Saturday, April 30, 2011

Badgering Your Consultants to Death

This article describes a fascinating and absolutely untenable situation with numbers that just defy comprehension.

At an academic teaching hospital in Korea, 75% required consultation towards their admission rate of 36% - and their ED LOS median was seven hours.  Then, they implemented this brutal system in which an automated computer protocol paged out a consultation - and then, at the three hour mark - if there was still no disposition, they autopaged every resident in the consulted department.  Then, at the six hour mark, a page went out to every resident and faculty member in the consulted department regarding the disposition delay.  And their median ED LOS and time to disposition basically each improved by an hour and a half with this intervention.

So, this situation is insane.  Their admission rate is pretty high, but I still cannot fathom consulting on 75% of my patients.  And, these time to disposition numbers are equally alien, especially to a community emergency physician.  At my hospital, if a consultation goes over one hour in our EDIS, the badgering begins - but it's more likely friendly, desperate begging as opposed to this hospital's automated irritant spam.

So, shed a tear for Korea and their dysfunctional ED.

Friday, April 29, 2011

Intracranial Extension of Sinusitis in Children

Interesting descriptive study of a decade's worth of children transferred/admitted to Texas Children's in Houston with intra-orbital or intra-cranial extension of their sinusitis.  It's really just a summary of the clinical and hospital courses of 118 patients identified through retrospective chart review.

Interesting tidbits:
- Of these patients, 40% had been prescribed outpatient courses of antibiotics prior to the time of diagnosis of intra-cranial or intra-orbital extension.
- All patients with intra-orbital involvement presented with eye swelling.
- Intra-cranial extension had substantially (and significantly) more headache and vomiting, and only 67% received antibiotics prior to transfer.
- Identical numbers in each group - 16% - of patients were afebrile upon presentation.
- 33% of patients with intracranial extension of sinusitis did not complain of a URI-like syndrome at presentation.
- Frontal sinus involvement was associated with 84% of their intra-cranial extension.
- All organisms recovered were sensitive to clindamycin or vancomycin plus cefotaxime except for a single pseudomonal infection.
- There were no deaths, and four patients had persistent neurologic or visual sequelae.

Short summary - orbital cellulitis was a little more straightforward in diagnosis than intracranial extension of sinusitis, and a significant minority of both groups would definitely diagnostic challenges.  CT imaging, anathema as it may be, is the diagnostic modality of choice.

Thursday, April 28, 2011

Psychiatry & ED Agreement

Not as helpful an article as I hoped when I pulled it to peruse.  Part of the issue is the surveys are administered to psychiatry and emergency department residents regarding their evaluation of the patient, so you're almost certain to have a lot more variability - not just in assessment, but in level of understanding of language and the process of acute psychiatric assessment.

Where I'm not surprised we have a low kappa with our psych colleagues are areas like mood disorders - as emergency physicians are looking more at threat to themselves, threat to others, acute psychosis, and other factors affecting their global level of function to determine whether they are safe for discharge.  What's interesting are the 2x2 tables regarding things like suicidality, where psychiatry is eliciting suicidality in a significant number of individuals where that was not reported by the emergency physician.  Out in community practice where psychiatry is not always readily available, the discharge of psychiatry patients is a high-risk endeavor - and I would have expected the emergency physician to be more attuned to suicide risk and document a lot more concern for suicidality that was deemed not an issue for the consulting team.

Mostly just an article to read out of passing curiosity that won't impact your practice.

Wednesday, April 27, 2011

More Conflicts of Interest

I don't know if I'm the only one who gets depressed by these sorts of articles.  You have the progression through medical school and residency, you finally start feeling up-to-date on current treatment, your Grand Rounds invited speakers present results from some trials, and you think you're fully armed to provide the best care modern medicine can provide.

And, then you discover that it's all a stack of cards predicated on results influenced by pharmaceutical funding.

This article is from JAMA, again, very important topic given studies performed with pharmaceutical funding have a fourfold greater chance of reporting positive results.  They looked at meta-analysis, one of the techniques we try to use to increase statistical power in our reading of the literature.  They discovered that nearly no meta-analyses included comment on whether the included studies were funded by pharmaceutical literature - even though 60% of the studies reported funding sources, and 70% of those studies reported receiving funding from the pharmaceutical industry - and the same sort of dismal reporting for author conflicts of interest.  What it means - it's another cautionary tale regarding how pervasive the masking of conflicts of interest really is, and how easily it creeps into the medical literature without our knowledge.

Tuesday, April 26, 2011

Adrenal Insufficiency in Pediatric Shock

This falls into the "don't use etomidate" pile of literature.  Well-demonstrated, primarily in the pediatric literature, that etomidate and its association with adrenal insufficiency results in poorer outcomes in shock.  This article doesn't look at etomidate, but rather it describes relative or absolute adrenal insufficiency in pediatric shock, and finds it relatively pervasive.  It then finds an association between their two definitions of adrenal insufficiency and length of stay, length of ventilator days, and required doses of vasopressors.  They only 5% mortality in their study, so they can't comment on any mortality association.

