Tuesday, April 17, 2012

Post-Arrest Troponin Measurements Predict Little

Taking post-arrest patients to cardiac catheterization improves outcomes - as long as they have a cardiac occlusion as the underlying etiology of their arrest.  Otherwise, you're simply delaying the diagnosis and treatment of alternative causes, as well as post-arrest ICU-level care.  Therefore, if there is some clinical feature that can be identified on initial Emergency Department evaluation that predicts a coronary occlusion, that would be of great value.

So, this is a retrospective analysis of a prospective registry of out-of-hospital arrests from Paris, where much of the post-arrest catheterization work has been done.  And, unfortunately, there isn't any useful association - 92% of their patients had elevated troponin on initial evaluation.  There was a nonsignificant trend towards higher troponin levels in patients with coronary occlusion, but even at their "optimum" cut-off of 4.66ng/mL, the sensitivity and specificity were nearly coin-flip at 66% each.  A troponin of 31ng/mL was required for 95% specificity.

ST-segment elevation, incidentally, was more predictive of a coronary occlusion - OR 10.19 (CI 5.39 to 19.26).

"Can early cardiac troponin I measurement help to predict recent coronary occlusion in out-of-hospital cardiac arrest survivors?"

Sunday, April 15, 2012

The Dexamethasone Dose for Croup is 0.15mg/kg

Unfortunately, this is still probably not the trial that convinces everyone.  In fact, it's been over 15 years since the original single-center trials/reports showing that 0.15mg/kg of dexamethasone was every bit as effective as 0.6mg/kg of dexamethasone.  This makes intuitive sense, considering the steroid equivalencies, and the doses used in studies that have established prednisolone as an adequate treatment for croup, as well.

Regardless, this is a very small - 30-odd patients - with mild croup, randomized to dexamethasone at 0.15mg/kg vs. placebo.  The point of this study was not to test the efficacy of dexamethasone, but rather to show that, despite it's long half-life, it had immediate effects.  And, I think it's fair to say this study demonstrates those significant effects in reduction in croup score, gaining statistical significance by 30 minutes.

I don't know where the attachment came from in terms of the 0.6mg/kg dose of dexamethasone, but it's just preposterously high.

"How fast does oral dexamethasone work in mild to moderately severe croup? A randomized double-blinded clinical trial."

Friday, April 13, 2012

Early Steroids Probably Better for Asthma

Not sure if this is the study that proves it - since due to ethical considerations it's simply observational, and doesn't control for confounders and introduces a lot of bias - but, it's a small piece of the puzzle.

This is a cohort in a Montreal pediatric emergency department in which they prospectively collected data on moderate and severe asthma exacerbations as patients progressed through their care pathway.  They see, essentially, a nonsignificant trend in increased odds of hospital admission for patients in whom administration of systemic steroids was delayed.  This is mostly a data mining exercise, so any significant associations should be considered hypothesis generating.  However, considering the patients who received delayed steroids had milder exacerbations overall - yet still seemed to go on to have higher admission rates - it might be tempting to interpret these findings as appropriately confirmatory of physiologic foundations of treatment.

At least, there's no suggestion of harm from early steroid administration in asthma with exacerbation in children.  Perhaps some prospective interventional data with patient-oriented outcomes will surface in response.

"Early Administration of Systemic Corticosteroids Reduces Hospital Admission Rates for Children With Moderate and Severe Asthma Exacerbation"

Wednesday, April 11, 2012

ABCD2 For Cerebrovascular Dizziness

This is a bit of an interesting idea - a repurposing of the ABCD2 prediction instrument for TIAs as a risk-stratification instrument for cerebrovascular causes of "dizziness."

Every ED physician loves the complaint of "dizziness."  It's either giddiness, unsteadiness, lightheadedness, vertigo, and it's frequently difficult to elicit any pertinent neurologic symptoms to clarify one of the benign causes of vertigo or a cerebrovascular cause.

This is a retrospective chart review in which they evaluated the charts of 907 "dizzy patients", 37 of which had a cerebrovascular cause - 4.1%.  It's a small sample size - so the confidence intervals for their odds ratios are very wide - but for multivariable adjusted odds, age > 60 had an increased OR of 5.1, BP >140/90 had an increased OR of 2.9, speech disturbance had an OR of 6.2, and unilateral weakness had an OR of 10.9.  Essentially, it's interesting to see - and it makes sense - that the same features that generally portend stroke after TIA also might help predict which of your dizzy patients will be higher yield for a more intensive evaluation.

