The Healthcare Summit

Here's the skinny from Medscape.

Anyone expecting some glorious "eureka!" moment at the White House healthcare summit today that would forge a compromise on contentious reform proposals between Democrats and Republicans has to be disappointed...

Was anything substantive decided at the summit? Obama and Democratic leaders strongly indicated that they may resort to the parliamentary procedure known as reconciliation if that is what it takes to get a bill passed. This would mean that the legislation could pass with a simple majority in the Senate, rather than the usual 60 votes needed to end a filibuster. Republicans characterize the tactic as pushing through the bill on a strictly party-line basis.

The public opposes using reconciliation by 52% to 39%, according to a USA Today/Gallup poll...

What's next? Democrats could try to push through their bills through the reconciliation method by a party-line vote, although they acknowledge that is a high-risk strategy, if even possible.

When hospitalist programs run on fumes

---it's diminishing returns for hospitals.

I ran across this post at Better Health by Dr. Wes via a tweet at Med Rants to a post at Kevin MD.

Dr. Wes raised a point which is under discussed and difficult to quantify but well known by those in the trenches of hospital care: every hospitalist program has an optimal patient load above which its economic value to the hospital wanes.

It appears hospitalist services are increasingly finding themselves overwhelmed with admissions and the promise of a reasonable lifestyle can be assured by either limiting the number of patients admitted to each hospitalist or hiring more of them. But new hires are becoming tougher to justify in this “do more with less” economic time in medicine. As a result, it appears existing hospitalists are quickly finding they’ve hit the peak speed of their clinical-care gerbil wheels.

Hospitals may think they're saving money by under staffing programs. But good resource utilization takes time, and under staffing may result in decreased efficiency.

Avandia and disclosure

In reference to yesterday's post there's an interesting thread on disclosure, both as it relates to Dr. Mintz's handling of his postings on Avandia and to disclosure in general, over at Retired Doc's Thoughts. Most of the public discussion on disclosure consists of posturing, platitudes and name calling. What's needed is frank, respectful and open treatment of the issue. The thread over at Retired Doc's is a good start. Dr. Poses, Dr. Mintz and I have already weighed in and I hope more readers will.

Revisiting Avandia and personal attacks against Dr. Mintz

Almost 3 years after the safety hoopla raised by Nissen's NEJM meta-analysis the issue has resurfaced. It seems a report on the Avandia controversy by Senators Grassley and Baucus was recently made public and covered by the New York Times. The Times piece was distorted and inaccurate (maybe I'll write a separate post about that later) and uncovered nothing new.

That prompted Dr. Mintz, who has written a great deal about it before, to reassess the controversy in his blog and as a guest blogger over at the Forbes health blog, The Science Business. He reviewed the evidence and pointed out that there's nothing new in the discussion concerning the risks and benefits of Avandia. Then Retired Doc, citing Mintz's analysis, asked readers why we're stirring the pot again. He got one response to his question and that was from Dr. Roy Poses at Health Care Renewal:

Perhaps Dr Mintz may have been influenced by his financial ties to GSK (not disclosed in his blog post that you linked to, but now mentioned in the Forbes Science Business blog version of it, see here:
http://blogs.forbes.com/sciencebiz/2010/02/another-unwarranted-avandia-scare/).

The undisclosed conflicts were first noted in the PharmaLot blog, see here:
http://www.pharmalot.com/2010/02/a-forbes-guest-blogger-and-his-pharma-ties/)

Dr. Poses's response is troubling in a way that is typical when issues of science are thrown into the arena of popular debate. At best it confuses things by conflating questions about Avandia's safety with those concerning the ethics of Dr. Mintz. Or, worse, it may represent the intellectually lazy approach of applying a simple litmus test (Pharma ties) to summarily reject Dr. Mintz's analysis. That sort of ad hominem attack may rarely be justified if ones opponent makes baseless claims without pointing to primary sources of evidence. While Dr. Mintz's analysis is not a systematic review it did appeal to primary sources. There is more than sufficient warrant to accept or reject Dr. Mintz's argument on its own merits. Personal attacks in this case are inappropriate and unnecessary.

