Dr. Bray Links

Wednesday, April 5, 2017

The Normalization Fallacy: why much of "critical care" may be neither

If our ancestors 100,000 years ago were getting infected with some organism and that infection was making their potassium low and they were dying as a result, would you not expect some sort of mutation in the aldosterone receptor that is activated during sepsis or some other compensatory mechanism? Did evolution fail? Must she lean on the diligent medical student with a K-rider to cover her shortcomings? Is that the most likely explanation, or is the most likely explanation that low potassium during sepsis is an epiphenomenon of all the compensatory cascades, resulting from millions of years of evolution, that protect us from the ravages of infection? Worse, could low potassium during sepsis be adaptive, and we are harming patients when we "replace" it? (Note that "replacement" implies that something is missing – even the way we talk about these things belies our enculturated biases.)

The same logic could apply for almost every perturbation we see in laboratory values and physiological parameters in sepsis and critical illness: anemia, electrolyte derangements, body temperature changes, tachycardia, hypo- and hyper-tension, tachypnea, delirium, leukocytosis, elevated biomarkers such as troponin and BNP, lactate (watch the linked video you will be glad you did), d-dimers, coagulopathies, cortisol levels, anorexia during infection or stress – you name it. The sicker a patient gets, the more values go out of whack and the greater are the deviations from normalcy. 


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