So, this is another study that helps describe why etomidate may be contributing to poorer outcomes.  The days of ketamine + rocuronium RSI are coming (we'll save the succinylcholine vs rocuronium debate for another day).

Monday, April 25, 2011

Out of Hospital Arrest Score Validation

There are nice studies in the U.S. defining and validating a rule that determines which patients are unlikely to have ROSC or survival to hospital discharge, e.g. BLS-TOR.  This is a study from France that looks at people who do have ROSC to see, not just if they'll survive, but survival where the patient is not severely disabled or vegetative.  One of the nice things about Europe is that their cultural perception of "life" really has to do more with living, and not just simply "being alive".  So, whether we can actually implement something like this in the U.S. may be difficult.

It's a chart review, which limits its quality to some extent.  The other real issue I have with this OHCA score is its complexity - it incorporates initial rhythm, no-flow and low-flow intervals, and admission levels of creatinine and lactate.  The U.S. validation cohort had 34% therapeutic hypothermia, which is pretty good - the derivation cohort was only at 11%.  Predictors of good neurologic outcome, consistent with other articles: ventricular fibrillation, bystander CPR, lower creatinine and lactate.

Unfortunately, for this rule to get up to 100% specificity, the sensitivity drops to 19%.  Alternatively, you could say that's 20% of out-of-hospital arrest ROSC that shouldn't have further intervention, which would be an important cost and medical resource utilization savings.

So, this is something that your colleagues in critical care are going to use to discuss prognosis, although I'd like to see something along these lines that helps attenuate the number of people we resuscitate until our post-resuscitation care demonstrates much, much improved outcomes.

Sunday, April 24, 2011

"Teachable Moments"

From the critical care literature, looking at whether the ICU admission represents a "teachable moment" for counseling against health-endangering behaviors.  It's a review article asking the question whether interventions at the time of admission to an ICU - i.e., a close brush with death - are effective.

This is relevant to the Emergency Department for those situations where you want to shake your patients and tell them "you did this to yourself, you fool!"

They look at the literature for nicotine cessation and for alcohol cessation.  The nicotine cessation literature is rather bleak.  They break down the interventions to <15 minutes vs. >15 minutes, and then whether contact after hospital discharge is helpful.  Pretty much, unless you have a mechanism for prolonged after-discharge contact and counseling, you won't get any meaningful results.

As far as alcohol goes - there are good studies that support questionnaires, lab work, or scoring systems to identify individuals at risk for alcohol-related injuries or illness.  However, all the studies in their review show regardless of behavioral intervention, no decrease in alcohol consumption at discharge is seen.

So, sadly, almost assuredly, the ED, with the minimal time and follow-up available to us, is unlikely to be a place where impactful counseling is feasible.

Saturday, April 23, 2011

Ultrasound Guided Subclavian Access

Ultrasound guidance and visualization of anatomy and/or the needle tip during jugular venous cannulation is, essentially, the standard of care given the frequency of complications using anatomic landmarks alone - not to mention the "growing" U.S. population that has outgrown their landmarks.  It's also the standard of care because residents finishing their training right now have never done an IJ without the ultrasound.

So, what do we do when we don't have ultrasound?  Then you're left with the decision to do subclavian or femoral.

Well, ultrasound-guided subclavians are well-described in the literature, and this is an article from our critical care colleagues with 400 subclavian access attempts - half with landmarks and half with ultrasound. Fewer complications, fewer attempts, less time to access.  Hard to argue with that.  If you aren't getting familiar with ultrasound, I would start thinking about ways to become more comfortable.

Friday, April 22, 2011

Fluoroquinolone-Resistant E. Coli

Doom and gloom from the Netherlands regarding antibiotic resistance in E. coli.  Although they focus on the resistance rates to fluoroquinolones, the more interesting take-home point from this article is the risk factors described for polypharmacy resistance.

Depending on your local resistance patterns, 88% susceptibility to E. coli for fluoroquinolones either sounds great or it sounds terrible.  What's interesting is that the strains of E. coli in this study that had fluoroquinolone resistance also had 33% resistance to amoxicillin-clavulanate, 65% resistance to TMP-SMX, and 14% had an ESBL gene.  So, you can really extend their findings to more a listing of predictive factors for resistance to multiple antibiotics.  In there study, the main univariate risk factors were indwelling catheter (OR 6.0) and prior fluoroquinolone use within six months (OR 18.6).  Less prominent, but still statistically significant were underlying urinary tract disorder (OR 2.3), recurrent UTI (OR 2.2), or recent hospitalization (OR 2.3).

Their conclusion that the presence of any of these risk factors should result in a urine culture being sent, which is reasonable - although even in the absence of risk factors, there was still an 8.2% chance of fluoroquinolone resistance.

