconds.

Can some COPD exacerbations be managed without antibiotics? How can we predict?

According to this study sputum change and an elevated CRP were predictors of failure without antibiotics. Keep in mind the findings apply to ambulatory patients. It is generally recommended that patients hospitalized with COPD exacerbation receive antibiotics.

Thursday, March 13, 2014


Flash cards and learning tools on just about everything.

Hyperchloremia and outcomes after noncardiac surgery

From a recent study:

BACKGROUND: The use of normal saline is associated with hyperchloremic metabolic acidosis...
RESULTS: The dataset consisted of 22,851 surgical patients with normal preoperative serum chloride concentration and renal function..Of the 4955 patients with hyperchloremia after surgery, 4266 (85%) patients were matched to patients who had normal serum chloride levels after surgery. These 2 groups were well balanced with respect to all variables collected. The hyperchloremic group was at increased risk of mortality at 30 days postoperatively (3.0% vs 1.9%; odds ratio = 1.58; 95% confidence interval, 1.25–1.98) (relative risk 1.6 or risk increase of 1.1%) and had a longer hospital stay (7.0 days [interquartile range 4.1–12.3] compared with 6.3 [interquartile range 4.0–11.3]) than patients with normal postoperative serum chloride levels. Patients with postoperative hyperchloremia were more likely to have postoperative renal dysfunction. Using all preoperative variables and measured outcome variables in a logistic regression analysis, hyperchloremia remained an independent predictor of 30-day mortality with an odds ratio of 2.05 (95% confidence interval, 1.62–2.59).

Maybe the surgeons have been right all along.

As the blogger at RESUS.ME put it:

Here’s something to add to the pile of data cautioning us to think before we acidify patients with saline.

Overdiagnosis of pneumonia

The overdiagnosis of pneumonia, which is becoming increasingly recognized, was the topic of a recent article in the Cleveland Clinic Journal of Medicine. As is apparent from the review the reasons for this trend in overdiagnosis are multiple and complex. One factor, I believe, is time pressure. This pressure comes in many forms including throughput initiatives to reduce ER crowding, time based performance measures, pressure to identify a “principal problem” on admission and incentives to place hospitalized patients on care pathways. Vague problem statements like “pulmonary opacity” and “breathing difficulty”, while often more honestly and accurately reflective of problem resolution at a given time, are frowned upon in today's regulatory and performance environment. “Systems improvements”thus lead to diagnostic inaccuracy.

Another problem pointed out in the article is the disconnect between application of a simple diagnostic label and discrimination between patients who will and will not benefit from antibiotics. As the article points out:

The central problem with pneumonia, as with many long-recognized clinical conditions, is that the diagnosis is separated from the treatment. In other words, although physicians are confident that antibiotics benefit patients who have what Sir William Osler would have called pneumonia (elevated white blood cell count, fever, cough, dyspnea, pleurisy, egophany, lobular infiltrate), we don’t know whether the treatment benefits patients whose pneumonia would have been unrecognizable decades ago (with cough, low-grade fever, and infiltrate on CT alone). Improvements in imaging may exacerbate the problem. In this sense, pneumonia exists on a spectrum, as do many medical diagnoses. Not all cases are equally severe, and some may not deserve to be labeled as pneumonia.

It goes on to say that there is equipoise for the performance of clinical trials to determine whether antibiotics can be withheld in dubious cases.

Wednesday, March 12, 2014

Perioperative insulin management

Here is a review from CCJM. The main point of the review is that it is best to continue at least some of the patient's basal insulin, modified if necessary according to the circumstances, through the perioperative period.  

The interpretation of troponin elevations and the definitions and classification of MI

I have posted updates and reviews on this topic before. The classification (types 1-5) has undergone some tweaks in the recent past. The topic was updated in a recent issue of CCJM. An expert consensus document on troponin elevations from ACCF can be accessed here. Here is a post linking to a review on the significance of troponin elevations in heart failure.

Whipple's disease review

Published in Postgraduate Medical Journal.

Via Hospital Medicine Virtual Journal Club.

Monday, March 10, 2014


Usually thought to be associated with thrombocytosis, there are other causes as well. Here is a summary from Nephron Power.

Results of three new sepsis trials to be announced soon

These trials re-evaluated early goal directed therapy as well as some of its individual components. Results should be announced very soon. More at RESUS.ME

Pain as the fifth vital sign: faulty ideas exposed

“Pain is the fifth vital sign” became the slogan of a movement that was launched about a decade and a half ago. It was a campaign to educate us health care professionals, who were not doing a very good job of treating pain. The movement was overhyped and unintended consequences were realized over time. Now at long last some of the original proponents of the campaign have admitted that they were wrong. It's the topic of a post at The Poison Review which references this article from the Wall Street Journal. The revelations in the WSJ piece should come as no shock to those who have been practicing in the trenches for the past few years, who know the negative consequences all too well.

