Quite bluntly, you’re more likely to die.
These authors analyzed the 2008 Nationwide Emergency Department Sample, using 4,225,973 patient encounters as the basis of their observational analysis. The absolute mortality differences between weekday emergency department presentations and weekend emergency department presentations is tiny – about 0.2% difference. However, this difference is very consistent across type of insurance, teaching hospital status, and hospital funding source.
The NEDS sample did not offer these authors any specific explanation of the “weekend effect”, but they expect it is due to decreased resource availability on weekends. The authors note specific systems in place (e.g., trauma centers, PICU, stroke centers) where weekend staffing is unchanged have demonstrated the ability to eliminate such weekend phenomena. However, it’s probably never going to be the case that weekend shifts are less desirable – so we’re probably stuck with this slight mortality bump on weekends.
“Don’t get sick on the weekend: an evaluation of the weekend effect on mortality for
This article is an overview of the critical procedures performed over a one-year period at Cincinnati Children’s, a large, well-respected, level 1 trauma center with a pediatric emergency medicine fellowship program. In theory, this facility ought to provide trainees with top-flight training, including adequate exposure to critical life-saving procedures.
In that one year period, the PEM fellows performed 32 intubations, 7 intraosseus line placements, 3 tube thoracostomies, and zero central line placements. This accounted for approximately 25% of all available procedures – attending physicians and residents poached the remainder of procedures during the year. Therefore, based on this observational data, these authors conclude the training in PEM might not be sufficient to provide adequate procedural expertise. Then, the authors note pediatric emergency departments have such routinely low acuity – 2.5 out of every 1,000 patients requiring critical resuscitation – that it is inevitable these skills will deteriorate.
Essentially, this means the general level of emergency physician preparedness for a critically ill child is very low. PEM folks might have more pediatric-specific experience – but very limited procedural exposure – while general emergency physicians perform procedures far more frequently – but on adults. The authors even specifically note 63% of PEM faculty did not perform a single successful intubation throughout the entire year.
Their solution – which I tend to agree with – is the development of high-quality simulation tools to be used for training and maintenance of skills. Otherwise, we won’t be providing optimal care to the few critically ill children who do arrive.
“The Spectrum and Frequency of Critical Procedures Performed in a Pediatric Emergency Department: Implications of a Provider-Level View”
The Annals of Emergency Medicine Journal Club regarding IST-3 has been published as free fulltext online. This article was written by myself, Yashwant Chathampally, and Gregory Press at The University of Texas Health Science Center at Houston.
It may be downloaded here:
“rt-PA and Stroke: Does IST-3 Make It All Clear or Muddy the Waters?“
Recent medical school graduates are familiar with the Step 2 Clinical Skills examination, a day-long charade of simulated clinical encounters intended to screen out medical students who are incapable of functioning in a clinical setting. This test was adapted from the ECFMG Clinical Skills Assessment, intended essentially to screen out foreign medical graduates with inadequate communication skills to safely practice medicine in the United States.
However, U.S. and Canadian medical school graduates pass this test 98% of the time on the first attempt, and 91% of the time on a re-attempt. This means each year $20.4 million are expended in test fees – and probably half again that amount in travel expenses – to identify 30-odd medical school graduates who are truly non-functional. The authors of this brief letter in the NEJM suggest, with interest compounding secondary to medical school debt repayments, it costs over a million dollars per failed student.
Clearly, some medical students are not capable of functioning as physicians. However, clinical skills teaching, evaluation, and remediation ought to be part of the purview of the medical school training program that has multi-year longitudinal experience with the student, not a one-day simulation. I’m sure some of the few who fail Step 2 CS twice are capable of safely practicing medicine, and certainly many who pass Step 2 CS still require additional teaching. I agree with these authors that this test is an expensive and ineffective farce.
Then again, as this NYTimes vignette points out, medical schools are having a tough time failing folks for poor clinical skills. However, the solution is not to pass the buck along to the NBME.
“The Step 2 Clinical Skills Exam — A Poor Value Proposition”
Featured today as a guest blog, revisiting the JAMA Clinical Evidence synopsis critiqued last month on this blog, here and here.
It’s rather an experiment in discovering just how influential social media has become – open access, crowdsourced “peer review” – and whether this mechanism for addressing conflict-of-interest in the prominent medical journals is more effective than simply attempting a letter to the editor.
KevinMD.com – “The filtering of medical evidence has clearly failed“
Endotoxin mediated circulatory collapse remains a theoretical target in the treatment of sepsis.
But, eritoran won’t be one of the agents used to ameliorate its effects.
After a phase II trial found sepsis patients randomized to eritoran had 37.5% mortality compared with 56.3% in the placebo group, the manufacturer sponsored a multi-national, multi-center phase III trial enrolling 1,951 patients. And, in short – no mortality benefit overall, and no individual subgroups of severe sepsis with any indication of benefit. The authors comments speak wistfully of the early favorable results before finally concluding: “Eritoran joins a long list of other experimental sepsis treatments that do not improve outcomes in clinical trials in these critically ill patients.”
Interestingly, the study concluded in 2010 – meaning it took 2 1/2 years for the results to reach publication. The reader will have to derive their own interpretation regarding whether this had anything to do with being negative results from a manufacturer-sponsored trial.