Thursday, April 21, 2011

Norepinephrine is Superior to Dopamine

Last day of Journal Club for April.

It is very interesting how generational medical practice is - currently training physicians are accustomed to using norepinephrine for virtually everything as the vasopressor of choice (except, well, when there's a medication shortage like this past month), while previous generations have a comfort zone with dopamine.

This is a very nice study in a lot of ways and it does a good job if illustrating that dopamine and norepinephrine have very small but relevant clinical effects.  Some of their inclusion criteria are a little odd - hypoperfusion/decreased CVP after only 1000mL of crystalloid or 500mL of colloid?  And 246 of their patients suffered from hypovolemia due to acute hemorrhage - so you can really question why anyone was reaching for a pressor instead of a Cordis or the OR - and, there are a few other instances with small numbers where neither dopamine or norepinephrine is your vasopressor of choice (e.g., anaphylactoid shock, spinal shock).

But, they had good randomization and their treatment groups are very similar.  And what did they find?  No difference.

Well, not completely true - no difference in ICU mortality with a p = 0.07 in favor of norepinephrine and no difference in in-hospital mortality with a p = 0.24 favoring norepinephrine.  So, norepinephrine is favored, but statistically the results are not bulletproof.  I think the trends are reasonable, but it's certainly worth keeping an open mind.  Alternatively, if you wanted to never use dopamine again, you can definitely argue that norepinephrine is no worse.

Secondary outcomes generally trend in favor for norepinephrine with a few reaching significance - although, when you look at 20 secondary outcomes, you're bound to find some significant differences.  The most important difference is the incidence or arrhythmias, primarily atrial fibrillation, which occurred in 24% of the dopamine group and 12.4% of the norepinephrine group at a p = <0.001.

It's an important paper to have around to be on the same page as the critical care colleagues.

Wednesday, April 20, 2011

Famoditine in Urticaria

Dredged up for Journal Club from The Year 2000 (that was the future, once).

You might scoff at this article because it enrolls a grand total of 25 participants with acute urticaria, ten of which receive diphenhydramine and fifteen receive famotidine.  You might be more impressed to know that this is pretty reflective of the evidence we have regarding H2-blockers in the treatment of urticaria.  Another study from 1993 compares diphenhydramine, famotidine, and cromolyn sodium - and only enrolls 20!

It is mildly amusing to see them report there is no significant difference between the groups when they don't have the power to detect any.  Regardless, our H2 blockers provide some relief, it's likely additive, and they're inexpensive and safe.

The "definitive" study at present supporting our H1 + H2 blocker for acute urticaria or allergic reaction in the emergency department enrolls 91, and it shows diphenhydramine + cimetidine is superior to diphenhydramine alone.

Tuesday, April 19, 2011

Antibiotics Are Unnecessary After MRSA Abscess Drainage

Almost a year old now, but it's been dredged up for Journal Club (spoiler alert: the next two days might have something in common with vis-a-vis dredging).

Small study randomizing skin abscess to placebo vs. TMP-SMX after incision and drainage in children.  I think it's a fair article with decent external validity, as I would say this directly addresses the practice pattern of pediatric emergency physicians, let alone community pediatricians.  The real issue is statistical power for their secondary endpoint and some minor differences between their two groups.  Treatment failures comparing placebo and TMP-SMX are identical - which just goes to show you that the I&D really is the most important element of treating abscesses.  They do a lot of packing!  I suppose I'm almost more surprised there isn't more packing, since that's the commonly accepted practice, but I digress.

The only fire remaining in their argument is that antibiotics will decrease recurrent abscesses.  And, I am willing to give them that - although, I really expect, if they had a longer follow-up period, a lot of those abscesses would return after the antibiotics were stopped because the environment requires eradication.  However, there's a significant difference in the number of each group with a history of recurrent abscesses favoring the TMP-SMX group, which might explain the magnitude of their difference in recurrent lesions within 10 days.

Too small a study to change our practice - although, our practice probably should never have changed from not treating abscesses with antibiotics in the first place.

Monday, April 18, 2011

Oxy-Free ED

A little bit of a follow-up to yesterday's post on adverse events - and because it was mentioned on EM:RAP a couple months ago.

This is the group up in Washington state that is trying to cut down on the number of narcotics being diverted from their Emergency Department into the community.  It's a nice discussion and something that if you're not already doing something about it, you're not doing enough.  A unified strategy across their entire department helps keep patients and physicians on the same page and standardizes their treatment.  I know at a small critical access hospital at which I work, some patients will call ahead to see which physician is working - since they know they won't be getting their usual fix with certain docs.

Sunday, April 17, 2011

Everything is a Poison...

...when taken in inappropriate amounts.