"Application of the ABCD2 Score to Identify Cerebrovascular Causes of Dizziness in the Emergency Department"

Monday, April 9, 2012

You Should Behave on the Internet

This is an interesting little research letter in JAMA regarding the incidence of state medical board review of unprofessional online behavior.  Of the 48 boards responding, 44 indicated that at least one complaint had been reviewed secondary to inappropriate online behavior.

The most commonly reviewed instances were inappropriate patient communication, online misrepresentation of credentials, and "inappropriate practice."  The most common responses noted by the survey were disciplinary proceedings, sanctions, and informal warnings - and half of medical boards reported license restriction, suspension, or revocation in response to proceedings.

Behave on the internet!

"Physician Violations of Online Professionalism and Disciplinary Actions: A National Survey of State Medical Boards"

Saturday, April 7, 2012

How Canada Does Chest Pain

Vancouver, Canada, to be specific.  The 37th most expensive city in the world to live in (ahead of New York and Los Angeles), a jewel on the coast of British Columbia, with breathtaking scenery, evergreens, rugged coasts, and mountains.

This is an observational series of their chest pain algorithm, and it falls into the category of "we do this and we like it" types of articles.  So, they do this, and they like it, and I can see why.

And the first thing you notice is that it is nothing like the United States.  Of the 1,116 patients they enrolled for this follow-up, they send home 25% of their potentially cardiac chest pain after an EKG and a single troponin.  These are patients whose mean age is 43 years old, and have TIMI scores of 0 or 1.  No outpatient stress test is arranged.  None of them had ACS within 30 days.

Another 20% had a negative 2-hour troponin and EKG and were sent home without outpatient stress testing, average age 49 years old and TIMI scores mostly 0 and 1.  None of them had ACS within 30 days.

Finally, at six hours, they were left with a group of 60 year old folks, 30% of their cohort, whose TIMI scores were >1.  They sent them all home, 25% of without an outpatient stress test and 75% with - and none of the no-stress cohort had ACS within 30 days.

Essentially, they send home over half their patients, aged 40 to 60 years old, and a couple cardiac risk factors - and they do fine.  We don't really know what sort of coronary disease the patients discharged without a follow-up stress test had, and it means they probably have some false negatives in their outcomes at 30 days simply because they don't receive any sort of additional diagnostic testing.  But, none of them had an unprovoked adverse coronary event, which counts for something.

About 20% of their patients referred for outpatient stress failed, and about half of those ultimately received a diagnosis of ACS - so, even then, in the patients they were most concerned about after negative ED testing, only 10% had ACS.  Seems like there's room to improve here, as well.

It's not crazy, it's Canada.

"Safety and Efficiency of a Chest Pain Diagnostic Algorithm With Selective Outpatient Stress Testing for Emergency Department Patients With Potential Ischemic Chest Pain"

Thursday, April 5, 2012

Rivaroxaban and Pulmonary Embolism

This is rivaroxaban, an oral Factor Xa inhibitor, part of the wave of potential warfarin replacements.  This is their phase III EINSTEIN-PE trial, which is a non-inferiority comparison against warfarin for the long-term outpatient management of pulmonary embolism.

Overall, it was slightly less effective at prevention of recurrent venous thromboembolism (2.1% vs 1.8%), but slightly safer with regards to bleeding episodes (10.3% vs. 11.4%).  Adherence to therapy was reasonable compared to other trials regarding the amount of time patients spent with therapeutic INR between 2.0 and 3.0.  So, really, it's pretty much a wash.

But, of course, when you have a new and expensive therapy that's essentially similar to the old, cheap option, the conclusion is: "Our findings in this study involving patients with pulmonary embolism, along with those of our previous evaluation involving patients with deep-vein thrombosis, support the use of rivaroxaban as a single oral agent for patients with venous thromboembolism."  

Of course, if you were expecting a different conclusion from an open-label, manufacturer-sponsored study, you are unfortunately mistaken.

So, make sure your hematology group is on board with PCCs, because there doesn't seem to be any other possible option for reversing life-threatening bleeding - and rivaroxaban is coming, whether it should be or not.

"Oral Rivaroxaban for the Treatment of Symptomatic Pulmonary Embolism"

Tuesday, April 3, 2012

Whole Blood Works For POC Pregnancy Tests

If there is such thing as a "cult favorite" article amongst Emergency Physicians, right now, this probably qualifies as the one receiving its 15 minutes of fame on Twitter.