Meanwhile over at Pharmalot (linked above by Dr. Poses) the whole thing morphed into a full-scale attack on Dr. Mintz---not so much in the body of Ed Silverman's post, but in the comments. And, to be fair to Silverman, he wrote with a singular focus and made no pretense of evaluating Avandia.

For those readers who take me at my word that I have no Pharma ties (not all readers do!) here's my skinny on type 2 diabetes treatments starting with the categories associated with greatest harm down to the ones with greatest benefit:

Known macrovascular harm
Sulfonylureas

Probable macrovascular harm (Dose and usage pattern related)
Insulin

Question raised about macrovascular harm without convincing evidence
Rosiglitazone (Avandia)

Preliminary evidence of macrovascular benefit, in need of confirmatory data
Acarbose

Probable macrovascular benefit
Pioglitazone (Actose)

Definite macrovascular benefit
Metformin
Diet, exercise

No evidence to guide clinicians as to macrovascular benefit, harm or neutral effect
All other agents!

Note that this listing is not a treatment algorithm (you can find that here). It is only concerned with macrovascular effects of diabetes treatments, because that's the focus of the current controversy. It ignores other benefits of glycemic control such as microvascular benefit.

On a related note, another area of obfuscation by the popular media and even some physician writers (who should know better) is the confusion of macrovascular harm with the heart failure issue. Although TZDs cause fluid retention and there are heart failure concerns the evidence is now clear that it is a peripheral effect with no direct adverse effect on the heart. This was well illustrated in a study which showed that although Avandia was associated with increased need for treatment of edema there was no finding of adverse cardiac effect as evidenced by lack of change in cardiac ejection fraction.

What do hospitalists need to know about stroke care?

...it is important now that the practicing hospitalist is facile in the treatment of patients with cerebrovascular disease-and it is likely to become progressively more important over time.

That's from the opening of a two part review on stroke in the Journal of Hospital Medicine.

Part 1. Part 2.

This two part series addresses issues in stroke care that bedevil hospitalists. I would suspect that, nation wide, as it is in many areas of medicine, best practice adherence in stroke care is low. This review should help.

First, the astute clinician is wary of stroke mimics. But when stroke is the working diagnosis an NIH stroke score should be done in the early moments in the ER (resource here).

In cases of intracerebral hemorrhage, although surgical indications are shrinking, patients may benefit from aggressive medical care and the review authors warn against an inappropriate rush to a DNR decision, citing literature that such a decision may be an independent risk factor for poor outcome (self-fulfilling prophecy).

In their discussion of tPA the authors mention the SITS-MOST study, a large phase IV study confirming that tPA performs as well as it did in the NINDS trial. The importance of informed consent for this risky therapy is emphasized (although written consent is not a firm requirement) and a discussion on administration of tPA when such consent is unobtainable is provided. Data in support of the new 4.5 hour time window are discussed although the authors come short of making a recommendation.

For patients who present too late for tPA but inside of 8 hours catheter based treatments (extraction or intra-arterial thrombolysis) are possible. Actually the most recent AHA/ASA guidelines only provide for a 6 hour window and read thusly:

Intra-arterial thrombolysis is an option for treatment of selected patients who have major stroke of <6>

If this type of treatment is “on the table” then CT angiography would be part of the stat imaging in the ER to identify or rule out a large vessel occlusion amenable to catheter based therapy. For this to go smoothly the interventional radiologist (either at your facility or the referral center) would need to be involved early in the ER planning to discuss timing, anticipated total dye loads, etc.

