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.
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.
…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.
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 meningitis…in 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.
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.
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.
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.
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.
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.
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.