By some measures, at least, you can claim that the Health Reform is working. I’ve seen a few articles out there saying it failed, because ED visits continue to rise. But, if this study is reliable, the increases in ED utilization are a result in increased illness severity, not inability to access a physician.
Non-acute visits for the uninsured/low-income cohort in Massachusetts went down, from 43.8% to 41.2% – a greater decrease as compared to their “control” group of private insurance that is supposedly unaffected by health reform, which decreased from 35.7% to 34.9%. So, one way to interpret this is that increased access has kept some of the non-urgent uninsured out of the ED.
…but they’re still seeing, by their definition, a solid nearly 40% of patients in our EDs that have less than a 25% of requiring true Emergency Department care. So things have incrementally improved – but the problem is not simply that a patient has nominal access to a PMD, they actually need to be able to access that PMD on a semi-urgent basis to truly reduce ED utilization…and that PMD needs to be more than simply a revolving door back to the ED.
Interesting analysis of the EMSHOCKNET cohort, looking to see if there was any association between time to antibiotic administration and survival benefit in septic shock.
And, no. Earlier antibiotic administration, as measured by arrival time in the the ED, showed no significant impact.
They do another secondary analysis where they try to say, well, if the patient received antibiotics before they met criteria for septic shock – then they had a 2.59 (1.17 – 5.74) OR for survival. I’m not sure how to interpret this finding – perhaps because they looked at 10 different cut-off points for antibiotic administration, they found one that favored antibiotics by chance.
Or, perhaps antibiotics really aren’t the lynchpin in treating sepsis – if you can give antibiotics ahead of SIRS, perhaps you have a milder case – but once you have end-organ dysfunction, the interventions that target improving the physiologic changes of sepsis are more important.
These are a couple interesting commentaries regarding the state of clinical evidence and the difficulty of applying it at the point of care. One, from the BMJ, worries about the sheer number of studies and trials being generated, and that the data will never be able to be appropriately digested, and we’ll all die slow deaths from information overload. And, to some extent, this is true – how many of us carry around “peripheral brains” in our pocket? Before smartphones, it was the Washington Manual or Tarrascon’s, and now we have MedCalc, Epocrates, etc. And, we desperately try to simplify things so we can wrap our brains around it and integrate it into a daily practice by distilling tens of thousands of heterogenous patients into a single clinical decision instrument like NEXUS, CCT, CHADS2, etc. While this is better than flailing about in the dark, it’s still repairing a watch with a hammer. These tools tell us about the average patient in that particular study, and have only limited external validity towards the patient actually sitting in front of us.
Dr. Smith’s BMJ article proposes the “machine”, which is a magical box that knows all and provides seamless patient-specific evidence. Dr. Davidoff isn’t sure that’s feasible, and, as a stopgap measure, promotes the rise of the informatician or medical librarian, a new role for utilizing the available electronic health databases. This librarian will be expert in reading medical literature, will be expert in data mining healthcare information systems, and discover the most relevant ways to target quality and guideline improvement initiatives.
They’re both right, in a way. And we should definitely train and mature the growing discipline of this clinical informatician while we keep working on the magic box….
I like that the big focus these days is on increasing cerebral perfusion pressure in cardiac arrest – sure, we can focus on more interventions to flog the heart back into coordinated activity, but, sometimes, it’s just not going to happen. But, for when we are able to get the heart rolling again, unless you’re a big organ donation proponent, we need to preserve neurologic outcomes. After all, that’s where a lot of our studies of ACLS fall off – we get short-term ROSC, but survival to hospital discharge is unchanged because the brain is unrecoverable.
Here’s another trick in pigs – sustained AA pressure resulting in measurable increases in CPP. Better CPP = better neurologic outcomes in other studies. Seems like a no-brainer.
I particularly like this intervention because it’s basically no-cost and should be easy to test for outcome efficacy in humans.
A nice comparison of the sensitivities and specificities of the various biomarkers for acute myocardial infarction at ~3.5 hours after symptom onset. Each biomarker was set at the 95th or 99th percentile based on manufacturers definitions for their reference table, and then they also show ROC curves and calculate AUCs for each.
