Not exactly the article I was expecting when I pulled it, but mildly interesting nonetheless. The real applicability of this article is towards those folks who say the LP for SAH is outdated, and we should just proceed with CTA to identify the culprit aneurysm.
As opponents say, many aneurysms identified by CTA are asymptomatic and unrelated to the acute headache in the Emergency Department, and, without the LP, you don’t know their clinical relevance. This study lets them also say that CTA doesn’t even necessarily perform well enough at this task to warrant use – it will miss 5% of aneurysms and overcall 3.8%.
However, it must be said, this meta-analysis uses data from a number of old studies that have older CT scanners that were very poor at detecting <4mm aneurysms. Once you get to 16 and 64 row CT, your sensitivity is closer to 98-99% – and then you have to fall back to the asymptomatic/clinical relevance argument.
“Diagnosing cerebral aneurysms by computed tomographic angiography: meta-analysis”
Catheter-based endovascular treatment of acute ischemic stroke has been around for several years – this is a nice, concise review of the published literature regarding their use.
The abstract sounds a little more favorably skewed than the actual content of the article – their discussion is appropriately skeptical regarding the efficacy and applicability of this particular treatment modality. It is certainly true that restoring flow to affected regions in stroke is advantageous, and the theory behind the use of these devices is to mechanically ensure open vessels in situations where systemic thrombolysis may not be efficacious and the disability is likely to be profound.
The problem is, there really isn’t any “evidence” in this article. The published literature on this topic is primarily retrospective cohort/case-reports by industry-affiliated inventors of these devices and, even despite this bias, that literature tends to report unacceptable levels of procedural complications while trying desperately to show benefit.
Regardless, as the authors mention, there are many studies of MERCI and Penumbra ongoing – slowly chasing that inexorable statistical probability of finally performing enough studies that, by chance, one of them will be favorable enough upon which to base widespread marketing efforts.
“Neurothrombectomy devices for the treatment of acute ischemic stroke: state of the evidence”
The sodium-channelopathy that went many years before being described, now increasingly well-known. More interestingly, the phenotype is apparently autosomal dominant in inheritance. These investigators use this inheritance to retroactively diagnose deceased family members with a Brugada cause to their sudden cardiac death.
They found, unfortunately, that not only were most individuals who died of Brugada young, most were asymptomatic – and of the five patients for whom they could find an antemortem EKG, only one of them had a typical Type I Brugada pattern, and one had a single lead with a Type III pattern.
I think my take-home point from this article is that, in the young patients presenting with syncope, it’s important not just to do the EKG, but also to enquire regarding family history of sudden cardiac death – and then hope whatever cardiologist you refer them to is insightful enough to order a amajaline provocation test if needed.
These are a couple studies from a family of publications that use population data, GIS mapping tools, and travel times by air and ground to estimate what percentage of the population has access to a certain healthcare resource. In these two papers, the resources in question are Primary Stroke Centers and Pediatric Trauma Centers. They estimate that 71% of the pediatric population is within 60 minutes of a pediatric trauma center by ground or air – which is appropriate, because trauma systems are set up to use aeromedical transport. However – and, depending on what direction the TPA pendulum swings – only 55.4% of the population has access to a stroke center within 60 minutes – by ground, which is typical. They say this could be increased to 79% within 60 minutes if aeromedical resources were involved, but I think we should wait to establish a greater treatment effect for acute stroke treatment before we go nuts with air travel.
I like maps; I worked with one of the authors (Dr. Branas) on previous iterations of descriptive articles similar to these. The problem with these articles is the statistic they describe – timeliness of care – may or may not have significant effects on patient outcomes. And, in theory, the solutions – moving trauma center designations, establishing new stroke centers, increasing aeromedical use, etc., have significant costs and unintended consequences.
Another interesting article regarding shoulder reduction techniques.
Essentially, what I read into shoulder reduction is that – if there many usually successful ways to do something, pretty much anything works. And, what seems to be the generally accepted way to do it – excepting the scapular manipulation technique – is pulling on it. What is different between methods seems to be how exactly you apply the traction.
This is a single-operator method with direct axial traction on the distal humerus with one hand and counter-traction on the acromium with the other hand. The trouble I foresee with this method is that you’re fighting a lot of large muscles on the patient with your own, smaller, rotator cuff and shoulder abductors. I think you’d end up fatiguing before a lot of your patients.
The variation I might suggest is the snowbird technique, where you use the weight of your leg to provide downward traction via stockinette around the forearm. You can sometimes get away from having to do full procedural sedation if you can perform a technique like this where the patient fatigues before you do.
When NovoNordisk writes an article analyzing safety data from the CONTROL trial, you get a skewed perspective on the data. Specifically, if you only read the abstract, you’re going to think that it’s safer in some ways(ARDS was less), and there was no difference in adverse events (except for all that investigator-reported AMI/NSTEMI). So, that sounds favorable.
