Correct me if I'm wrong, but I just read this chapter in tintinalli's.
typically the adrenal crisis that occurs with exogenous steroid withdrawal (ie prednisone patient who stops suddenly) is secondary Adrenal insufficiency and there is no hyperkalemia associated with this as aldosterone is NOT under the control of the hypothalamic/pituitary axis, but rather is controlled by the renin-angiotensin-aldolsterone system. Hyperkalemia in itself stimulates the kidneys directly to secrete aldosterone.
so unless you have primary Adrenal insufficiency (ex. addison's) then aldosterone isn't typically affected.
later
Yes. I was just about to write the same thing.
In primary adrenal insufficiency (Addison's, bleeds, TB, histo), you need to worry about mineralocorticoid production. Of course this is very very rare. BKN certainly has a point in that not all glucocorticoids are created equal with regards to mineralocorticoid effect. Hydrocortisone is the most "mineralo" of the bunch but don't forget that is has 125 less potency than fludrocortisone.
As an aside, although cortisol (=hydrocortisone) does have mineralocorticoid effects in supra-physiologic doses, it has no sich effect in physiologic doses. There are exceptions to that rule. Two well-described conditions, apparent mineralocorticoid excess (AME) and licorice ingestion, lend the mineralocorticoid receptors more sensitive to cortisol. These are important for medicine boards but probably less so for EM boards.
Now, in secondary adrenal insufficiency, like steroid withdrawal or pituitary insult, you don't need to worry about mineralocorticoid effect. ACTH does have a slight, but important, permissive effect on aldosterone production so florinef can still be a consideration in very long-standing secondary adrenal insufficiency.
But.... then there's "relative adrenal insufficiency" and this is where the ACTH (cosyntropin) stim test comes in. If you have a septic patient, he may or may not be able to mount a proper cortisol response. Most recommendations go like this:
Start Dex on admission to the ICU
Do a Stim test
If your delta cortisol (change before and after 250 mcg cosyntropin) is less than 9, you treat.
If your delta is more than 9 some and your patient seems to be improving, you still treat. There is little evidence for this approach; in fact, a big study (CORTICUS) is coming out this summer to clarify this approach. Which agent to use? No one knows. Once your stim test is done, you can use whatever you want. Hydrocortisone is best studied (including in CORTICUS). Some studies include florinef, some don't.
If your delta is more than 9 and the cortisol does not seem to make the patient better, you stop. Although in real life lots of people will keep it going.
BKN brings up baseline cortisol. That's a nebulous concept in relative adrenal insufficiency. The problem is lab variability, physiologic variability. There is no censusus regarding interpretation. However, most people would say that a cortisol greater than 25 is sufficient. Less than 2 is diagnostic for adrenal insufficiency - but it's never less than two.
I should say that a baseline cortisol in primary or secondary adrenal insufficiency is clearly indicated and I believe that's what BKN was talking about.