For patients presenting past 8 hours anti-platelet therapy is the only anti-thrombotic option early on. Aspirin should be given early. It is the only anti-platelet agent that has been studied for acute stroke. For patients already taking aspirin there is little to guide clinicians. That issue is discussed in detail in the text of the review.

Systemic anticoagulation is not recommended for any situation except cerebral venous sinus thrombosis, although in a few other situations systemic heparinization is considered. From part 1 of the review:

...a number of exceptions exist, based more on tradition and theory than on evidence. These exceptions, for which an IV heparin drip will at times still be considered, include acute ischemic stroke due to dissection of the carotid or vertebral arteries, cardioembolic stroke with fresh clot seen on echocardiogram (ECHO), and a clinically progressive syndrome suggestive of basilar artery occlusion...

Long term systemic anticoagulation with warfarin is indicated for patients with atrial fibrillation, but not with systemic heparinization in the acute phase. Nuances are discussed in the text of the review and in the guidelines.

Basilar artery occlusion syndrome and malignant middle cerebral artery occlusion syndrome are special situations which may warrant intra-arterial intervention and decompression craniotomy, respectively.

Discussions on general supportive care are included. A couple of points from the guidelines bear mention. The conservative threshold for acute hypertension treatment is well known, but absent such extreme blood pressure elevations what should be done with the patient's home blood pressure medication? The guidelines suggest starting them approximately 24 hours post stroke onset.

Glycemic control in hospitalized patients is controversial right now. In stroke, hyperglycemia is known to be associated with worse outcomes, but neither the target nor the threshold for intervention is precisely known. Accordingly, the guideline statement is vague:

The minimum threshold described in previous statements likely was too high, and lower serum glucose concentrations (possibly greater than 140 to 185 mg/dL) probably should trigger administration of insulin, similar to the procedure in other acute situations accompanied by hyperglycemia (Class IIa, Level of Evidence C).

Indications for carotid endarterectomy, arterial dissection and PFOV are discussed but a discussion of other indications for warfarin and for TEE (based on the TOAST classification) were conspicuously absent.

Interpreting HIT antibody results

When evaluating patients for heparin induced thrombocytopenia (HIT) we commonly order two tests: antibodies to heparin-platelet factor 4 complex and a serotonin release assay (SRA). Both tests are sensitive but the antibodies are nonspecific. Invariably the antibodies come back first. If they come back positive you're faced with a dilemma: should you go ahead and treat or wait for the more specific SRA result? According to a study in the Journal of Thrombosis and Haemostasis the magnitude of positivity of the antibody result, expressed as optical density, correlates well with strong SRA positivity, thus predicting true HIT:

Results: For patient sera investigated for HIT antibodies, a weak-positive result (0.40–less than 1.00 OD units) in either EIA indicated a low probability (less than or epual to 5%) of a strong-positive SRA; the risk increased to approximately 90% with an OD greater than or equal to 2.00 units. Quantifying the EIA–SRA relationship for 1553 referred patient sera, we found that for every increase of 0.50 OD units in the EIA–IgG, the risk of a strong-positive SRA result increased by OR = 6.39 [95% confidence interval (CI), 5.13, 7.95; P less than 0.0001]. For every increase of 1.00 OD units in the EIA–IgG, the risk increased by OR = 40.81 (95% CI, 26.35, 63.20; P less than 0.0001). Conclusions: The probability of HIT antibodies (strong-positive SRA result) inferred by a positive PF4-dependent EIA varies considerably in relation to the magnitude of the EIA result, expressed as OD values. In our laboratory, the probability of HIT antibodies being present reached greater than or equal to 50% only when the OD level was greater than or equal to 1.40units.

In the concluding paragraph the term “HIT antibodies” means truly functional antibodies, thus predictive of HIT.

