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.

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.

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.


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.


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.


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.

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.

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 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.


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.


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.