The movement was in high gear when I became a hospitalist in 1999. It was apparent to me early on that this was pure dogma being shoved down doctors' throats. I felt a little intimidated in calling out the pseudoscience at the time, though, because as the WSJ article notes, adherents to the movement were driven by an almost religious fervor:

Steven Passik, a psychologist who once worked closely with Dr. Portenoy and describes him as his mentor, says their message wasn't based on scientific evidence so much as a zeal to improve patients' lives. "It had all the makings of a religious movement at the time," he says. "It had that kind of a spirit to it."

Back then if you challenged the groupthink tempers were likely to flare.

What still baffles me is why so many doctors accepted the biggest and most obvious load of nonsense, the idea that pain, long established in clinical medicine as a symptom, could suddenly become a sign. Even The Joint Commission and my own professional organization, the Society of Hospital Medicine (then known as NAIP) were serving the Kool-aid.

Other nutty ideas were promulgated:

Opiates are safe.
Uh huh. How's that working these days?

Doctors' concerns about opiate addiction are overstated; true opiate addiction is in fact rare.
Ten years or so ago if you pointed out narcotic seeking behavior you would be told, dismissively, that this was not addiction but pseudoaddiction. Pseudoaddiction, they said, was merely behavior exhibited by a patient whose pain was uncontrolled. Put another way, if your patient engaged in seeking behavior it meant you were not doing your job.

Pain can be measured.
Translate: pain is not subjective. Pain does not have emotional components. How many people knew that was a crock but were too intimidated to call it out?

No one should have to experience pain. Pain can be made to disappear from the planet.
Really? How about all those patients on chronic narcotics who have had their doses increased, time and time again, to ridiculously high levels, and are still suffering?

As pain retires from its position as the fifth vital sign the pendulum will swing. Likely it will swing too far. Draconian medical board policies with their unintended consequences lie ahead. NSAID use is likely to increase, despite the cardiovascular risks which for many patients are greater than the hazards of opiates.

Be that as it may it's time to stop the madness. Twenty years ago the field of pain management was in need of improvement. But the improvement needed to be informed by science, not dogma.

Sunday, March 09, 2014

Overview of influenza activity in the US, 2013-14

From MMWR, HT to Hospital Medicine Virtual Journal Club.

The rise and fall of the PA catheter

From an article in Annals of Intensive Care:

The birth of the intermittent injectate-based conventional pulmonary artery catheter (fondly nicknamed PAC) was proudly announced in the New England Journal of Medicine in 1970 by his parents HJ Swan and William Ganz. PAC grew rapidly, reaching manhood in 1986 where, in the US, he was shown to influence the management of over 40% of all ICU patients. His reputation, however, was tarnished in 1996 when Connors and colleagues suggested that he harmed patients. This was followed by randomized controlled trials demonstrating he was of little use…
While a handful of die-hard followers continued to promote his mission, the last few years of his existence were spent as a castaway until his death in 2013. His cousin (the continuous cardiac output PAC) continues to eke a living mostly in cardiac surgery patients who need central access anyway…
In the 1980s 20% to 40% of seriously ill patients who were hospitalized were reported to undergo pulmonary artery catheterization [4]. This phenomenon occurred despite that fact that the safety, accuracy, and benefit of the device had never been established.

This has a familiar ring. It’s where we are today with techniques such as point of care ultrasound and pulse contour analysis. I think the problem with the PA cath was a lack of skill applied to interopretation of the data derived from the catheter. There is no reason to think PCWP and all the other measurements weren’t valid surrogates. Applying the measurements to clinical decision making is another matter. The use of POC echo and application of results to patient care is even more demanding. The new techniques are rapidly gaining in popularity but have not been validated in high level studies.

In the review some problems inherent in the technology itself, particularly in the measurement of cardiac output, are cited.

Rapid response teams and transition to end of life care

The data on RRTs are mixed but on the whole do not suggest meaningful impact on important outcomes. Some studies, however, suggest that RRTs decrease in hospital codes. One reason may be that RRTs transition many patients to end of life care.

Friday, March 07, 2014

Medical Criteria

A quick reference site with classifications, criteria, guideline summaries and more.

Procalcitonin as a marker for septic arthritis and osteomyelitis

From a recent paper:

Patients of all age groups (n = 82) with suspected Acute Osteomyelitis and Septic Arthritis were prospectively included in this study. All patients were subjected to TC, CRP, PCT, IgM Dengue, IgM Chikungunya, pus and blood culture and sensitivity. At the end of the study, patients were classified into 3 groups: Group 1 = Confirmed Pyogenic (n = 27); Group 2 = Presumed Pyogenic (n = 21); Group 3 = Non – infective inflammatory (n = 34).
Group 1 has higher mean PCT levels than Group 2 and 3 (p less than 0.05). PCT, at 0.4 ng/ml, was 85.2% sensitive and 87.3% specific in diagnosing Septic Arthritis and Acute Osteomyelitis. In comparison, PCT at conventional cut – off of 0.5 ng/ml is 66.7% sensitive and 91% specific.
Serum Procalcitonin, at a cut – off of 0.4 ng/ml, is a sensitive and specific marker in the diagnosis of Septic Arthritis and Acute Osteomyelitis.

