Tag: anion gap

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Another hyponatremia Tweetorial

This was a great case. The full the tweetorial is unrolled below.

🧂 Hyponatremia #CaseReport #Tweetorial

(and a gif for the people who want to rename this hyperhydronemia)

Chug Water GIF

Patient came to the hospital with abdominal pain, nausea, and vomiting. Patient has alcohol use disorder. Last drink was about a day prior to admission.

After arrival to the ER the patient has a seizure.

gross james van der beek GIF

Besides the weirdly elevated anion gap, and the hypokalemia, the initial labs just show some AKI. I don’t have an ABG but I suspect combined metabolic alkalosis and lactic acidosis.

This can be demonstrated by looking at the Delta Ratio which compares the change in bicarb to the change in anion gap. The ratio should be 1. If it is less than 1, there is an additional non-anion gap metabolic acidosis, > 2 additional metabolic alkalosis

A delta ratio of 6 is crazy high.

Kate Mckinnon Snl GIF by Saturday Night Live

A related calculation, called the “bicarb before” can tell you the serum bicarb without the anion gap acidosis, so if the patient has two disorders it allows you to look at the metabolic alkalosis (or non-anion gap metabolic acidosis) without the anion gap metabolic acidosis.

The “bicarb before” comes to a mostly unbelieable serum bicarb of 60.

But the reason I was intrigued by the case are the next two labs that come 10 and 20 hours after the initial labs…The sodium drops to 125 despite getting 150 an hour of 0.9% NS and the patient making 3600 ml of urine.

Additionally the full force of the metbolic alkalosis is revealed with the bicarb shooting from 29 to 41. I suspect this is due to vomiting. The urine chloride < 20 is consistent with this. This is Cl responsive metabolic alkalosis. It will (eventually) respond to the NS.

The urine also has a massive anion gap, around 90. What is the unmeasured anion?

(BTW the answer is bicarbonate)

But what is driving down the sodium? The patient appears volume depleted, and the steadily improving serum creatinine points to a patient with pre-renal AKI.

In volume depletion hyponatremia, giving fluid improves the serum sodium, it doesn’t make it worse. Also these patients do not typically make 3600 ml of urine

In it is highly unusual to make that much urine and have the sodium fall, usually that kind of urine output is associated with arising sodium. A hint to what is happenning can be found in the electrolyte free water clearance (Clefw).

The high urine sodium and really high urine potassium makes the urine essentially isotonic to plasma. Even though the patient is making 3.6 liters, it is like taking ladles of soup from a big pot, no matter how many ladles you take out it doesn’t change how salty the soup is.

pot wo GIF

Because the electrolyte free water is close to zero, those 3.6 liters of urine are not afffecting the serum sodium at all. So why is the sodium falling? I suspect this is due to the patient drinking (unrecorded) water.

So what would you do if faced with a falling sodium in a volume depleted patient?

I chose Tolvaptan plus continued 0.9% NS at 150/hr. The following day, the labs look…better.

I think this patient had nausea induced ADH in addition to severe metabolic alkalosis and volume deficiency. I found it interesting.

Originally tweeted by Joel M. Topf, MD FACP (@kidney_boy) on July 30, 2021.

What I loved about it is that the full lab interpretation required six different equations:

  • Anion Gap
    • the rare case of a relevant anion gap despite an increased serum bicarb
  • Gap Gap analysis
    • First the Delta Ratio
    • Then the Bicarbonate Before
  • Urine chloride in metabolic alkalosis
    • <20 mEq/L is chloride responsive
  • Urina anion gap
    • People think it is just for RTAs…not true
  • Electrolyte free water clearance

And I got great comments from Twitter. Some highlights:

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Acid-Base

Acid-Base (Powerpoint)
  • This is a lecture written for medical students getting their first exposure to acid-base physiology.
  • This is a version for residents where the learners have previous experience with acid base. (Powerpoint | PDF)
  • Scope:
    • primary disorder
    • second primary disorders affecting compensation
    • anion gap
    • osmolar gap
    • bicarbonate before
  • The presentation depends on a brand new supplemental questions handout (Word, PDF). This is an 11 page book of 67 unique practice questions with answers
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Resident lecture on NAGMA

One hour lecture on NAGMA. Just some small changes edits from the last time I gave it. It is one of the few lectures that is still in PowerPoint. It is due for a complete overhaul. It also needs a slide on the treatment of RTA that covers the amount of bicarbonate in a 650 mg tablet (8 mmol) and the fact that distal (type 1) RTA requires a limited amount of bicarbonate (at most 1 mmol/kg). This is appropriate for residents and medical students.

