February 2019 Journal Club

Hi All

Have a look at this month’s paper here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184351/
I warn you now it’s a bit of a long one.
It’s also a bit leftfield but if you stick with it has some really pertinent implications for what we do in critical care and peri-operative medicine, failing that it also explains how bears hibernate…….
“Hi Everyone

I guessed from the stunned silence that followed me sending out this month’s paper you probably all think I have now officially gone too far…….
But honestly there were some little gems of information in this monster of a review article!
The first point to make is that yet again we can see how staggeringly complex and intricate human homeostasis (and ergo pathology) really is. However trying to understand human disease states by thinking of humans as totally distinct from every other life form on the planet (with which we share the vast majority of our genetic material) is also unlikely to be a winning strategy. By broadening our field of study we can see that torpor (the hypometabolic state induced in hibernators to a period of reduced energy supply/adverse environmental conditions) is a genetically driven process that seems to have been conserved by evolution across a wide range of species. Furthermore it bears striking similarities to the organ “dysfunction” seen in sepsis…….
As yet there are no real therapeutic options available from this insight (cooling as mentioned in the paper has as many bad points as good) but research is happening as we speak.
There are, perhaps, implications however for how we make decisions and prognosticate on the ICU.
I think we have to be very cautious about making any judgements about “poor LV function” in the context of sepsis when we do our FICE scans because as the paper shows there is a huge amount of evidence out there that the systolic impairment we are seeing is likely to be adaptive and reversible. Likewise “AKI” in the non-obstructed, euvolemic patient (especially in the early phase of sepsis) may not require any intervention to resolve it (other than treating the sepsis). However how, as yet, we are meant to know which individual will rapidly return to normal and which will progress to acute renal failure requiring organ support I’m afraid I don’t know; so in the mean time we watch them all carefully…..
The other slightly off piste revelation I got from reading this paper is being reminded that eukaryotic cells (and therefore the organisms from which they are made) made an evolutional pact with another organism (mitochondria) billions of years ago in order to thrive in the newly toxic oxygen rich environment. If we didn’t “host” the mitochondria we’d have to rely on our own vastly inferior ATP producing processes (i.e. the anaerobic pathways) in order to survive. In which case we’d still be a single celled organism floating in the sea somewhere instead of the multicellular, ATP producing powerhouse that we are, I guess that counts as a happy accident……😊

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