If there is any singular agony known to all Emergency Physicians it is the inability to obtain urine samples in a timely manner.  Sometimes, this is for the urinalysis.  Other times, this is for the qualitative pregnancy test result.  If only there were a better way....

And, perhaps, there is.  This is a two year study of sensitivity/specificity of the POC pregnancy test using the Beckman Coulter ICON 25 - comparing the performance of using urine vs. whole blood, with laboratory quantitative bHCG >5 as the gold standard.  95.3% sensitivity for the urine test, 95.8% sensitivity for whole blood, with 100% specificity.  Most of the false negatives were due to beta hCG < 100.

Interesting alternative!

"Substituting whole blood for urine in a bedside pregnancy test"

Monday, April 2, 2012

One Year of EM Lit of Note!

Happy Birthday to my blog - one year old.  No longer neonatal, but still an infant.

Blogging has been interesting - it is, indeed, time-consuming to read all these articles.  However, I'd be reading them regardless - so the time commitment is mostly the part with the typing.  Luckily, in academics, your clinical time is scaled down specifically to encourage these sorts of activities (although, blogging has so far only been parlayed into an endowed chair by Michele Lin).  And operating a blog is nothing like the amazing podcasts other folks put together - I have no idea how they do it.

At the moment, we're on a schedule of a post every other day or so - and up to about 11,000 views per month.  In contrast, my article in JAMA from last summer has been downloaded 2,250 times.  Which has more value?  So far, the blog seems to be leading to more opportunities.  The traditional model of knowledge and opinion dissemination in medicine is certainly shifting.

Firefox and Safari are literally tied at 30% of my site traffic, as well as Macintosh vs. Windows at 30%.  Australia is in second place behind the U.S., and counts for about 10% of my traffic.

The top five most frequently viewed articles:
#1. Yet Another Highly Sensitive Troponin - In JAMA
#2. Too Many Traumatic Arrests Are Transported
#3. Cardiology Corner - More Brugada Tidbits
#4. C-Collars Cannot Stabilize Unstable Injuries
#5. Must We Use Paracetamol/Acetaminophen?

Thank for reading!

Sunday, April 1, 2012

Don't Hold It!

The hidden threat to patient safety in the Emergency Department - impaired cognitive performance secondary to suppressing the extreme urge to urinate!

Of course, this is only eight volunteers who consumed an average of 2.2 liters of water - and, by impaired cognitive performance, I mean to say they were slightly slower - but, it's certainly suitable for an April Fool's Day blog post.

This study shared the 2011 IgNobel Prize for Medicine.

"The Effect of Acute Increase in Urge to Void on Cognitive Function in Healthy Adults"

Friday, March 30, 2012

Glucose-Insulin-Potassium For MI?

"Investigators, led by Dr Harry Selker (Tufts Medical Center, Boston, MA), are pleased with the results, believing that after years of futile study, they have finally found some clinical evidence to support the experimental data suggesting that GIK [glucose-insulin-potassium] myocardial metabolic support could protect the heart in the ACS setting."

...which lead to the press release tweet of "Intravenous GIK Slashes Death Risk in Acute Coronary Syndrome: CHICAGO – Glucose, insulin, and potassium given i..." by @ACEPNews.  That press release can be seen here.

There have been trials enrolling over 20,000 patients to date that have been negative.

Despite all these previous negative trials, the authors believed the problem was timeliness - the critical time in which to provide metabolic support to the infarcting myocardium was in the prehospital setting, upon the earliest recognition of ACS.  The original goal was to enroll 15,450 patients.  They ended up with 880.  Then, after data collection, they changed the primary endpoint from all-cause mortality to progression to myocardial infarction at 30 days and at 1 year.  And they only have the 30 day data right now, they'll get back to us with the 1 year outcomes.  How this made the cut for publication in JAMA is outside the scope of my speculative powers.

So, they enrolled folks prehospital with signs and symptoms of potential acute coronary syndrome whose prehospital EKG was read as STEMI or met the ACI-TIPI prediction instrument probability threshold of 75%.  They received the GIK solution with 90 minutes, on average.  And, the primary outcome measure was negative for progression to MI, trend favoring GIK with OR 0.88 (CI 0.66-1.13).  Negative for 30 day mortality, OR 0.72 (0.40-1.29).  For STEMI patients, negative for progression to MI, OR 0.74 (0.40-1.38), and negative for 30 day mortality, OR 0.63 (0.27-1.49).
So, yes, there is a trend.  And some subgroups even had significant trends in favor of GIK.  But for JAMA and the rest of the internet to be promoting this as practice-changing at this juncture is absolutely inappropriate.

