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Non-anion gap metabolic acidosis screen cast

This is my NAGMA lecture. It contains a thorough, but not exhaustive, overview of renal tubular acidosis.

Any feedback would be appreciated.

NAGMA from joel topf on Vimeo.

I need a better technology to make these. Still way too tedious.

8 Replies to “Non-anion gap metabolic acidosis screen cast”

  1. Great lecture and very nice slides ! Some observations:
    1. In your chloride intoxication group of causes, I would add TPN
    2. In your GI loss of HCO3, I would add "HCO3 or 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
    3. 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
    4. In the renal HCO3 loss group I would add post-treatment of DKA, and post-hypocapnia
    5. 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
    6. Pentamidine also blocks ENaC and can cause hyperkalemia

  2. Thanks. Awesome insights.
    Some questions:
    In bullet point 2 do you mean stool is alkalotic?
    In bullet point 3 did you mean NH3 production in the proximal tubule instead of NH4+?

  4. Excellent lecture. I have two minor comments, though.

    1. In my view, the mechanism behind so called dilutional acidosis is simply dilution of the HCO3 buffer in the plasma of an (often) HCO3-deficient patient. Meanwhile, the low pH of normal saline is due to the dissolution of atmospheric CO2 in a non-buffer solution. The H+ content in this solution as measured by titratable acidity, however, is low. Please see http://www.medsci.org/v10p0747.htm
    2. The ABG for case 2 in the lecture is different between the first and second slides. I believe the second is the right one, as the first one does seem to be appropriately compensated.

    I look forward to any future lectures.

    Eric Mohlin, last year medical student / junior doctor, Sweden

  5. Thanks for your insightful comment.

    Unfortunately, I am not talented enough to fully understand and certainly would be unable to explain that reference to a bunch of bewildered interns.

    How would you teach that point? Do you think the additional complexity has a meaningful payoff in increased ability to explain how patients and metabolic disorders behave?

  6. I do think it helps in understanding dilutional acidosis to focus on the buffer side of acid-base balance, and to realize that a volume contracted patient may have a HCO3-deficit which is underestimated if only the concentrations in plasma are taken into account. If vigorously replaced with chloride-rich fluids, such a deficit may be unmasked.

    Conversely, I view the mechanism behind the slightly acidic pH of saline bags to be of purely academic interest, and that it adds little to the understanding of clinical problems. I do not really pay much attention to the pH of the infusate. For example, I found the pH of one 'balanced' solution (Ringer's acetate) to be annotated as pH 5.0-6.0, which in my eyes just adds to the confusion.

  7. Dr John Gennari in my division makes it a point to tell every fellow that it is 'normal anion gap acidosis' and not 'non anion gap acidosis'.

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