CMS ED Quality Measures Are Coming

When the government is the largest healthcare payor, you pay attention when they start measuring “quality” – because it’s usually not long after that payments are tied to “quality”.

This is an Annals study looking at the pilot reporting program from CMS, which includes seven metrics that hospitals are going to have report in the next two years.  These metrics are:
 – Throughput time for admitted patients.
 – Throughput time for discharged patients.
 – Admit order to bed placement for admitted patients.
 – Time to pain management for long bone fractures (discharged and admitted)
 – Time to chest x-ray after order placed (discharged and admitted)

I love the pain management metric.  The literature that supports how poorly ED physicians manage pain is extensive.  Not a day goes by where have a resident trying to give a 2 milligram dose of morphine to treat acute pain.  The other metrics – well, so, faster is more and more is better, so therefore more, faster is “quality”, right?  Well, there are some studies that show improved outcomes when patients reach the floor more rapidly, so, perhaps that’s what they’re getting at.  I don’t know if we’ll ever really know how improving these measures affects quality, because there are so many other confounding variables affecting these issues.

What is good about these metrics is that it should make a lot of EDs re-examine their processes and see how they can maximize the resources they have.  But, after the low-hanging fruit, you run up against issues of physical and financial resources – many of which are hospital-wide issues.  It will be interesting to see how our workplace changes in response to this.  Unsurprisingly, academic centers and busy EDs had the worst throughput statistics; not sure about magical solutions there.

“A Field-Test of Time-Based Emergency Department Quality Measures.”
www.ncbi.nlm.nih.gov/pubmed/21868129

How Do We Miss Aortic Dissection?

This is a retrospective look at 109 cases eventually diagnosed with aortic dissection – with a focus on the differentiating clinical features present in the 17 cases where the diagnosis was initially missed in the Emergency Department.

Confounding clinical attributes that were associated with a missed diagnosis were walk-in vs. ambulance arrival and presence of anterior chest pain.  Chest x-rays lacking a wide mediastinum were nonsignificantly associated with missed aortic dissection, and with only 55% of their diagnosis cohort having a wide mediastinum vs. 25% of their misdiagnosis cohort.  Interestingly, over 75% of each group received a d-Dimer and they were all positive in the misdiagnosis group as well as all but one in the diagnosis group.  It would seem that they order so many d-Dimers that they’ve become fatigued to its clinical usefulness due to its poor specificity.

The good news is the patients who were initially misdiagnosed had similar mortality (18% vs. 15%) – despite 7 of the 17 being treated with antithrombotic agents.  Most of the missed diagnoses were classified as undifferentiated possible ischemic chest pain, but two were diagnosed with renal colic.

As always, the main problem with missed-diagnosis literature is there’s no guarantee the authors didn’t miss another set of cases themselves.

“Factors leading to failure to diagnose acute aortic dissection in the emergency room.”
www.ncbi.nlm.nih.gov/pubmed/21889877

Ondansetron, Just Like Droperidol

Droperidol used to be one of the most widely used anti-nausea medications, particularly in the peri-operative period.  Now, none of my residents are familiar with it because it’s rarely used since the FDA gave it a black box warning for its QT-prolonging effects.  We have largely and copiously replaced it with ondansetron, the supposedly safe alternative.


Now, the FDA is asking GlaxoSmithKline to go back and look at the safety profile for ondansetron…due to QT-prolonging effects: http://reut.rs/pDq6Yw  They are already changing the labels to reflect cardiovascular risk in the meantime.

It should be interesting to see the results.  It is fairly clear that ondansetron prolongs the QT interval probably nearly, but not quite, as much as droperidol.  The droperidol black box was based on cardiovascular events including only a mere 10 patients receiving doses in the therapeutic range of 0.625mg to 1.25mg, and those events had multiple confounding factors or drug co-administrations.  It would not surprise me if ample, if equally flimsy, evidence exists implicating ondansetron as well.

“Food and drug administration black box warning on the perioperative use of droperidol: a review of the cases.”

“Droperidol and ondansetron-induced QT interval prolongation: a clinical drug interaction study.”

“The effects of droperidol and ondansetron on dispersion of myocardial repolarization in children.”

Putting Acetylcysteine To Rest

Essentially, another study to nail the coffin shut for using n-acetylcysteine to prevent contrast-induced acute kidney injury.

