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Luscious question. Generally, burst suppression (BS) can occur in most any encephalopathy (eg., GABAergic drugs, hypoxic-ischemic encephalopathy, Ohtahara syndrome, etc.) with the proposed common aetiology being decreased CMRO and decreased ATP regeneration 1/n https://twitter.com/cpaolag/status/1345912694268964865
in cortical pyramidal neurons and interneurons ( https://sci-hub.st/10.1073/pnas.1121461109). So, provided the acidosis were severe enough to either prevent oxygen delivery to the brain, or to prevent ATP regeneration in the cortical neurons/interneurons, then the answer would be "yes!". 2/n
The story gets more toothy because acidæmia almost never occurs on its own, and some assoc. abnormalities (low CBF from cardiogenic shock, neuro-inflammation from sepsis, cerebral hypoxia c/ acidosis, etc.) can themselves produce burst suppression. https://bit.ly/3oVzpUX 3/n
What's more, extracellular measurements of pH
may not correlate with the internal environment of the nerve cells. There is some good [old] work to suggest that the internal pH of neurons may be somewhat independent of that of the extracellular fluid https://bit.ly/39INEWL 4/n
may not correlate with the internal environment of the nerve cells. There is some good [old] work to suggest that the internal pH of neurons may be somewhat independent of that of the extracellular fluid https://bit.ly/39INEWL 4/n
To ground ourselves at the bedside, imagine pts c/ severe acidæmia (say, DKA without severe cerebral oedema). Most are stuporous, but few are frankly comatose. This would seem to suggest that blood pH<7 is supportive of CMRO that is at least *somewhat* normal (conjecturally). 4/n
Ultimately, I suppose the answer to your question is:
"No, it is not "normal" to see burst suppression with a pH of 6.87 alone, but it would seem totally appropriate that whatever process were driving the acidosis could, alone or in combination with the acidæmia, cause BS."
"No, it is not "normal" to see burst suppression with a pH of 6.87 alone, but it would seem totally appropriate that whatever process were driving the acidosis could, alone or in combination with the acidæmia, cause BS."
Caveat: I am no expert on this, and I haven't even begun to broach the confusion overlay of CBF, CO2 physiology, and concomitant effects of drugs and temperature. If anyone has other thoughts, I would be curious to hear them!
@AndrewKofke @ICU2EEG @phluaria @IctalGroup @stlegriel
@AndrewKofke @ICU2EEG @phluaria @IctalGroup @stlegriel