The NYT reports on a recent AHRQ release that doesn't tell us a lot that's new - more hospital and ED visits are coded with medication side effects - a "50% increase since 2004".  The problem with the lay article is that it focuses on these issues as "medication errors" as some alarming decline in quality in U.S. healthcare.  Part of the problem with this release is that it's simply data - it's not a study or a statistical analysis that attempts to control for other confounding influences - have the number of prescriptions for each of these classes gone up?  What's the average age of these patients presenting with errors (i.e., aging boomers)?  There are a lot of other factors contributing to whether a medication results in an adverse effect, and they aren't just "errors".  The ED data isn't all that insightful, although it is interesting to see how it differs from the inpatient errors.  The #1 culprit for the ED is "Other", which is 261k compared to 118k opiate adverse events - which basically invalidates their data when most of your data points fall into an unknown category.

Saturday, April 16, 2011

Heparin-Binding Protein for Bacterial Meningitis

This study came out highlighted by the last Emergency Medicine Journal Watch.

Now, I don't want to steal Emergency Medical Abstracts thunder, since I'm sure they're going to tear this article to shreds in a few months, but let me just comment on the conclusion of the Journal Watch reviewer that this is a "promising new biomarker that...might play the same role in bacterial meningitis that D-dimer does in venous thromboembolic disease" and that "an HBP level >20 ng/mL should prompt empirical therapy for bacterial meningitis" like this assay is something we should incorporate into our practice.

Part of the problem with this study is their methodology.  They used HBP to diagnose bacterial patients where they could diagnose bacterial meningitis.  Which means, these are all patients in which they already were able to make the diagnosis of bacterial meningitis without this magical new test.  So, immediately from that standpoint, it doesn't add any value.

They also used two different samples, including, apparently, some they had on file from a decade ago - but their justification seems reasonable.

They compare the sensitivity and specificity of their test to the sensitivity and specificity of CSF polynuclear cells and CSF WBC count - and they're statistically identical.  And, specifically, they are marginally better in absolute terms and likely in AUC vs. any of those tests individually, but when taken against the combined information given by all the CSF tests we already send off, there is likely no clinical difference.

Lastly, the most important words are on the first page: "Hansa Medical AB has filed a patent application on the use of HBP as a diagnostic tool in meningitis.  Dr. Linder, Dr. Christensson, Dr. Björck, and Dr. Åkesson are listed as inventors."

My conclusion: this is an unnecessary test to add to your arsenal.  Read the article, make your own conclusion.

Friday, April 15, 2011


I went to a Scotch tasting event the other day hosted by Glenmorangie - which is, supposedly, the top-selling Highland single-malt - and while the event itself was rather bland, their line of double-barreled scotches are worth mention.  Essentially, they take their regular 10-year Highland single-malt, and then they spent two more years aging it in barrels from Port, Sherry, or Sauternes.  They are all worth trying and tasting, simply because they really have a lot of interesting flavor, and mostly sweetness, onto the base Highland.  The Nectar D'Or - really for no reason - has a $20 markup over the other double-barreled variants LaSanta and Quinta Ruban, and, while quite good, is kind of a lot of markup when you consider the competition in that $40 to $60 dollar range.

And, more importantly, they have them in the state-run liquor stores out here in rural areas where I currently live.  When I do feel like purchasing one, I tend to go for the LaSanta.

Addendum:  Hiding a FFBall team logo secretly on the inter webs.

Dexamethasone in Asthma

Steroids are part of the mainstay of therapy for acute exacerbations of reactive airway disease - but does it matter which steroid we use?

I think it's clear that answer is: "no".  Multiple studies support using dexamethasone rather than prednisone - best described in pediatrics, but this study reaffirms its utility in adults.  The advantage is its half-life of 72 hours, meaning it requires fewer doses and, in theory, greater compliance.  Although, really, this study is limited directly as a pharmacologic comparison study specifically because of the compliance issue - there's no guarantee every patient finished their course of prednisone, while it's pretty likely patients managed to take at least the 2nd non-placebo dose of their dexamethasone.  However, in terms of clinical relevance - it reflects the compliance issues encountered in reality.

There's an underpowered single-dose dexamethasone pediatric study out there, as well, which appears promising.  I like the idea of 100% compliance guaranteed by a single-dose in the ED, but it's something that needs more data.

Thursday, April 14, 2011

Emergency Response Teams

This is an idea that sounds great in theory - if you have a roving team of skilled resuscitation professionals in your hospital assisting nurses who are concerned about their patients, you can intervene on these patients before they deteriorate, keep people from escalating into the ICU, and improve outcomes.  It's such a great idea that the entire country of Australia has been spurred into implementing these.  My hospital has them, and, no doubt, many other hospitals do as well.

The problem is, they're having a hard time demonstrating their efficacy.

A study out of Stanford last year reported that, at their VA hospital, implementation of emergency response teams (ERTs) reduced mortality.  Unfortunately, on closer reading, ERTs reduced mortality on the floor, and their primary intervention was to move people to the ICU - where their mortality was no longer counted in the study.  While it is rather graceless to have people coding and dying on the floor, unfortunately they did not show the outcomes they claimed.

