No but what I’m saying is, many patients get vanco who don’t have meningitis at all. They get the vanco before the LP, and the LP is negative for meningitis. So the denominator is all LPs done to evaluate for meningitis including those that are negative.

Yes, we recommend adding vanco only for purulent meningitis, AFTER LP. One thing, there is no way 9% of LPs are S. pneumo. 9% of meningitis maybe. But vanco goes in before LP, so all those non meningitis LPs still got vanco and aren't counted in your calculations. I htink it's more lik 1 in 100 LPs.

If 1% of ED LPs end up being for Pneumo, and 1% of Pneumo in adults is R, you will do 10,000 vanco courses for every 1 patient with CTX-R pneumococcal meningitis. That will definitely cause a large amount of AKIs and VREs.
In LA, we recommend NOT adding vanco until LP CSF WBC/% PMN known.

Yup, posted on the other platform. For PK, 2 gm CTX Cmax blood 250 mcg/ml, 10% CSF = 25 at peak. 4-6 hr half life:
T0 = 25
T4 = 12.5
T8 = 6.25
T12 = 3.125 --should be above MIC whole interval.

As far as the massive overuse of vanco, does depend on geography. In much of US, CTX-R rare in adults...

If we know it’s pneumococcus i do not use a second agent. The beta lactam is adequate. I do not find the theory of “anti inflammatory” benefit compelling or useful. Now, we could consider steroids for severe cap.

People told me it was too radical at my place too. But then we walked everyone through the policy, which was developed with Counsel and Risk input. It is an actual structured policy that creates a due process mechanism for doing the right thing. It turns out to be rational, rather than radical.

The main take away is to implement a Policy to Override Policies at your institutions too.

Yeah but you’re Lawful Good. That’s ok. We need Lawful people too. It’s all about balance, right?

I was thinking Samuel Clemens. “…lies, damn lies, and statistics.”

It’s also an absurd conclusion based on wonky stats. A 48% chance dalba was superior? Seriously? How about, no chance. Based on both pre test prob and the actual clinical endpoint results.

I love Dalba
I just don’t know why we should do a PhD in statistics to understand a trial now
Or maybe am just getting old and grumpy

#5/5 You have not actually prevented any infections. You simply suppressed colonization growth from non-sterile sites. We are clear in our Discussion that the studies found a statistical reduction in infections that was likely not a true reduction in infections. The trials were poorly designed.

#4/5 When you randomized pts to receive abx or not, and then take cultures from non sterile sites, you will OBVIOUSLY grow more bacteria from the patients randomized to NOT receive abx. You are suppressing colonization with abx. This makes it appear that an infection was prevented. But...

#3/4 The #2 infection type was "pneumonia". Again, numerous studies over the last 20 years have shown that a high percentage of "pneumonias" diagnosed in hospital are not actually pneumonias.
Which brings us the fundamental error in the design of all of these trials...

#2/4 The #1 "infection" type in these RCTs was "UTI" based on positive urine culture, with no description of symptoms being present. Since we know that >50% of "UTIs" in hospitals are not UTIs, but asymptomatic bacteriuria, the majority of infections were not actually infections.

#1/5 The problem is even worse than that. It's not simply a trade off of preventing infections vs. worsening resistance & adverse effects. Indeed, it is not at all clear that infections were actually prevented at all in these RCTs. As we discuss, the definition of infection was highly problematic.

As @bradspellberg.bsky.social would say CRP is missing a letter as a test "A" (CRAP) - www.sciencedirect.com/science/arti...