“Effect of Eritoran, an Antagonist of MD2-TLR4, on Mortality in Patients With Severe Sepsis”
This entertaining brief communication refers to Chvostek sign – the twitching of the facial muscles after tapping the facial nerve purportedly associated with hypocalcemia.
This neurologist notes, after one of his residents presented with bilateral Chvostek sign, he convenience sampled other residents and medical students on the wards – and 6 out of 11 exhibited Chvostek sign. He otherwise notes 25-43% of healthy individuals exhibit this sign and 29% of patients with hypocalcemia do not. He bluntly states Chvostek sign should simply be retired as a clinically relevant entity.
Stick with the Trousseau sign!
“Chvostek sign, frequently found in healthy subjects, is not a useful clinical sign”
The content of these recommendations is what made the rounds in various news outlets – the first begrudging revelations that antibiotics are possibly unnecessary for many of acute otitis media. This isn’t news to us, of course, but it’s entertaining to see the precise moment the Rock of Gibraltar starts to make its slow course corrections.
As far as clinical policy statements go, however, this is beautifully constructed. For every actionable statement, these authors offer a concise summary of the benefits, harms, value judgements, intentional vagueness, patient preferences, and exclusions. Whether I agree with the hairs they split on each recommendation is almost overwhelmed by how pleasant it is to understand the basis of their reasoning.
My big irritation: their implication that symptom severity or temperatures greater than 102.2F are somehow specific for bacterial disease more likely to benefit from antibiotics. Odd – or am I missing a notable piece of literature? Please point it out if so!
The other new item of interest is the “Strong Recommendation” for analgesic treatment in cases of AOM. Thank goodness!
“The Diagnosis and Management of Acute Otitis Media”
Two negative studies weren’t enough to stop the Medicines Company from CHAMPION PHOENIX, the third attempt at demonstrating cangrelor is useful during PCI.
Cangrelor is a direct-acting platelet adenosine diphosphate inhibitor – same as prasugrel and clopidogrel – that differs in its half-life and route of administration. Rather than clopidogrel, which is a long-acting oral loading dose during STEMI, cangrelor is a continuous intravenous inhibitor that wears off after minutes. This has some theoretical advantages, such as when multiple lesions are found on invasive angiography and coronary bypass need not be delayed for the antiplatelet effects of clopidogrel to wear off.
So, PHOENIX follows up CHAMPION PCI and CHAMPION PLATFORM, each of which were negative for their primary combined endpoint of death, myocardial infarction, or ischemia-driven revascularization. In fact, these studies were stopped at their interim analysis for futility, as they were unlikely to show superiority given the planned enrollment.
So, why does PHOENIX succeed where others have failed? Well, they changed the primary endpoint to a new composite – death, myocardial infarction, ischemia-driven revascularization, or stent thrombosis. And, PHOENIX shows a 0.8% vs 1.4% advantage to cangrelor for stent thrombosis – which accounts for most of the new advantage in primary outcome. In previous CHAMPION studies, stent thrombosis was 0.2% vs. 0.3% and 0.2% vs. 0.6%. So, truly, cangrelor succeeds here mostly because the clopidogrel group fares so much more poorly, rather than on its own merits. Considering 25.7% of the clopidogrel group received only 300mg rather than 600mg, and 36.6% received their clopidogrel during or after PCI, it’s no wonder they had greater stent thrombosis in this study.
It’s pretty clear the Medicines Company learned from its two negative studies and rigged the third one to succeed – and kept it just underpowered enough that severe or moderate bleeding with cangrelor didn’t reach statistical significance (0.6% vs. 0.3% p = 0.09). This reinforces a bias frequently seen in sponsored trials – failure at first begets further trials, while initial success doesn’t lead to confirmatory RCTs that might cast doubts upon the authenticity of the golden goose.
“Effect of Platelet Inhibition with Cangrelor during PCI on Ischemic Events”
This piece of literature is incredibly important – not because of the specific clinical question it addresses, but, rather, because of the fundamental principle in medicine it illustrates.
In large, heterogenous populations – frequently clinical trials – the risks and benefits are not evenly distributed throughout the cohort. However, when the primary outcome reported, this is based on the aggregate results. This leads us to one of the primary flaws in evidence-based medicine, that statistical power typically comes at the expense of external validity to the individual patient.
This retrospective evaluation of the cohort from RE-LY, the trial comparing dabigatran to warfarin for the prevention of stroke in atrial fibrillation, evaluates genetic polymorphisms and their association with primary and safety outcomes. In short, each minor allele of CES1 SNP rs2244613 was associated with lower trough concentrations and statistically significant interaction between treatment with warfarin and bleeding – hazard ratio 0.59 (0.46 – 0.76) for carriers and hazard ratio 0.96 (0.81 – 1.14) for noncarriers. No difference in the primary stroke prevention outcome was apparent – but outcomes were infrequent and the study was underpowered to detect such a difference.
My take on these results is simple – the 32.1% of patients who are carriers for the rs2244613 allele account for most of the bleeding benefit seen in RE-LY, and the non-carriers have no bleeding advantage compared with warfarin. We ought to be specifically tailoring and reducing the dabigatran treatment population to this subgroup with the most favorable risk profile – and we need to be developing tools that support this kind of individualized treatment throughout medicine.
“Genetic Determinants of Dabigatran Plasma Levels and Their Relation to Bleeding”