Via Hospital Medicine Virtual Journal Club.

The impact of externally applied “quality” measures

Note the quotation marks. The various performance measures that pass for quality in today's health policy groupthink have little to do with real quality. I've been saying that for several years, pointing to unintended consequences and lack of demonstrable benefit.

This was the topic of a recent review in the open access Journal of the American Heart Association. If focuses on cardiovascular disease but has a lot to say about the performance movement in general. It traces the history of performance metrics and their various iterations (public reporting, P4P, value based purchasing, etc.) and asks whether they have had any meaningful impact. The short answer is no.

Wednesday, March 05, 2014

Hepatic encephalopathy: what the hospitalist needs to know

Free full text review from Mayo Clinic Proceedings.

Antisynthetase syndrome

Here is a free full text review.

Inflammatory myopathies (polymyositis and dermatomysotis) occur in distinct subsets based on antibody profiles. Antisynthetase syndrome is one of them.

Anti Jo-1 is by far the most common antisynthetase antibody but there are others.

Antisynthetase syndrome has a distinct clinical profile based on extramuscular manifestations.

Extramuscular manifestations (e.g. ILD, polyarthritis) may dominate the clinical picture or be the initial manifestation.

ILD is the most important extramuscular manifestation. Its histology (NIP) differs from that of IPF and is somewhat responsive to steroids and other immunomodulatory agents.

Pulmonary hypertension may be out of proportion to parenchymal lung involvement.

Donald Berwick running for governor of Massachusetts

His recent interview at Medscape with Editor-in-Chief Eric J. Topol, MD was not exactly hardball. I ranted extensively about Berwick a few years ago, around the time of his recess appointment as head of CMS, mainly concerning his duplicitous statements about health policy. He is a man of contradictions. I have long struggled to find clarity in his positions. The Medscape interview did not help. It was a great opportunity to press Berwick to resolve his inconsistencies but Topol did not take advantage. Let's take a look at some of the double talk.

Double talk on rationing

Berwick has expressed views favorable to health care rationing. In the health care policy debates of a few years ago he said:

“the decision is not whether or not we will ration care, the decision is whether we will ration with our eyes open.”

But when Topol asked him about his views on rationing:

Dr. Berwick: It was ridiculous. Rationed care? I'm a pediatrician, for Pete's sake. I've gone to the mat over and over again for my patients.

For more on Berwick's rationing flip-flops see this article by Wesley Smith.

Double talk on waste, efficiency and evidence based medicine

From the Medscape interview:

We've built this kind of volume-based, do-more-and-more-stuff healthcare industry, and I've very systematically looked for years at the levels of overuse... We now have the data that 30%-40% of care is just wasted...
We just go back to the question, "What will help the patient?" And if there is something we're doing that doesn't help the patient that means we can stop doing it. It's the intellectual route out.

But then there was this from a few years ago (hardly the intellectual route out):

For example, “leaving choice ultimately up to the patient and family means that evidence-based medicine may sometimes take a back seat,” Berwick says. “One e-mail correspondent asked me, ‘Should patient “wants” override professional judgment about whether an MRI is needed?’ My answer is, basically, ‘Yes.’ On the whole, I prefer that we take the risk of overuse along with the burden of giving real meaning to the phrase “a fully informed patient.”

Straight out of Dr. Berwick's mouth. Both sides of his mouth.

If Berwick were still just brainstorming at IHI this might be humorous. But he is seeking public office and wants to help shape policy. I'm a little concerned.

Inscrutably, Berwick seems to vacillate between the incompatible extremes of central control and radical consumerism. Orac, the blogger at Respectful Insolence, has commented on this before:

Finally, unfortunately Dr. Berwick’s philosophy is custom-made to be an enabler of the very woo that I so frequently rail against on this blog. After all, if patient empowerment and “patient-centeredness” trump science- and evidence-based medicine (except in “rare” circumstances that Dr. Berwick declines to define), then there really is no reason not to give the people what they want when they want it, all the time, so to speak. They want woo? Give it to them! They don’t want to vaccinate? No problem...
Sadly, his idealism is not grounded in the real world and, worse, it does not place science- and evidence-based medicine on even close to the same level as it does to turning patients into “consumers” and physicians into people who cater to those consumers no matter what.

If Berwick is so radically patient centered why, when he was head of CMS, were the Republicans so afraid he would favor government intrusion and rationing? It's because he has talked out of both sides of his mouth on this issue so many times, not only in the examples above but in many other speeches and writings including, for example, his well known remarks on the British National Health Service.

Radical consumerism and central control are at opposite ends of a spectrum and we may never know where he really stands. One thing is certain though. Neither is compatible with evidence based medicine.