I’ve avoided posting technical stuff so far - but I’m in a bind, my (brief) research is leading me nowhere.
Why does salicylate intoxication not raise osmolar gap?
Though I am unable to help you, I truly wish I could, since you were gracious enough with your time to help me…Sorry, I know that doesn’t help, but the thought is there!!
Not sure if this will help. Something jogged in my memory from my pharmacology courses 20 years ago and from the biochem course I’m taking now.
Here’s what I found in Goodman and Gilman’s, The Pharmacological Basis of Therapeutics 7th ed.
Salicylates stimulate respiration directly and indirectly.
Full therapeutic doses of salicylates increase oxygen consumption and CO2 production primarily in skeletal muscle due to the uncoupling of oxidative phosphorylation. Increased CO2 stimulations respiration which balances the CO2 priduction and the therefore the plasma CO2 tension doesn’t change. Once the salicylate gains access to the medulla (diffusion across the blood brain barrier is slow) it directly stimulates the respiratory centre causing hyperventilation (marked increase in cases of poisoning leading to respiratory alkalosis).
Compensation for the respiratory alkalosis ensues due to an increase in renal excretion of bicarbonate accompanied by Na and K thereby lowering plasma bicarbonate and normalizing blood pH.
Anyway, not sure if this helps because I’m not 100% clear on what the osmolar gap is (general sense but don’t remember that term specifically).
Hopefully one of the docs or folks in med school can chime in.