prognostication after cardiac arrest involves a structured series of tests performed over time.
this may vary a bit between patients and institutions.
most often, decisions center around the trifecta:
๐บserial clinical examination
๐บcontinuous EEG
๐บMRI
MRI is the weak link:
๐๏ธ least robust evidence
๐๏ธ interpretation is subjective
๐๏ธ logistically challenging (eg pacemaker)
MRI can help if there is *no* anoxia, or if there is an unexpected *alternative* dx.
MRI isn't great at sorting out bad anoxia from moderate anoxia.
CT has advantages over MRI:
๐ช measurement of Houndsfield units allows it to be objective
๐ช expanding evidentiary base
๐ช high specificity for poor outcome
๐ช can be applied to all pts
the problem with CT has been that it's done immediately post-arrest, before edema develops
the immediate post-arrest CT has poor sensitivity.
but *delaying* the CT >24 hours improves sensitivity, as found in this study from 2018:
the new study by Nielsen's group extends these findings, by showing that delayed CT scan >24 hr
๐ โฌ๏ธ sensitivity for severe anoxic injury (~70%)
๐ retains high specificity for prognosticating a poor outcome
so CT seems to perform very well when evaluated at the right timepoint
overall, CT scan may be poised to *replace* MRI for post-arrest neuroprognostication in many patients.
of course, each patient must be approached individually
if data isn't lining up (e.g., inconsistencies between exam / EEG / imaging) - wait & get more data!
what do folks think about CT-vs-MRI?
the evidence base for CT isn't gigantic, but I think it's better than the data for MRI.
MRI requires subjective interpretation which introduces a source of bias ๐ค
I think it's time for a difficult discussion, folks.
Let's talk about CSF lactate ๐ซฃ
CSF lactate has been shown to be *superior* to traditional CSF studies in sorting out viral vs. bacterial meningitis in several studies & meta-analyses...
a subset of patients with viral meningitis will initially have a *neutrophilic* pleocytosis.
this can lead to unnecessary admissions & antibiotics
some patients are subjected to repeat LPs ๐ฉ
a low CSF lactate could avoid all of this, allowing patients to go home from the ED
CSF lactate measurement is recommended in guidelines from the United Kingdom, Europe, and France.
(it's not recommended in the ID society of America guidelines, but they're from *2004* and require revisions)
hot take on the LOVIT trial of vitamin C... I'm probably going to regret this but I can't resist...
as a preface, it seems that Marik's initial paper might have been fabricated - which may have pushed the field in the wrong direction for years. the VITAMINS trial largely halted the use of vitamin C... and surely nobody is going to use it now for sepsis. medpagetoday.com/special-reportโฆ
back to LOVIT: the primary endpoint was a composite of mortality or organ dysfunction at 28 days. the paper states that vitamin C caused statistically significant harm (p = 0.01)...
an asymptomatic adult human presents with these findings...
should you institute therapy or repeat lytes?
EKG shows classic findings of hypoK (ST depression & pronounced U-wave that produce a "wavy baseline" pattern). so the hypokalemia is real - treatment should start immediately.
(more on EKG findings of hypoK:hqmeded-ecg.blogspot.com/search?q=hypokโฆ )
Waveform capnography! I've been meaning to cover this for years. Finally posted an IBCC chapter on it. The chapter is pretty long (filled with subversion, physiology, and zentensivism), so here is a thread with some key points.๐งต emcrit.org/ibcc/co2/
end tidal CO2 (etCO2) will ~always be lower than the arterial CO2 (b/c dead space dilutes CO2 as the patient exhales). the gap between the etCO2 and the arterial CO2 varies depending on lung function. in normal lungs, the CO2 gap is usually ~2-5 with an upper limit of ~10-15
Imagine that we intubate a healthy patient for airway protection 2/2 intoxication. A safe pH for this patient might be ~7.2-7.5 (no good data!). To achieve this, we need an arterial pCO2 to be ~32-64 mm. So all we need to do is target an etCO2 of ~30-35 and we should be good.
oh, the life & times of remdesivir! - let's review the bizarre trajectory we've taken with this medication! with emoji's to represent each study ๐คฃ
we start with a retrospective series of patients treated with remdesivir under the banner of "compassionate use." most patients didn't die. this paper has so many flaws, at this point it's merely a case study in horrific research design ๐คฎ (commentary: bit.ly/2XBwnx1)
next: the 1st placebo-controlled trial. the primary endpoint (time to clinical improvement) was negative, as were most 2nd endpoints (including viral load). the only glimmer of benefit was faster clinical improvement in one slicing of the data ๐ฅด (bit.ly/3lIxnXZ)