Glycemic control in cardiac surgery patients

Recent evidence has been disappointing concerning tight glycemic control in the general critically ill population, and the suggested threshold for intervention is now 180mg/dl. Different considerations may apply in special populations, and for cardiac surgery patients the target is unclear. A new literature review of glycemic control post cardiac surgery, published in the Baylor University Medical Center Proceedings, concluded thusly:

Based on recent information, the new Society of Thoracic Surgeons guidelines and the AACE/ADA consensus statement seem appropriate and allay the concern for hypoglycemia with the new recommended range of less than180 and 140 to 180 mg/dL. More studies analyzing blood glucose target ranges seem necessary to further recommend an intensive blood glucose goal range of 80 to 110 mg/dL, especially in the cardiac surgery population. Even throughout the Van Den Berghe trials, the average blood sugar of patients in the intensive control arm was approximately 140 mg/dL. Thus, aiming for blood glucose levels around 140 mg/dL appears reasonable. Mortality and morbidity benefits are seen with overall control of hyperglycemia; however, the exact range is still not clearly defined, as previously thought.

More free educational and entertainment resources

H/T to Clinical Cases and Images for pointing me to this repository. Open course-ware, free movies, free books, you name it.

How many consumers are willing to pay for Internet content?

Most, by far, are going for the free stuff.

H/T to STLMedia.

Some hospitalists are reducing readmissions

---by not being hospitalists anymore. Disturbing.

There's an interesting discussion on the use of check lists

---over at DB's Medical Rants.

On a hectic and busy medical service the checklist can be an important housekeeping tool for the tired, distracted and constantly interrupted hospitalist. I'm trying to develop my own, and these are the items I'm considering for inclusion:

Have today's labs been addressed and appropriate action taken?
Is chemical VTE prophylaxis being given where indicated?
Is discharge planning underway (including order entry for case management consultation and entry of the anticipated discharge date)?
In patients on steroids for asthma or AECOPD is tapering proceeding apace?
Is it time to modify antibiotic orders based on culture results, clinical status or duration of therapy?
Are medications properly reconciled, i.e. are home medications being held that should be and are those being continued (statins, beta blockers) that should be?
Is the patient's activity order appropriate and has PT been ordered if needed?

This list may not be appropriate for everyone, but reflects things that don't have reminders built in at my institution.

Related post at Wachters' World.

Here's one to add

---to Joint Commission's list of unapproved abbreviations.

More on Emily Rosa and Therapeutic Touch

Out of the mouth of a babe.



Background on Emily Rosa here.

Remember the girl who debunked therapeutic touch in JAMA?

Background:

Conclusions.—Twenty-one experienced TT practitioners were unable to detect the investigator's "energy field." Their failure to substantiate TT's most fundamental claim is unrefuted evidence that the claims of TT are groundless and that further professional use is unjustified.

Torsade de Pointes in hospitalized patients: prevention is key

AHA/ACCF has issued a new scientific statement on this topic.

Here are a few background comments and points I found interesting:

Prolongation and distortion of repolarization is the defining characteristic of TdP, more so than the twisting of the QRS complex about the isoelectric point. The latter feature may not be apparent in a given lead.

Although the traditional assessment for prolongation of repolarization is the measurement of the QT interval, that assessment is simplistic and fraught with error due to controversy about normal limits and rate corrections, poor T wave demarcation, poor distinction between the T wave and the U wave and cycle length dependency. More subjective features including pause dependency, particularly in short-long cycle sequences, splayed T waves (or TU fusion) and macroscopic T wave alternans may be more important.

Among drugs that prolong the QT interval amiodarone has a uniquely low risk of producing TdP because the prolongation of repolarization it induces is homogeneous. Heterogeneous repolarization abnormality is the more likely substrate for TdP.

The list of QT prolonging drugs is evolving. As new ones are added older ones (quinidine, erythromycin, droperidol (inapsine) are disappearing from hospital wards. Aside from anti-arrhythmic drugs methadone and haloperidol have the highest profile right now in hospitalized patients.

