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.
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.
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.
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.
…when taken in inappropriate amounts.
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.