Tag: metabolic acidosis

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How I made that short video about interpreting ABGs

Here are the tweets (I’m using WordPress’ ability to post a tweetstream, pretty cool)

We need to know if it is alkalosis or acidosis, so we ordered an ABG.

Thought I’d try my hand at a @HannahRAbrams style explanatory animation for the above ABG. Need to get it down under 2:20 to fit in a tweet.

And the last bit

Originally tweeted by Joel M. Topf, MD FACP (@kidney_boy) on October 7, 2020.

I made the video with Keynote, it is a single slide with a lot of animation. Here is the slide (all 750 kilobytes):

Creating the animation just takes patience. This slide has 44 steps to the animation. It is a mixture of build ins, actions, and build outs.

Once I had the animation perfect I used “Record Slideshow…” to record the animations and my narration, then exported the movie using “Export To Movie…”

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Mini-Tweetorial on Metformin Associated Lactic Acidosis (MALA)

How small can you make a tweetorial? This one is only 5 tweets.

A lot of patients are on metformin and a lot of people get lactic acidosis. One does not always cause the other.

But in this case I think the metformin did cause the lactic acidosis. The patient did not have sepsis. There wasn’t any dead bowel, shock, or other typical cause of lactic acidosis. And thanks for asking, the thiamine was normal, they were not being poisoned with arsenic. No aspirin toxicity. No malignancy causing an occult type B lactic acidosis.

They had acute tubular necrosis causing acute kidney injury.

The lactate was sky high

Perfusion was intact. Blood pressures were in the 160s.

And they were taking a coupe grams of metformin a day. The thing about a creatinine of 8 is you need to have a GFR of around zero for almost week to get there. So imagine the patient has about 14 grams of metformin on board.

I think this was MALA.

I think this patient should have gotten hemodialysis.

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Non-anion gap Metabolic Acidosis

Non-anion gap metabolic acidosis (Powerpoint, PDF)
  • 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
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OUWB Question: Acid-Base

Hi Dr. Topf,
(I don’t have Twitter) I wanted to ask you about question 6 on the week 2 quiz:
“An unresponsive woman is brought to the emergency room. She has a history of a suicide attempt a few years earlier. The lab tests are: Serum Na 140 mmol/L Serum K 4.0 mmol/L Serum Cl 100 mmol/L Serum HCO3 14 mmol/L, BUN 17 mg/dl, creatinine 0.7 mg/dL, serum osmolality 323 mOsm/Kg, Blood glucose 72 mg/dl, Blood gases: pH 7.28 pCO2 27 mmHg. What would you expect the urine pH to be in this patient?”
Why is it that we would expect the urine pH to be acidic? Since blood pH is 7.28, I would imagine that urinating out HCO3- (explaining the low serum HCO3) would have caused the acidic blood pH, thus making urine pH basic?

 

Thanks for your help,

When answering multiple choice board-style question try to figure out what they are looking for. Let’s break this down.
“An unresponsive woman is brought to the emergency room. She has a history of a suicide attempt a few years earlier.

This is the “tell” of the stem. Acid base + suicide = ethylene glycol toxicity

The lab tests are: Serum Na 140 mmol/L Serum K 4.0 mmol/L Serum Cl 100 mmol/L Serum HCO3 14 mmol/L, BUN 17 mg/dl, creatinine 0.7 mg/dL , Blood glucose 72 mg/dl, 

They don’t tell you the anion gap. Calculate it.

Anion gap = Na – (Cl + HCO3)
Anion gap = 140 – (100+14)
Anion gap = 26 (normal 6-12)

High anion gap.

serum osmolality 323 mOsm/Kg

More of the tell. They won’t tell you the osmolality unless they want you to calculate the osmolar gap (or it is a hyponatremia question)

Osmolar gap= Measured osmolality – (Na x2 + glucose/18 + BUN/2.8 + ethanol/3.6)
Osmolar gap = 323 – (280 + 4 + 6 + 0)

Osmolar gap = 323 – 290
Osmolar gap is a massive 33 (Upper limit of normal is 10, over 20 starts to gain a lot specificity for toxic alcohol)
This confirms our earlier suspicions of ethylene glycol toxicity

Blood gases: pH 7.28 pCO2 27 mmHg. What would you expect the urine pH to be in this patient?”

The ABG confirms the metabolic acidosis.

Let’s do Winters formula (not really needed for this question, but you know…practice)
1.5 x 14 =21 + 8 =29, measured CO2 is within ±2 of predicted so an appropriately compensated metabolic acidosis.