This more recent report, from Australia, as mentioned above, is a before and after analysis of hospital-wide mortality, CPR rates, etc. with their ERTs.  They likewise show benefits, with ICU admissions, CPR rates, and mortality all declining after implementation.  However - and they very astutely point this out themselves - one of the most significant functions of the ERTs was to clarify code status and affirm a greater number of people as DNR or futile resuscitation.  While this function, if it reduces ICU admissions, is absolutely a cost and resource savings, I don't think it's precisely how they wanted to justify implementation of ERTs.

There are many reasons to have ERTs, but a mortality and cost-benefit justification has not yet been well-demonstrated.

Wednesday, April 13, 2011

News Flash - Better Electronic Medical Records Are Better

In this article, providers are asked to complete a simulated task in their standard EMR - which is Mayo's LastWord supplemented by Chart+ - vs a "novel" EMR redesigned specifically for a critical care environment with reduced cognitive load and increased visibility for frequently utilized elements and data.  In their bleeding patient scenario, their novel EMR was faster and resulted in fewer errors.  So, thusly, a better EMR design is better.

While it seems intuitively obvious - you still need studies to back up your justification for interface design in electronic medical records.  Their approach in testing is one I'd like to see expanded - and perhaps even implemented as a regulatory standard - evaluation on cognitive load and a certain level of task-based completion testing with error rates at a certain level.  Electronic medical records should be treated like medical devices/medications/equipment that should be rigorously failure tested.  While EMRs are far more complicated instruments, studies such as this one, illustrate that an EMR with interfaces designed for specific work environments to aid in effective and efficient task-completion save time and reduce errors.

The main issue I see with EMR these days is that the stakeholders and motivators behind this initial wave of implementation in financial - systems in place to capture every last level of service provided to a patient in order to increase revenues.  Now, the next generation and movement with EMRs is to look at how they can increase patient safety, particularly in light of threats of non-payment for preventable medical errors.  Again, financial motivation, but at least this financial motivation is going to motivate progress and maturation of medical records as tools to protect patients, not simply to milk them for profits.

Chest Pain and Recent Negative Stress Test

If your hospital is anything like our hospital, you have tons of low- and intermediate-risk chest pain.  Every one is stressful, but hopefully you have a friendly hospitalist, or better yet, an ED-run chest-pain unit that gives you a place for observation admissions.  They go there, get their rule-out, and get some sort of provocative test, as discussed in the most recent AHA guidelines.  The test is negative, they go home.

...and then they come back a week later with the same symptoms.

This is a great paper to have in your pocket when you need to justify why this patient still needs to be ruled out; I heard about it when it was mentioned on the April EM:RAP during the low-risk chest pain discussion.  Patients with negative stress tests may still be diagnosed with CAD on angiography - 20.7% incidence of CAD in their cohort which had negative or non-diagnostic stress within 3 years - and 7.8% were diagnosed with AMI.

When you add negative troponins and the negative stress from the previous visit, you've met the guidelines and standard of care to say they did not have acute myocardial ischemia and you cannot induce ischemia on provocative testing, and they are risk-stratified into a group of patients very unlikely to have ACS in the next 30 days/60 days/6 months.  However, you get that high NPV because you're performing these tests on a low-risk population, not because the sensitivity of those tests, particularly stress testing, is good enough.  While this patient likely does not need another provocative test - although, depending on individual factors, they may be candidates for angiography of some sort - if their story is concerning for cardiac etiology, they still need enzymatic rule-out.

Tuesday, April 12, 2011

Prehospital STEMI Diversion to PCI

Time is muscle and the earlier you get to PCI the more muscle you can save.  So, we should just drive by all the critical access hospitals and go straight to PCI-capable centers?  The Dutch, in this retrospective study, think we should.  Everything in their protocol hinges on EMS reading a computer interpretation of the EKG, and, if it says STEMI, they go to the PCI center.  At the end of the day, everyone who went to the PCI capable center first rather than the spoke hospital first had a mortality benefit between 2% and 2.6% at one year.  

What they really don't discuss much are the outcomes of the 5.7% of their intention-to-treat analysis that had false positives.  False positives, at least, are typically not harmful to the patient - the alternative diagnoses for chest pain that would benefit from immediate treatment at one of their non-PCI "spoke" hospitals are probably not that frequent - aortic dissections and submassive PEs tend to be the sorts of things that would benefit.  But, even if they did a true intention-to-treat analysis, they'd probably still have a mortality benefit.  The other problem with false positives is the financial costs associated with unneeded cath lab activation and the costs to the system associated with taking EMS out of service.  It's obvious that treating patients for their disease in the most timely fashion for certain diseases improves outcomes - but we must always beware of the unintended consequences.