"Out-of-Hospital Administration of Intravenous Glucose-Insulin-Potassium in Patients With Suspected Acute Coronary Syndromes:  The IMMEDIATE Randomized Controlled Trial"

Wednesday, March 28, 2012

CCTA Is A Bad Shortcut Around Bad Care

"Although an acute coronary syndrome is ultimately diagnosed in only 10 to 15% of patients who present with chest pain, the majority of these patients are admitted to hospitals, at an estimated cost of over $3 billion annually."

This is, essentially, the statement of problem from the NEJM article, sponsored by Siemens, regarding the use of coronary CT angiograms in the Emergency Department on low-to-intermediate risk chest pain.  They are clearly huge fans of CCTA up at the University of Pennsylvania, and I hate to think it has something to do with the parade of imaging technology companies and patent applications listed as disclosures by the authors.

In this study, the authors enrolled 1,392 patients with chest pain with the goal of testing the primary hypothesis that "patients without clinically significant coronary disease on CCTA (i.e., no coronary-artery stenosis ≥50%) would have a 30-day rate of cardiac death or myocardial infarction of less than 1%."

Good news!  They were right.  Bad news:  their entire enrolled cohort had a 30-day death or MI rate of only nearly 1%.  It's rather incredible, really, that they have this entire article in which they sing the praises of CCTA for identifying low-risk chest pain, when in reality, they gloss over the fact that they simply could have sent home every single patient in the study without doing a single additional test and only nearly 1% would have had death or MI within 30 days.

Going back to their essential statement of problem, it might be true that CCTA were valuable if they were looking to apply it in a population and practice environment in which we were actually hospitalizing patients with a 10-15% rule-in rate.  However, the opposite of what these authors propose is the real truth - clinically identify all the low-risk chest pain and stop doing all these expensive tests!  They claim it expedites discharge from the Emergency Department, which, in theory, saves money - but it isn't!  Despite 90% of their CCTA being negative for stenosis >50%, they still end up admitting half their CCTA cohort.  Even the negative CCTA cohort, while their length of stay is reduced to 12 hours, still means they're being placed in observation status and billed an additional separate observation code - which in many places is a protocolized chest pain observation unit run by the Emergency Department.

This is simply a bad solution to bad baseline practice patterns.  The measurable benefit here isn't to the patient, it's to the malpractice risk of the physician, to Siemens and other sponsors of the study, and likely to the Emergency Departments whose billing increases for these short stay observation patients.

"CT Angiography for Safe Discharge of Patients with Possible Acute Coronary Syndromes"

Monday, March 26, 2012

Pan-Scan & Zero-Miss

In an interesting contrast to a prior article regarding over-scanning in trauma, this article takes a different perspective.  While the authors do note that there is controversy regarding the impact of "pan scan" on survival, they are rather focused on the sensitivity/specificity of the "pan scan," rather than the appropriateness.

This is a review of 982 consecutive patients undergoing "pan scan" in Germany.  The indications for scanning were a set of "red flag" criteria, which included impaired patients, patients with obvious injuries, "suspicion of severe trauma" or "high risk mechanism".  The diagnostic reference standard was chart review by two reviewers of the electronic notes for any injuries missed on the initial scan.

The results are rather interesting in a couple ways:  the prevalence of injuries per organ system is not terribly high, and the sensitivity of scanning was rather low.  The highest prevalence of injuries for an organ system was 37%, for chest, followed by head and neck at 34%.  However, the sensitivities range from a high of only 86.7% for chest down to a low of 79.6% for face - likely because dedicated fine cuts of the face were not part of their protocol.  Regardless, with sensitivities in the mid-80s meant they missed almost one seventh of the total number of injuries.  Of these 70 missed injuries, almost half required surgery or a critical intervention as treatment.

So, pan-scanning: expensive, low yield, yet still misses important injuries.  The authors do not try to fully address whether their yield is reasonable or not, and wisely simply state further research is needed regarding triaging patients into groups likely to benefit from scanning.

"Accuracy of single-pass whole-body computed tomography for detection of injuries in patients with major blunt trauma."

Saturday, March 24, 2012

More Nails In the Coffin For Epinephrine

The news for epinephrine in cardiac arrest keeps getting worse - it restarts the heart, but at what cost, and with what outcomes?