Why is it that we would expect the urine pH to be acidic? Since blood pH is 7.28, I would imagine that urinating out HCO3- (explaining the low serum HCO3) would have caused the acidic blood pH, thus making urine pH basic?

So the bicarbonaturia you are talking about would happen if the cause of the metabolic acidosis is renal loss of bicarbonate (what we call renal tubular acidosis).

RTA should only be considered if you are dealing with an normal (or non-anion gap) metabolic acidosis. Since we have an anion gap metabolic acidosis and functioning kidneys the kidneys will be working as hard as possible to clear the exogenous acid. This means the urine is acidic.

The urine would also be acidic if the patient had a non-anion gap metabolic acidosis from diarrhea.

Hope this helps

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More metabolic acidosis than you can shake a stick at…

The set up

28 year old under going treatment for metastatic testicular cancer presents with a history of recurrent kidney stones.

pH 7.13
pCO2 22
pO2 96

Na 138

Cl 114
BUN 14

K 3.2
HCO3 8
Cr 1.0
glucose 96

urine lytes:
Na 56
Cl 78
K 12
Measured osmolality 292

Step one


Determine the primary acid-base disorder. The pH, bicarbonate and pCO2 are all moving in the same direction (down in this case). When all the Henderson-Hasselbalch variables are moving in the same direction (up or down) the primary disorder is metabolic. The pH is decreased so this is a metabolic acidosis. 

Step two


Is the compensation appropriate, or do we have a primary respiratory disorder as well as a metabolic acidosis? 
We use Winter’s Formula to get the predicted pCO2 based on the bicarbonate.
1.5 x bicarbonate + 8 = 
1.5 x 8 +8 = 20

His actual pCO2 is 22 which is close enough, so a pure metabolic acidosis with appropriate respiratory compensation.

Step three

If there is a metabolic acidosis is there an anion gap?
138 – (114 +8) = 16
Yes, this is an anion gap metabolic acidosis.

Step four

If there is an anion gap, is there an osmolar gap? I usually don’t bother to look for an posmolar gap uness the patient is particularly toxic with a large anion gap, neither of which describe Lance, but since the information includes the measured osmolality we should check this. You know, Chekhov’s gun and all.
2 x Na + Glucose / 18 + BUN / 2.8 + Ethanol / 4.6 = calculated osmolality
2 x 138 + 96 / 18 + 14 / 2.8 + 0 / 4.6 = 286
Osmolar gap = measured osm – calculated osm

Osmolar gap = 292 – 286 = 6

This is a normal osmolar gap. Poor foreshadowing by the question writer.

Step five

If there is an anion gap, what was the bicarbonate before the anion gap? To calculate the bicarbonate before, take the anion gap, subtract 12 and add that to the current bicarbonate:

Bicarbonate before the anion gap = Bicarbonate + (Anion gap -12)

Bicarbonate before the anion gap = 8 + (16 –12)
Bicarbonate before the anion gap = 12

So the bicarbonate before the anion gap was 12 indicating a large non-anion gap metabolic acidosis and a relatively mild anion gap metabolic acidosis.

Step six

If there is an NAGMA, what is the urinary anion gap? What does it mean? The patient has a NAGMA as discovered in step 4. The differential of NAGMA is:

  1. chloride intoxication
  2. GI losses
  3. RTA

The patient doesn’t seem to be suffering from chlorine gas intoxication or have an isotonic saline drip running so number one is not likely.

The low potassium could indicate GI losses as well as type 1 or 2 RTA. The urine anion gap in the face of severe metabolic acidosis will help here. In GI losses and chloride intoxication the urine amnion gap will be negative, in RTA it should be positive.

Urine anion gap = (Na + K) – Cl

Urine anion gap = (56 + 32) – 78

Urine anion gap = + 10

The positive anion gap indicates a lack of NH4+ in the urine. In diarrhea, the kidney will up ammonium excretion to get rid of the acid load. The increase cation load in the urine will be balanced by an increased in chloride in the urine. The increase Cl– will make the urine anion gap negative (in reality it is an unmeasured cation, or a positive cation gap, but by convention we use an anion gap). The positive urinary anion gap is the face of a severe acid load indicates a renal tubular acidosis.

Put it all together

This patient has a well compensated metabolic acidosis. The metabolic acidosis is partly anion gap and non-anion gap. The non-anion gap is a distal RTA. The AGMA may be a lactici acidosis from the neoplasm as these are not uncommon in metastatic neoplastic disease.

The chief complaint of kidney stones points to type 1 RTA. Patients with testicular cancer receive platinum-containing chemotherapy. Platinum can cause proximal or distal RTA. However, proximal RTA is not associated with kidney stones. So I suspect this  is classic distal RTA due to platinum.