This is actually a big deal sort of topic in EM right now as it relates to the regionalization of care, which is something that the Academic Emergency Medicine consensus conference is dealing with right now.  Attempting to mirror what's happened with trauma networks, they're trying to extend the benefits to other acute conditions that otherwise benefit from transfer to higher levels of care.  Clearly, a myriad of life-threatening conditions benefit from the resources of tertiary referral centers - but the logistics and political issues associated with centralizing care for different conditions remains a significant barrier.

Friday, April 8, 2011

Sodium Nitroprusside with CPR

Here's another interesting piece of animal literature to fight with your IRB about for performing studies on human subjects in your ED.  The article itself is a little hard to follow because of the terminology used - eCPR, SNPeCPR, and S-CPR, but, essentially, they have regular CPR, then they have their enhanced CPR which consists of an impedance device and compressive trousers, and then they have enhanced CPR plus sodium nitroprusside.  Additionally confounding, on top of different CPR methods, they only gave standard CPR epinephrine, while the other two methods received no epinephrine.  Sodium nitroprusside pigs did much better than the other two methods and medications.

So, with n = 8, in pigs, there's only a couple statistical conclusions we can make.  Their pigs that received their no-drugs enhanced-CPR did no differently than standard CPR with epinephrine.  Then, their pigs that received sodium nitroprusside plus enhanced-CPR do way better than their no-drugs enhanced-CPR.  So, sodium nitroprusside is doing something.  As far as external validity, 1) it's pigs and 2) it's probably financially and logistically infeasible for our ACLS-equipped paramedics to go through the additional steps of enhanced-CPR.  I'd really like to see what would have happened in a blinded, three-arm, nitroprusside vs. epinephrine vs. placebo where each group had the same CPR.

That being said, if you can get your IRB to approve a prospective study in human subjects - more power to you.  All the literature shows our current ACLS is mostly useless - and the definition of insanity is doing the same thing over and over again and expecting different results - so I'm all for looking at new agents in cardiac arrest.

Thursday, April 7, 2011

Carbapenem Resistant Bacteria in India

More public health doom and gloom from the infectious disease world - multiple bacterial found carrying stable and transmissible plasmids for the NDM-1 gene, a form of beta-lactamase that endows bacteria with carbapenem resistance.  In the sewage.  And in the drinking water.

...but only South Asia, for the time being.  But, they also note that India is a popular destination for "medical tourism" to save money on surgical procedures, and patients have returned as carriers for bacteria with the NDM-1 gene.

This is not a unique development - there's MDR tuberculosis, inducible clindamycin resistance for MRSA, and, my favorite, macrolide-resistant streptococcus.  Macrolide resistance in streptococcus can be directly linked to the overuse of azithromycin, a patient-friendly drug with terrible pharmacokinetics.  In contrast to the medication it replaces, erythromycin, it has such a long half-life (68 hours when multiple doses are administered) after you take your fifth dose that it spends a long period in the body below its therapeutic concentration, just sitting there as substrate to induce resistance without bacteriostatic properties.


Wednesday, April 6, 2011

Antibiotics for Acute Otitis Media

These are two articles coming to us from January's NEJM - one from Pittsburgh and one from Finland.  For a ridiculously prevalent disease managed daily in the ambulatory setting by thousands of providers across the world, we really don't know what we're doing.  Firstly, we know there are bacteria in the middle ear - plenty of studies have aspirated out a variety of pathogens.  Secondly, undertreated AOM may lead to suppurative complications - the surgical emergency of mastoiditis.  Finally, however, we also know the natural history of AOM is to resolve without intervention and treatment in most cases.

The commentary accompanying these articles seemed to think these two studies tilted the balance in favor of routine antibiotic use for AOM.  And, you can read the articles in that fashion - the Finnish article makes an argument that by their standard of care, the placebo group had 45% treatment failure and required antibiotic rescue 30% of the time.  However, I read the article and their definitions of treatment failure are, for the most part, not clinically relevant.  A red ear that still looks red on day three does not predict much - and, actually, a lot of their primary outcome measures were not statistically significant until they added in the 30% they used rescue treatment on to boost their definition of treatment failure.  So, this study doesn't tell much much - except that Augmentin causes diarrhea 40% of the time.

The Pittsburgh study reads much more straightforward and, partially, justifies my criticism of the Finnish study.  By day 7, 80% of their Augmentin group had symptom improvement compared to 74% of their placebo group.  However, the ears still looked terrible in the placebo group - but, obviously, weren't correlating with symptoms.  So, is it clinically relevant to define treatment failure based on the appearance of the ear?  I would say that improvement in symptoms is the appropriate measure of clinical cure - and in that respect, the 80% vs 74% numbers match up better with previously published literature.