Over 1000 patients each in the acetylcysteine and placebo groups, this study showed exactly equal 12.7% chance of acute kidney injury resulting from contrast exposure during cardiac catheterization.  In addition, the 30-day mortality was nearly identical at 2.2% for acetylcysteine and 2.3% for placebo, and only 3 patients in each group required dialysis within 30 days.
Perplexingly enough, the only advantage acetylcysteine had was a lower incidence in adverse effects versus placebo, 2.2% vs. 1.3%.  They do not mention what formulation their placebo formulation was, but apparently it caused more nausea & vomiting.
The authors also do a mini meta-analysis to evaluate why previous studies showed a benefit, and they additionally find that studies that had appropriately blinded allocation showed identical outcomes while patients with inadequate blinding demonstrated an acetylcysteine advantage.
“Acetylcysteine for Prevention of Renal Outcomes in Patients Undergoing Coronary and Peripheral Vascular Angiography.”

Rivaroxaban Can Be Reversed, But Not Dabigatran

We all hate coumadin – difficult to control levels and causes life-threatening bleeding, but at least we can measure its activity and reverse it in a straightforward manner.  However, coumadin’s days are at an end with the approval of the new oral anticoagulants – and the two most extensively evaluated are dabigatran (direct thrombin inhibitor) and rivaroxaban (factor Xa inhibitor).

This is a randomized, placebo-controlled trial of the reversal of dabigatran and rivaroxaban using prothrombin complexe concentrates – which, most importantly, have been theorized to be the only used agent for dabigatran.  Their results – in groups of 12 healthy volunteers – is that PCCs have no effect on any of the laboratory clotting parameters for dabigatran, but fully reverse rivaroxaban.
So, while there are no studies as of yet describing the acute reversal of either of these agents in a clinical situation, this is definitely concerning that we still have no theoretical way to treat life-threatening bleeding with dabigatran.
“Reversal of Rivaroxaban and Dabigatran by Prothrombin Complex Concentrate.”

Predicting Poor-Performing Residents

This is an entertaining look into the residency training experience in the United States, which is renowned for its brutality in certain specialities.  As far as sleep-deprivation goes, it ranks right up there with some of the lowest quality of life professional jobs.

This is, basically, the quality-of-life information from the Internal Medicine in-service training examination, as reported in JAMA.  The authors have linked it to in-training examination results for the, probably predictable, association of poor work/life balance and poor in-training scores.
Interesting tidbits I noticed:
 – 15.3% of residents stated that life was as good as it could be.
 – PGY-1 and PGY-2 residents had nearly equal poor quality-of-life and work/life balance – which improves significantly PGY-3.
 – Over 40% of residents have >$100,000 in debts – and that was associated with poorer quality-of-life scores.
 – Improvements in quality-of-life for PGY-3 was mirrored by a corresponding increase in depersonalization.
Not a healthy experience, by a longshot.  Pity those whose residencies are longer than the bare minimum of 3 years.
“Quality of Life, Burnout, Educational Debt, and Medical Knowledge Among Internal Medicine Residents.”

More Platelets In Massive Transfusion

Where are we going to get all these blood products?  The rapidly growing body of literature backing early transfusion of FFP and platelets in massive transfusion protocols continues to tilt towards the 1:1:1 ratio.

This is a retrospective review of whether platelet transfusion impacts survival in trauma.  They identify three categories of ratios of platelets to RBCs (>1:20, 1:2, and 1:1) and measure a variety of different outcomes.  Briefly, more platelets helped with survival to 24 hours, but more platelets also increased multi-organ failure.  In the end, the initial survival differences were great enough that they outweighed the additional multi-organ failure for a significant survival benefit (52% vs. 57% vs. 70%).

They exclude 25 patients who died within an hour in an effort to mitigate survival bias.  However, looking at the breakdown of survival times, it looks as though almost all the mortality benefit to increased platelet ratios was realized in the first 6 hours – and then the mortality numbers worsen in tandem after that.  The authors state they were unable to truly quantify retrospectively whether the patients survived because they received more platelets vs. whether patients surviving longer were able to receive more platelets, and note that prospective trials will need to be performed.

I would also note that a significant portion of their high ratio patients also received Factor VII, for whatever that’s worth.

So, we continue to await high quality prospective trials that specifically address the impact of survival bias.