This is a study, published in JAMA, of 417,188 out-of-hospital cardiac arrest patients in Japan - only 15,030 of which received epinephrine during prehospital transport - a far cry from the U.S., where the toolbox has typically already been emptied prior to the ED.  Nearly every baseline characteristic favored the epinephrine group - more witnessed arrests, more received bystander CPR, a physician was more frequently in the ambulance, more patients in ventricular fibrillation/PEA.  However, more of these patients also received an advanced airway, which has also been associated with worse outcomes.

In their unadjusted analysis, the epinephrine cohort was three times as likely to have ROSC, and had an OR of 1.15 to be alive at one month.  However, they were half as likely to be functional as the non-epinephrine survivors.  Then, when they do all their statistical adjustments for all the favorable baseline factors in the epinephrine cohort, all these numbers become less favorable for epinephrine.  They also do a propensity-matched cohort of 26,802 patients that has favorable ROSC with epinephrine, but dismal 1 month and functional outcomes.

This data is from before the era of routine hypothermia - which may be beneficial - but it certainly supports what we already expected regarding the damaging physiologic effects of epinephrine while senselessly flogging the heart back into action.

"Prehospital Epinephrine Use and Survival Among Patients With Out-of-Hospital Cardiac Arrest"

Thursday, March 22, 2012

TPA is Dead, Long Live TPA

I'm sure this saturating the medical airwaves this morning, but yesterday's NEJM published a study which they succinctly summarize on Twitter as "In trial of 75 pts w/ acute ischemic , tenecteplase assoc w/ better reperfusion, clin outcomes than alteplase."

Well, that's very exciting!  It's still smashing a teacup with a sledgehammer, but it does appear to be a more functional sledgehammer.  Particularly encouraging were the rates of sustained complete recanalization - which were 36% at 24 hours for alteplase and 58% for tenecteplase - and the rates of intracranial hemorrhage - which were 20% for alteplase and 6% for tenecteplase.

However, the enthusiasm promoted by NEJM, and likely the rest of the internet, should be tempered by the fact that there were only 25 patients in each arm, and there is enough clinical variability between groups that it is not yet practice changing.  This was a phase 2B trial, and it is certainly reasonable evidence to proceed with a phase III trial.

Unfortunately, in a replay of prior literature, the authors are all affiliated with Boehringer Ingelheim, the manufacturer of tenecteplase.

"A Randomized Trial of Tenecteplase versus Alteplase for Acute Ischemic Stroke"

Addendum:  As Andy Neil appropriately points out, tenecteplase has been studied before - 112 patients over several years, terminated early due to slow enrollment - without seeing a significant advantage.

Tuesday, March 20, 2012

Over-Prescribing of Antibiotics Happens Everywhere

On Twitter a couple weeks back, in response to my plea to reduce empiric macrolide use for benign clinical syndromes, there was an allusion suggesting Pediatricians were the culprits of a poor antibiotic stewardship.

Of course, that's clearly not the case.  And, while we all envision Urgent Cares and customer-service medicine contributing to the over-prescription of antibiotics, it's happening in our academic medical centers, as this article indicates.  This is a retrospective chart review from San Diego that evaluated 836 patients receiving a diagnosis of "acute bronchitis", a typically self-limited disease that evolves into pneumonia only in a minority of cases in elderly patients or patients with significant pulmonary comorbidities.

The average age was 46, 10% had comorbid COPD noted, 17% asthma, 8% diabetes, and 4% HIV/AIDS.  All told, 74% were prescribed antibiotics - 50% received a macrolide, 15% a tetracycline, 6% a fluoroquinolone, along with a few others.


And certainly not just the Pediatricians.

"Antibiotic and bronchodilator prescribing for acute bronchitis in the Emergency Department."

Sunday, March 18, 2012

Is It Reasonable to Keep Using Vasopressin in Shock?

The authors of this meta-analysis seem to think so.

Unfortunately, they identify a very heterogenous set of evidence for analysis, which reduces the statistical power of every comparison.  They identify only a couple studies of vasopressin vs. placebo, and most of their studies are vasopressin vs. an increased dose of norepinephrine.

It's hard to generate any unreasonable conclusion from this data - the error bars cross one, so you can either take this as permission to drop vasopressin from your usage patterns because its use has no measurable mortality benefit, or you can continue to use vasopressin because it doesn't seem to be harmful, and allows you to reduce the dose of norepinephrine.

I'd really like to see more vasopressin vs. control - there's only one reasonably sized vasopressin vs. placebo trial - and it heavily, but non-significantly, favors control with a risk ratio for mortality of 1.94 (0.74 to 5.10).

More to be done!

"Vasopressin for treatment of vasodilatory shock: an ESICM systematic review and meta-analysis"