Tag: delta 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:

Posted on

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.