The risk of drug induced TdP, even though idiosyncratic, is generally dose related. A notable exception to the usual dose relationship is quinidine, because at higher doses its sodium channel blocking effect has a counterbalancing effect on action potential duration.

The idiosyncratic susceptibility to drug induced TdP appears to be based on a forme fruste of LQTS.

A repository of QT prolonging drugs every hospitalist should have bookmarked is the Arizona CERT.

A multi-hit model for incident TdP is emerging where two or more risk factors conspire (e.g. genetic susceptibility + drug#1 + drug#2 + hypokalemia=TdP).

Among the recommendations in the scientific statement:

Continuous QTc monitoring is appropriate for drugs deemed most at risk to cause not only QT prolongation but also TdP. After administration of an at-risk drug, if the Qtc exceeds 500 ms or there has been an increase of at least 60 ms compared with the predrug baseline value, especially when accompanied by other ECG signs of impending TdP, prompt action is indicated. Appropriate actions include alternative pharmacotherapy; assessment of potentially aggravating drug-drug interactions, bradyarrhythmias, or electrolyte abnormalities; and the ready availability of an external defibrillator. Patients should not be transported from the unit for diagnostic or therapeutic procedures, and they should be in a unit with the highest possible ECG monitoring surveillance. ..

When discharged, the patient should be educated about avoiding the culprit drug, other related drugs, and potential drug-drug interactions. A list of possible QT-prolonging drugs (available at www.qtdrugs.org) should be provided to the patient and appro-priate documentation made in the medical record. If drug- induced TdP has occurred, a careful review of the patient’s personal and family history should be obtained, because it may be the sentinel event heralding the presence of congenital LQTS. If a personal/family history of unexplained syncope or premature sudden death emerges, a 12-lead ECG should be recommended for all first-degree relatives, and consideration should be given to clinically available genetic testing for congenital LQTS.

Guidelines and principles for interaction with hospitalists

Although this was released by AAFP for its members it has the imprimatur of AAFP as a guideline document and so would apply to all specialties who participate in the hospitalist model.

I thought this was of interest:

If patients present to the emergency department (ED) and the ED physician assesses them, the ED physician should then contact the patient's family physician to determine if admission is necessary or if close follow up or outpatient work up is more appropriate.

If admission is necessary, the family physician should communicate information on pre-hospital treatment, work up, co-morbidities and ongoing specialty consultations, along with family and social concerns, advanced directives, etc., to the inpatient care physician who is assuming management of the patient's care.

In other words not just the hospitalist but also other providers bear some responsibility in the transfer of information.

And this says a lot:

The inpatient care physician should be readily available to discuss the patient's medical problems and hospital course with the family and should provide timely updates to the family physician designated by the patient. Communication with the family physician is extremely important at the time of any changes in the patient's status, complications or new diagnoses (e.g. cancer).

The inpatient care physician should communicate the treatment plan and follow up recommendations to the patient's family physician or the covering physician on the day of discharge. This may be best accomplished by having the discharge summary dictated and faxed to the family physician.

When family physicians refer their hospitalized patients to the care of an inpatient physician, the AAFP strongly encourages them to maintain ongoing communication with the patients, their families, and the inpatient care physician throughout the hospitalization.

So communication between hospitalist and PCP is a two way street, a push-pull mechanism. And, according to this guideline, the responsibility for patient satisfaction rests in part with the PCP. When PCPs maintain communication with hospitalized patients and their families it builds confidence and defuses a lot of issues.

Free fluid, electrolyte and acid-base e-book

Along with other e-books. Via Clinical Cases and Images.

In nosocomial MRSA pneumonia

---adding rifampin to vancomycin may help.

Liver disease and perioperative risk

From the Perioperative Medicine Summit.

SIRS assessment to predict severity of acute pancreatitis

Traditional assessment tools for severity of acute pancreatitis require data collection over 24-48 hours. I this new study SIRS criteria enabled assessment with high sensitivity and specificity at day 1.