But, the real reason there’s no significant differences in outcomes – and the reason why they terminated the trial early – is because the interim data is underpowered to detect a difference. As you see, the 30-day mortality is 12% vs 11% in favor of placebo – and that wasn’t helping NovoNordisk, so they quit before they could reach sufficient statistical power to prove their product was unhelpful. However, they can now benefit from that same lack of power to detect differences by applying it to the safety aspect, and trumpeting its equivalency in terms of AEs.
When taken in the context of the original trial, this is just a flawed piece of pharmaceutical propaganda to try and prevent the building crackdown on off-label Factor VII use.
The ACEP guidelines still have, as level B recommendations, that a single cardiac biomaker “8 to 12 hours” after symptom onset is adequate to exclude the diagnosis of NSTEMI.
This study looked at all of Highland’s patients that received more than one troponin measurement in their ED. Then, they looked at all the patients with initially negative troponins, and subsequently positive ones. And, finally, they tried to see how many of those had symptoms >8 hours. Their definitions are that troponins <0.06 ng/mL are negative, between 0.06 and 0.6 are indeterminate, and >0.6 are positive.
After starting with 5,596 patients, they had 125 that were negative initially, and then positive. And, for symptoms greater than 8 hours, a grand total of seven troponins ≤0.06 ng/mL and then subsequently positive, and 18 others that were indeterminate and then subsequently positive. They then say only two had a diagnosis of ACS.
Regardless, despite the size of the study, when you start talking about these sorts of tiny numbers and getting into splitting hairs on the diagnosis, you’re basically working on anecdotal evidence. So, take it with a grain of salt – you’re usually safe in a patient with that symptom duration, but you’re working off mostly consensus opinion as opposed to great evidence.
More interesting, really, would be some kind of follow-up on the 1,086 patients that were discharged after a single negative troponin (many of which probably fulfilled the >8 hour criterion) – but there’s no way to actually make that sort of follow happen realistically.
Disclaimer: I despise CCTA for low-risk chest pain in the ED. It leads to additional unnecessary testing, interventions, and harms that outweigh the risk of coronary events in its target population. Our liability-sensitive practice has us evaluating an ever-increasing cohort of low- and (mostly) zero-risk young chest pain patients, and this is purported to be a test of choice for identifying a zero-zero risk population.
But there are just far too many false positives that have coronary artery disease of uncertain clinical significance.
This is a Korean study that compared 1000 matched controls that did not undergo CCTA with 1000 who did. 215 asymptomatic patients had positive CCTA – defined as any atherosclerotic plaque. 52 had >50% stenosis and 21 had >75% stenosis.
Their control cohort and their CCTA cohort were very similar – and 55-59% low risk, 34-29% intermediate, and 10% high risk based on NCEP risk stratification.
And their control group had a grand total of 1 cardiac event within their 18 month follow-up period, as did a single person in their positive CCTA group. However, the CCTA group ended up with more additional testing and cardiac revascularization procedures during their follow-up time frames – with no change in outcomes.
Now, these are asymptomatic patients chosen for screening – not the same as our chest pain patients in the ED – but it’s another call for caution regarding overtesting and overtreating.
Is it too late to buy stock in the company that makes linezolid?
This group up in Detroit reviewed 320 patients with MRSA bacteremia and found that 52.5% experienced Vancomycin failure. Their conclusion states several significant OR for failure, but review of the between-group differences doesn’t show a lot of significant differences. Nursing homes, for example, were the only p < 0.05, and predicted vancomycin success with a p of 0.02.
What is more important than their clinical predictors, however, is their review of the bactericidal activity of vancomycin – and that higher MICs and higher troughs are needed to effectively treat patients. I’ve seen our pharmacists recognize this at my hospital as well – the 1g IV Vancomycin standard initial load is transitioning to a weight-based dose.
But, more importantly, what we’re probably really observing is the initial stages of the end of vancomycin’s utility for MRSA. And, I hate to see what happens when TMP/SMX stops working, too….
Another over-testing over-diagnosis article effectively illustrating issues endemic to our current medical culture.
They do a retrospective national database review regarding the impact of the introduction of CTPA protocol for rule-out PE, and note that we’ve diagnosed three times as many PEs in 2006 as we did in 1998. And, by detecting more PEs, we managed to reduce mortality attributed to PE…along the same gradually decreasing trendline that was present prior to the introduction of CTPA.
Figure 2 is the truly damning graphic – look at all those extra PEs we’re finding and treating for effectively no substantial benefit. Their secondary analysis was in-hospital anticoagulation complications on patients with any diagnosis of PE, which has jumped 71%. Thank goodness we can put them on dagibatran now instead of coumadin and not be able to reverse their life-threatening bleeding episodes….
Again, we are testing people who shouldn’t be testing, finding disease of uncertain clinical significance, and harming them with overtreatment – and let’s not even start with the costs.