To me, these articles don't help.  I don't necessarily mind the AAP recommendations of treating AOM with antibiotics under a year of age - although, really, after their third set of immunizations, it's not as though this is going to be a nidus for SBI.  Clearly, antibiotics offer some advantage - but not to everyone.  When I have a three year-old I have to hogtie to get a one-second glimpse at a red TM, how do I know whether this is a patient whose AOM will resolve on its own, or whether he falls into the subset of patients who will derive benefit from antibiotics?  And, is that 6% absolute difference in clinical outcome worth giving 40% of children horrible diarrhea (not that anyone uses Augmentin first-line for AOM, anyway).  With the NNT with antibiotics to prevent one case of mastoiditis estimated at 4100 from cohort data from the United Kingdom, that's a lot of useless (and harmful) antibiotic prescriptions.  If we want to reduce the amount of antibiotic resistance in this country, I think these studies support a conservative non-antibiotic strategy initially in appropriately selected patients.

Addendum 5/11: Scott Weingart & David Newman did a bit of a rant on this topic on the most recent EM:RAP where they attacked the Pittsburgh article specifically regarding result reporting integrity.  Dr. Newman delved into far more detail regarding the multiple primary outcomes listed and found the original research protocol listed only time to resolution of symptoms as the primary outcome - which was statistically equivalent between the two groups.  He and Dr. Weingart seem to suggest there was not sufficient editorial oversight regarding the publication of this article due to these flaws, and that the author's conclusions are suspect to the point of disingenuous.

Tuesday, April 5, 2011

Mandatory EKG Screening for Athletes

Discussion today in the public forum about this article:

Has been going around the internet.  I only have access to the abstract, however, so I can only base my discussion on what data I see there.  This is one of those articles that reviewed the rate of death in NCAA athletes for the last few years, and, essentially, they found that the incidence of sudden cardiac death was 2.28 event per 100,000 participant years.  The commentary in the media: if only we had better screening!

Well, they tried that in Israel.  Mandatory EKG screening was instituted in 1997 in an attempt to curtain SCD in athletes.  The death rate before screening was 2.54 events per 100,000 participant years.  Afterwards, 2.66 events per 100,000. 

So, yes, if only we had better screening - because EKG alone doesn't cut it.  EKG + echocardiography?  EP study?  At some point, you have to take a rational look at the costs of something and realize it's not taken out of an infinite pool of money - money that almost certainly could be put towards a much higher yield public health effort.  Reactionary calls for more screening at this time are simply increased costs without proven benefit.

Monday, April 4, 2011

Olanzapine Versus Droperidol

This is a fun study because it's always nice to have new things to try for common problems.  Keeps life interesting.

I started out residency taught to use metoclopromide+diphenhydramine for treatment of refractory headache in the Emergency Department.  And then I discovered droperidol.  Yes, there are studies out there that say prochlorperazine is equivalent to droperidol in efficacy, but prochlorperazine gives people the same akathisia that metoclopromide does.  Droperidol kills people dead, if you believe the black box - though I don't.  The QT-prolongation is essentially no different than ondansetron, the supposedly-safe alternative we now use for nausea.

In any event, now you can add olanzapine to your mix.  You can legitimately critique the study because the p-value for pain improvement between olanzapine and droperidol was actually 0.30 in favor of droperidol  - so without more power and/or a second confirmatory study, you can say it really might not be as effective.  But, the good thing is, nearly everything has some legitimate effectiveness - and the more different classes of medication you have available to knock down that headache, the better.

Suntory Yamazaki 12-Year

EM literature, you say?  Well, in addition to reading and critiquing literature, I've begun to enjoy trying new and interesting Scotch, and tonight the tasting is Suntory Yamazaki.

Now, the purists among you are absolutely correct that the Yamazaki is not Scotch - technically, it is a single-malt whiskey - because it is not from Scotland.  Where I'm at in North Carolina, there are government-run ABC stores that all tend to have a generally homogenous selection of the major distributors, with very few "interesting" Scotches.  On my way back from SAEM this past weekend, we walked by an ABC store in Virginia, where, in contrast to North Carolina, the stores are open on Sunday.  Curious to see if their mix was any different than ours, I popped in to look - and picked up this slightly more exotic selection.

I'm not a Scotch snob, so I'm not going to give you a play-by-play of the vanilla vs. cardamom vs. brine-soaked Wellingtons on the palate.  It's either bland, tasty, or delicious with me.  This one qualifies as tasty.  Sweet, pleasant nose, enjoyable finish.  Would not hesitate to buy a reasonably priced bottle from this distillery again.  I'm sure the connoisseurs among you would probably prefer the 18-year, but in the $40-odd range for Scotch-style whiskey, going up against the introductory-level McCallen, Glenmorangie, etc., it won't disappoint.

ASPECT 2-Hour Rule-Out

Low-risk chest pain - if your ED doesn't already have a chest pain unit set up for you to painlessly move patients through their enzymatic and non-invasive testing, you're probably trying to find safe ways to discharge your chest pain patients home to avoid the repetitive calls to an unsympathetic hospitalist.  Problem is, without some kind of imaging or functional study, you're going to invariably get burned.  This is another one of the TIMI-score-plus-X attempts at risk-stratifying patients in a prospectively applied dry run of their protocol.  It's TIMI 0 patients plus normal EKG plus negative zero and two-hour CKMB/troponin/myoglobin.  Basically, 10% of their chest pain cohort fit this essentially zero-risk profile and were enzymatically ruled out.  And 0.9% (0.02 to 2.1%) of this slam-dunk non-cardiac group came back with an MI within 30 days.

