Anion Gap and Osmolal Gap

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Calicliffs

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Why does methanol and propylene glycol ingestion cause elevation of both while drug ingestion, e.g. salicylates or isoniazid only causes elevation of the former?

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Why does methanol and propylene glycol ingestion cause elevation of both while drug ingestion, e.g. salicylates or isoniazid only causes elevation of the former?
Think of the osmolal gap as an “unmeasured anion gap “ in that your standard anion gap calculation will not account for something like methanol and propylene glycol .

That being said as the methanol is metabolized to Formic acid and ethylene glycol is metabolized to oxalic acid (and glycine) , those components will no longer contribute to an osmolal gap and will begin to contribute to an anion gap .

Lesson is if anyone is concerned about a toxic prodrome , the ED physician , ICU consultant , or nephrologist must get the measured osmolality as soon as possible

If the “intrepid pgy2/3” decides to order osmolal gap a few days into the admission after reading mksap , uptodate , or pocket medicine , then the osmolal gap may not be present anymore .

Still it’s always something to consider for an “unexplained anion gap during routine labs “ while on the floors for an “alcoholic.” Maybe a toxic prodrome was missed during admission .
 
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That being said as the methanol is metabolized to Formic acid and ethylene glycol is metabolized to oxalic acid (and glycine) , those components will no longer contribute to an osmolal gap and will begin to contribute to an anion gap .

I get that they contribute to the anion gap after they're metabolized (the metabolites are 'anions' in water). But why do these metabolites not contribute to the osm gap? The strict defn' of osmolality is a measure of dissolved particles in solution. Is there not an increase still in the # of dissolved particles? Or is it just too inconsequential to measure?

If the “intrepid pgy2/3” decides to order osmolal gap a few days into the admission after reading mksap , uptodate , or pocket medicine , then the osmolal gap may not be present anymore .

No matter. When this idiot patient---who drinks home-made moonshine from his bathtub---leaves AMA and is readmitted next week for the same thing, we'll be sure to get a fresh osmolal gap then. And of course, we'll counsel the patient, get social work involved, and it'll never happen again.
 
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not every anion contributes to tonicity or osmolality

Tonicity is the effective osmolality and is equal to the sum of the concentrations of the solutes which have the capacity to exert an osmotic force across the membrane.​


Osmolality is a measure of the number of particles present in solution and is independent of the size or weight of the particles. It can be measured only by use of a property of the solution that is dependent solely on the particle concentration.

for day to day clinical practice, its not so important to differentiate these two.

Rather, something that contributes to tonicity will cause fluid shifts from the intracellular fluid compartment into the extracellular fluid compartment. This has implications of worsening pulmonary edema perhaps (from ICF compartment to ECF, specifically the interstitial fluid compartment) or perhaps causing water to leave neurons (like hypernatremia).

We don't want things that can cause those kind of problems in our toxic ingestion patients of course...


once it gets metabolized to its metabolite, that metabolic still contributes to the AG as it is an "unmeasured" anion. But that metabolite no longer has the ability to exert fluid shifts across cell membranes. Hence this is why methanol and EG patients get some good old ethanol in the old days or fomepizole currently where available.
 
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