Essentially, none of the biomarkers is completely adequate for ruling out AMI given the constraints of their study. Their best combination, for both sensitivity and specificity, is combining the heart fatty acid binding protein and the troponin – which they state provides an NPV of 95.6%, outperforming the “triple rule out” of troponin, CKMB, and myoglobin at 92.1%. Interestingly, they also state that if they used clinical risk stratification, they could select a population in which HFAP and troponin together get up to 96.9% NPV…showing that regardless the resources we throw at the problem of “low risk chest pain”, it is an absolutely Quixotic quest to definitively rule out every MI in the Emergency Department. 3% of their “very low risk” population that was biomarker negative with the best sensitivity they could muster ended up ruling in for AMI during their subsequent hospital stay. They only way we’re going to prevent healthcare from becoming bankrupt is increasing our levels of acceptable risk.
As a side note, this article gets the award for “best vs. least professional” title so far this year.
The presence of near-daily updates is somewhat an artifact that I’ve had an easy time finding interesting research papers to queue up, plus I’ve been in a bit of a lull regarding clinical responsibilities.
The eventual goal will probably be to have something up 3 to 5 days a week from myself, and, if other clinicians start contributing, then, even more than that.
Speaking of which, if you’re at least a senior resident in Emergency Medicine, have opinions, and like writing little blurbs about new literature, you’re welcome to drop a comment regarding potentially contributing to this blog.
Or, alternatively, never bathe in fall and winter.
Data mining expedition evaluating the event rate of out-of-hospital arrest where activity could be determined, and then using the Japanese averages of time-per-day to evaluate for hourly rates of arrest per activity.
Working was the most cardioprotective per hour spent – and it had the best ROSC and survival, mostly because it was highly witnessed. Sleeping and exercising were riskier behaviors than working – sleeping moreso, because it was infrequently witnessed and had minimal survival. So, you might as well just keep working.
But, definitely don’t bathe because 1) no one is watching you bathe, so the survival is dismal and 2) the risk of cardiac arrest was a preposterous 40 times greater than working, and when the time of year was taken into account, bathing in cold winter months led to up to 100-fold increase in arrest rate.
The authors believe this is specifically related to Japanese homes being poorly insulated, leading to predictable large blood pressure drops when entering their traditional very hot baths.
Work harder, live longer.
Retrospective data out of the ketamine vs. etomidate prospective survival study.
Doesn’t prove anything – and it makes me want to go back and look at the original ketamine vs etomidate article to see if difficulty of intubation was included as a demographic factor – and, I wish this study indicated which sedative medication was used as well.
In any event, the more complicated an intubation was, the more likely there were complications with the intubation. And, further down the road, more patients who had intubation complications were deceased at the end of their follow-up period. Things that predicted complications during procedure included age, illness severity, BMI, specific medical disorders, respiratory distress, and difficult intubation.
Nothing here changes practice – since intubation is not an elective procedure. This is more a recognition that, yet again, sick people die.
While the protections for individuality make America the colorful place it is today, it sure is easy to run massive cohort studies in European countries where they sacrifice a little bit of anonymity for the common good.
Everyone in Denmark has a number, and they tracked every patient in Denmark with a history of MI to see if they had any adverse events after receiving a prescription for NSAIDs. There were a few significant differences in the populations receiving each different kind of NSAID – rofecoxib and celecoxib tended to be given to older, female populations, and there were some differences throughout their groups regarding the prevalence of other co-administered cardiac medications.
This article really annoys me because the page with which they present their incidence of death by week has six charts that lend themselves immediately to visual comparison – but their chart scales are grossly different. Ibuprofen looks terrible at first glance, but then you realize it has the smallest y-axis scale, and actually performs quite well. In the end, they all demonstrated worsening of outcomes regarding death/MI compared to the total study population rate of death/MI not proximate to NSAID use.
In the end, ibuprofen and naproxen had the least effect on the OR for death; it is fair to avoid rofecoxib, celecoxib, and diclofenac in your routine prescribing without specific indications.
I have to say, the outcomes of this study both surprised and did not surprise me. A couple years ago, I read a few articles regarding erythropoietin administration in animal models of myocardial ischemia, and they actually tended towards cardioprotective effects. However, there have been some other retrospective reviews looking at erythropoietin levels in humans that have not been quite as conclusive.
The efficacy cohort rather favored the intervention group – the most important significant difference was primary vs. rescue PCI, and significantly more EPO group patients received primary PCI. But, then, their results section is mostly a long list of non-significant differences, and some secondary outcomes favoring placebo. Adverse events also favored placebo. So, I don’t think we’ll be seeing EPO on the code STEMI order sheet anytime soon.
As another aside, and sort of a follow-up to the Annals of Internal Medicine article a month ago regarding conflicts of interest in the new ACC Guidelines – the disclosure list for this article is massive. It is clearly the standard of care in Cardiology to be on the payroll of multiple pharmaceutical companies in one fashion or another.