Now, for a rational person who thinks that we're spending altogether too much money and resources to capture every last potential cardiac event - that sounds pretty reasonable.  Home with follow-up.  The problem is, the non-invasive testing in basically the same sort of low-risk cohort, whether stress or CTA, the negative tests have 6+ month event-free periods.  So, the standard of care is unfortunately moving away from "no heart attack today!" to prognosticating distant events.

The other great thing about this article was their mini systematic review where they say there's 115 of these prediction rules in the literature in the last fifteen years.  Clearly someone everyone wants, but also something we can't get right....

Saturday, April 2, 2011

More Sensitive Troponin Assay Saves Lives?

These authors show us something very interesting about "negative" troponin testing in their prospective review.  Like my facility, they had an assay with a certain level of detectability.  I will say, though, that their assay detection level of 0.20 ng/mL is different than our assay, that goes down to 0.02 ng/mL.  But, basically, they implemented a new assay that was sensitive down to 0.05 ng/mL but didn't tell their clinicians any of the newly detectable troponin numbers below 0.20, but they built a database of the cohort in that detectable-but-previously-undetectable range.  Then, they showed clinicians their new detectable numbers and let them do what they wished with it.  It turns out, the population with the 0.05 to 0.20 troponins had similar cardiac morbidity/mortality risk as their >0.20 troponin population - while the truly undetectable did much better over their 1-year follow-up.

Additionally, after the new threshold was introduced, clinicians treated the 0.05 to 0.20 more similarly to the >0.20 group with additional testing, cardiology consultation, and medications - and their outcomes improved 20%.

So, this study really makes you think what it means to have a "negative" troponin and wonder what the disposition and follow-up should be at different points.  At my institution, we've traditionally said 0.10 ng/mL is the cut-off for "positive", and the lesser, yet still detectable troponins, are "negative".  But, this study clearly suggests that a lot of the patients we're labeling "negative" really need to have more aggressive treatment.  This study doesn't tell us whether they need to be inpatient, or have expedited follow-up, or precisely how to manage them in order to improve their outcomes, but it suggests a lot of great new questions to ask regarding how to use the information we receive from our troponin assay.

The Cost-Effectiveness of Cardiac CTA

I was really hoping this would be a great article that convinced me that my hesitancy towards cardiac CTA is unfounded.  I feel, based on the literature, that we're misusing cardiac CTA - or at least, the current generation of technology and reconstruction methods aren't leading us in the right direction.  Angiography, whether radiographic or invasive, describes anatomy, and then we use the anatomy as our basis whether to attribute chest pain to cardiac causes or not.  Many situations, this works - the STEMI goes to the cath lab and the occlusion correlates with symptoms.  But, we're trying to use CTA in our low-risk population to draw conclusions about the etiology of chest pain - and it's much harder to say someone's troponin-negative and EKG non-specific chest pain comes from a stenosis of a certain percentage.

The problem with their article is that they completely underestimate the number of false-positives cardiac CTA is generating.  There are several articles out there showing that the population considered for cardiac CTA is generally a population that just does great in follow-up, and that the number of negative follow-up studies generated after cardiac CTA - nuclear stress and invasive angiography - tend to far outnumber the number of positives.  They base their cost estimates on numbers that just don't reflect reality, and I just can't believe that cardiac CTA is a test that saves money and gives me better answers compared to functional cardiac testing.  If you wanted to use it as a screening tool for identifying a population that needs aggressive secondary-prevention of progressive atherosclerotic coronary disease, it would do great at that - but we know that plenty of ACS comes from ruptured plaque and hemodynamically insignificant disease, and someone who had a "negative" cardiac CTA that morning doesn't preclude them from needing an enzymatic rule-out.

Patient Reported Symptoms in STEMI and NSTEMI

Here's an article with a lot of great numbers to keep you from sleeping well at night.  It's a prospective look at the symptoms patients present with when their eventual diagnosis is STEMI or NSTEMI.  6.4% of their STEMI patients and 5.6% of their NSTEMI patients didn't complain of any chest symptoms (pain, pressure, etc.).  There's a lot of arm pain, epigastric pain, shoulder pain, and then multiple anginal-equivalents on their list of symptoms, but it's a great example showing that if you write off ACS in your patients without chest pain, you're going to get burned - 1 in 16 STEMIs in their cohort.  Even better, only 45.1%/53.9% of their patients thought their symptoms were cardiac related, which probably means there's a population of STEMIs just sitting at home figuring they'll feel better in the morning....