Non-anion gap Metabolic Acidosis

Non-anion gap metabolic acidosis (PowerpointPDF)
  • Case-based
  • 70 slides, 1 hour
  • Revised May 2013
  • Now optimized for App.GoSoapBox
  • Now available as a screencast.
  • In your chloride intoxication group of causes, add TPN
  • In your GI loss of HCO3, “change HCO3 to HCO3 precursors” since what we lose in diarrhea is not HCO3 per se since pH of the stool is not acidic, we lose citrate, etc which transform into HCO3 eventually
  • Interesting comment on renal bicarb loss: I would add an extra group and call it decrease renal NH4+ excretion and add distal RTA, renal insufficiency and hypoaldosteronism. You don’t lose HCO3 in distal RTA or hypoaldosteronism. You could argue that NH4+ synthesis in proximal tubule generates “new HCO3” but the student will get lost in that concept
  • In the renal HCO3 loss group I would add post-treatment of DKA, and post-hypocapnia
  • Toluene can cause both anion gap and non anion gap metabolic acidosis but the non anion gap is more common because the unmeasured anions are rapidly excreted by the kidneys
  • Pentamidine also blocks ENaC and can cause hyperkalemia

OUWB Non-anion gap question

Where does the chloride come from.

XXXXX and I had a question following the Acid-Base workshop. What is the origin of the increase in chloride ions in patients with NAGMA due to GI or renal causes?  

Thanks, 

 

So the key here is not to think of the body as static. As patients lose bicarb in the stool or in the urine, this will result in volume depletion which will be compensated for by renal retention of sodium and yes, chloride.

Great review of non-anion gap metabolic acidosis here: