Our EMR lets us generate reports of our 72-hour returns – and it’s a fun toy, but, reading through it is rarely illuminating. On a rare occasion you see a “true miss”, where one of your colleagues finds something through another line of thinking. But, mostly, it’s wound checks, admissions for failed outpatient antibiotic therapy for cellulitis, or the town drunk coming back in again. It is a valuable tool, at least, in the sense that our ED is the only one for 40 miles and is the only tertiary center for 90 miles, so we should get most of our own bouncebacks.
This is a paper cited in the most recent ACEP Weekend review that tries to draw more profound conclusions than it probably should.
It’s another piece of the growing body of literature that says “Hurry! Prehospital activation is all we need in STEMI!” From Israel, it’s a retrospective review of performance variables and patient outcomes between a cohort that was assessed in the ER and a cohort that went straight to the lab. They draw a few conclusions, some of which are valid.
First, time. One of the two “primary” outcome variables is door-to-balloon time. No argument that skipping steps along the way will save you time. No study is needed to prove that.
The second “primary” outcome variable is MACE within 30 days – another combined endpoint kludge of death, CHF, reinfarction, CVA, TIA, and urgent revascularization. This one favored the direct-to-ICCU group, 22% to 30%. How is 30-day CVA/TIA directly related to the effectiveness of PCI? Looking at their secondary outcomes – death was not significantly different – but CHF was 8% different, which therefore accounts for essentially the entire difference between groups in this primary outcome.
And the problem? Well, they also show in a secondary outcome that LVEF >30% was 7% greater in the direct-to-ICCU group…from which it follows there would obviously be less heart failure in that group. But, in their demographic information, they don’t know the pre-intervention LVEF for their patients – only the Killip class on presentation, which is a measure of the heart failure associated with the acute cardiac event, not their pre-existing LVEF.
So, the only thing they’ve effectively proven in this study is that skipping steps saves time. And, they don’t comment on the number of false positives in each group, either.
…or, at least, that’s the gist of the New England Journal Article making rounds in the news.
And, while a close reading of the article doesn’t offer great support for harm, it certainly supports saying that albumin, saline, or nothing were equivalent.
The absolute difference in survival was 3% – and, looking at the demographic breakdown, there were 2-3% differences or trends in favor of the control group regarding dehydration, acidemia, base-deficit, and bacteremia. Enough that it lets me cling in denial to standard practice and teaching here in the U.S., in addition to whatever you want to say about external validity of a study in resource-poor settings in Africa.
It is an odd and unexpected finding, so say the least. The authors attribute at least part of the unusual discovery to the high percentage of malaria cases they treated, and that fluid resuscitation in malaria is controversial – but regardless, this is going to be a frequently discussed study on the Pediatric Critical Care side of things for some time. I also expect follow-up confirmatory studies to be a tough sell to U.S. IRBs.
“Red cell distribution width is a robust predictor of… all-cause patient mortality.”
I saw this article when I was browsing abstracts, and I thought, “Huh! That sounds interesting, though, probably not relevant.”
So, yes, increasing red cell distribution width is associated with increased mortality. However – and this is something I’ve never seen before in an article – looking at the table describing the differences between their various divisions of RDW% – every other descriptive statistic is different between groups. More septic patients with high RDW%. More renal failure. Differences in hematocrit. More organ failure. They claim by statistical multivariate massage, that RDW shakes out as an independent factor, but, sheesh…it’s almost like saying decrease in temperature is highly associated with death, when they’re cold because the blood isn’t circulating, the breathing has stopped, the brain has shut down, etc….
Another fine example of where reading the abstract is absolutely no replacement for perusing the article.
Another sort of goal-directed sepsis study, this time in Pediatrics at Primary Children’s. They implemented a protocolized triage system in their ED designed explicitly identify more cases of sepsis – which led to increased percentages getting early fluid resuscitation, early lactate level measurements, and more frequently antibiotics in the first three hours.
An important negative study of an inflammatory biomarker that’s been getting a fair amount of push.
It is absolutely true that procalcitonin levels may be elevated in an inflammatory states such as sepsis. This group tried to make a clinically relevant protocol for procalcitonin trends by saying, if the procalcitonin level is not decreasing with current therapy, then antibiotic coverage should be expanded and aggressive testing should be undertaken to evaluate for missed source control.
Unfortunately, in the treatment arm where procalcitonin was used in clinical decision making, there was extensively greater broad-spectrum and multiple-antibiotic utilization without any demonstrated mortality benefit. In addition, LOS and ventilator-depended days were longer in the procalcitonin arm.
There were very minor differences between the two groups, probably favoring the control, but not nearly enough to suggest that procalcitonin has any value in assessing failure of current therapy.
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.