If you are interested in ward teaching and RTA, take a look at this post by Robert Centor.

Also this is a nice article on the issue of saline having a pH of 5.5, covering both the reason (its the PVC bag) and the implications (none).

NAGMA (PPT)

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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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Acid-Base Chapters (Chapters 10-16) from Fluids

Chapter 10: Introduction to Acid-Base

Chapter 11: Introduction to Metabolic Acidosis
Chapter 12: Non-Anion Gap
Chapter 13: Anion Gap Metabolic Acidosis
Chapter 14: Metabolic Alkalosis
Chapter 15: Respiratory Acidosis
Chapter 16: Respiratory Alkalosis
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Delta anion gap. Not as good as we think it is.

One of the concepts that is regularly taught in the evaluation of acid-base status is determining if there are multiple acid base disorders by evaluating the ratio of the delta anion gap/delta bicarbonate.

I teach this concept as determining what the bicarbonae would be in the absence of or prior to the anion gap.

The concept comes from the idea that for every mEq of bicarbonate that is consumed by the strong acid (other anion) the anion gap should rise by one. So if the bicarb is 16, a delta of 8, we would expect an anion gap of 20, a normal anion gap of 12 plus the delta bicarbonate of 8. This is a ∆AG/∆Bicarb of one.

If the patient had a pre-existing metabolic alkalosis with a bicarbonate of 30, then the patient would have a bicarbonate of 22 and an anion gap of 20. This would give ∆AG/∆Bicarb of 8/2 or 4.
If the patient had a pre-existing metabolic acidosis (non-anion gap) with a bicarbonate of 16, then the patient would have a bicarbonate of 8 and an anion gap of 20. This would give ∆AG/∆Bicarb of 8/16 or 0.5.
Concurrent metabolic alkalosis leads to ratios over 1 and preexisting metabolic acidosis (non-anion gap) yield a ratio below 1.
I had always been suspicious of this because the assumption of the one for one change in anion gap and bicarbonate. This didn’t seem to be very biologic. Turns out my suspicion was justified as numerous studies (Androgue, Elisaf) have shown that the ratio does not hold up.
In this paper by Paulson et al they found:
[Some authors] suggested that mixed disturbances should be considered if the ratio is less than 0.8 or greater than 1.2. Paulson, applying this rule to a group of normal control subjects and patients with simple metabolic acidosis, noted that the formula erroneously categorized 56% [specificity of 44%] of this group as mixed disturbances. Use of the 95% confidence interval of ±8 mEq/L increased the specificity to 97% but with a poor sensitivity of only 27%.
That’s terrible. Why torture the brains of medical students with this type of worthlessness.
Good review here.
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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.
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Coal Miner

The set up

Picture by Nicolas Holzheu

Coal miner presents to the ED with fever and vomiting

pH 7.23
pCO2 67
pO2 88
Na 144
Cl 96
BUN 8
K 3.2
Bicarb 27
Creatinine 0.6
glucose 128

Step one: determine the primary disorder

the pH is down, the HCO3 and CO2 are up so this is a respiratory acidosis

Step two: check to see if the compensation is appropriate

The CO2 is 67, since his chief complaint is not respiratory and he is a coal miner we will assume black lung and chronic COPD. So we will use the estimate for chronic respiratory acidosis
67 is almost 30 above normal pCO2, and for every 10 the CO2 rises the HCO3 should go up 3 (1 is this was acute). So a pCO2 of 67 should have a HCO3 of 2.7 x 3 = 8.1 above a normal bicarb of 24 = 32.1.
His actual bicarb is 27 so he has an additional metabolic acidosis (bicarb lower than predicted means metabolic acidosis).

Step three: if there is a metabolic acidosis what is the anion gap

The patient has a metabolic acidosis, so the anion gap is relevant. We calculate it and it is 21.

Step four: if there is an anion gap, calculate the bicarbonate before

The patient has an anion gap so to calculate the bicarbonate before the anion gap we subtract 12 from the calculated anion gap and add the difference to the current bicarbonate:
21-12 = 9 add that to the bicarbonate of 27 to get a bicarbonate of 36. This is higher than the predicted compensated bicarbonate from step two (32.1) so the patient has an additional metabolic alkalosis.

Final step: put it all together

The patient has black lung and COPD. His largest acid-base disorder is chronic respiratory acidosis. He does have an acute illness. This illness is causing an anion gap metabolic acidosis. Sepsis and multi organ failure does this. Prior to developing the anion gap the vomiting caused a metabolic alkalosis.
Its a triple disorder!