“Increased Platelet:RBC Ratios Are Associated With Improved Survival After Massive Transfusion.”
http://journals.lww.com/jtrauma/Abstract/2011/08003/Increased_Platelet_RBC_Ratios_Are_Associated_With.2.aspx

Impedance Threshold Devices Are Useless

So, supposedly, impedance threshold devices installed inline for ventilation during CPR potentially improve hemodynamics via negative intrathoracic pressure.  This is a prospective, randomized, multi-center, placebo-controlled sham study that really meets a very high standard for internal validity.  Over 4000 patients in the ITD group, the sham ITD group, and the not-enrolled comparison cohort.

Short summary:
 – Minimal differences between groups.
 – 27.8% sham vs. 27.1% active device ROSC in the ED.
 – 8.2% sham vs. 8.2% active device discharge from the hospital.
 – No apparent harms from the ITD device, but no benefits either.

The most important point from this article is that we have gotten sloppy in our rush to implement supposedly new and beneficial therapies in medicine.  Hypothermia, TPA for stroke, Factor VIIa, direct thrombin inhibitors, etc. and we should add impedance threshold devices to the list.  The AHA has had ITD as a class IIa recommendation to improve hemodynamics since 2005 – six years of useless therapy and costs based solely on a theoretical model without proof of improved outcomes.  Hammering this point home never gets old.

“A Trial of an Impedance Threshold Device in Out-of-Hospital Cardiac Arrest.”
www.ncbi.nlm.nih.gov/pubmed/21879897

More Mistakes In An Unfamiliar System

Probably tells us what we already know – and likely underestimates the problem.

These authors take a retrospective look at all the reported medication errors between 2000 and 2005, and then try to associate increased errors with the involvement of a temporary staff member.  The problem is, they don’t actually have staffing documents that report which employees are temporary – they rely on the population of a QA field listing “contributing factors”, under which temporary staff is an option.  So, you can dismiss this as a bit of garbage-in/garbage-out depending on how accurate the reporting is – but, I figure, if anything, people will forget to implicate temporary staffing more frequently than not.
More interesting – and potentially confounding re: temporary vs. permanent – are the perceived reported reasons behind the medication error.  Temporary staff were more likely to be reported to have knowledge deficits, performance deficits, and fail to follow appropriate procedures.  I might read into that data that it’s easier for an unfamiliar temp to appear knowledge-deficient, although that’s just my own imagination.
From a risk management standpoint, the solution seems to be: whatever the retention costs of your permanent staff members, they are almost assuredly lower than the costs associated with the errors inflicted upon patients by temps.
“Are Temporary Staff Associated with More Severe Emergency Department Medication Errors?”

Epinephrine Neither Wins Nor Fails

The crux of the problem – epinephrine continues to improve short-term ROSC with uncertain long-term outcome improvement.

This is a prospective out-of-hospital arrest study from Australia in which epinephrine or saline placebo was given to patients during resuscitation by EMS.  And, like many studies before it, it fails to show a meaningful difference between patients receiving epinephrine and patients receiving placebo.  Rather, their primary outcome of survival to hospital discharge had 1.9% with placebo and 4.0% with epinephrine – but this result was not statistically significant with a p-value of 0.15.

Of course, what the lack of statistical significance means in this case is that this difference could have occurred by chance 15 times out of 100 times they performed this study – which, while not meeting the gold standard of 5 out of 100, is still a reasonably interesting clinical trend.  Like all studies before it, the short-term endpoints met statistical significance, including ROSC of 8.4% for placebo and 23.5% for epinephrine.  There are a few confounding differences between groups: more placebo patients had witnessed arrest, although the number with bystander CPR was the same; more placebo patients were endotracheally intubated in the field, which usually confers a survival disadvantage; and more epinephrine patients were ultimately transported to the hospital from the field.

So, there’s two ways to look at it: 1) epinephrine works, and we just need to figure out how to salvage more of those ROSC or 2) epinephrine is flogging far too great a number of lost husks back to life that will go on to consume ICU resources and expire regardless.

But, if we’re not going to give epinephrine, how do we otherwise look busy during a code?  And, what happens downstream to our epinephrine ROSC that fail to leave the hospital or the ER, and can we prevent it?

I am still not sure what the right answer is – like many diseases, cardiac arrest patients are a heterogenous group in which there is almost certainly a subset of patients that benefits from epinephrine, but we don’t yet know who that might be.

“Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial.”
www.ncbi.nlm.nih.gov/pubmed/21745533

Thanks to @cliffreid of Resus M.E! for first noting this article.