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In theory, very little protein breakdown and utilization occurs in Coma's accompanied by hyperglycemia. This is evidenced by the body's inability to utilize simple molecular chains like glucose.
If so, is the increase in urea due to protein metabolism or dehydration?
Increased urea can result from dehydration. Again we are dealing with multiple variables. As you know it is thought that increased urea levels are caused by renal failure, which is sometimes accompanied by the failure of other organs (including the brain).
I'm sure that you are considering their hydration status, cardiopulmonary state, liver/kidney/GI function, neurosis, pain, and behavioral state.
You have ruled out coagulopathies and genetic anomolies particularly structural.
I think I know what puzzles Debbi. In something so much like DKA, how come there's no Ketones which are the indicator of protein breakdown. Well, I'm just fishing around the ol' memory banks (which gets more and more risky as I grow older) but I seem to recall that the HHNC patient is typically a type II diabetic. In fact, I recall 'learning' in a class sometime that it is how some people learn they're diabetic. And the explanation was that a bare minimum of endogenous insulin exists that allow the cells to maintain glucose metabolism--so no ketones. And the remarkable urine output (driven by the amazing high glucose level-- > 1000) explain the high BUN/Creatinine.
I didn't look that one up, which I guess I ought to have done. But I think it's the answer you're looking for.
In theory, very little protein breakdown and utilization occurs in Coma's accompanied by hyperglycemia. This is evidenced by the body's inability to utilize simple molecular chains like glucose.