Tag: electrolyte cards

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Polyuria, polydipsia

The set up

Patient is the ICU, you receive a consult for hypernatremia resistant to therapy for three days.

Na 174
Cl 128
BUN 38

K 3.2
HCO3 27
Cr 1.6
glucose 128

urine lytes:
Na 56
K 12
Body weight 45 kg
urine output 2,800

Step one


Calculate the fluid deficit:
We assume the increase in sodium is entirely due to loss of water. If the patient is hypotensive, tachycardic orthostatic or has other clues that he maybe volume depleted, the situation is more complex. We calculate the percentage that the sodium is elevated above an imagined “ideal sodium.” Many equations use 140 as the idealized sodium, I tend to use 145. The percentage the sodium is above the ideal is identical to the percentage of the total body water that is needed to lower the sodium to the target level.

174-145 / 145 = 0.2 (the sodium is 20% above 145)

Multiple that by the estimated total body water (weight x % body water) = 5.4 liters

I used 60% for estimated total body water. The patient looks like a young boy. Rose suggests lowering the estimated % body water by 10% so 50% would be okay also. In the elderly and obese this number can go below 50%. 

Step two


Going from 174 to 154 is too much change in 24 hours. The speed limit is 12 mmol/L/day so we will target a change from 174 to 162.

I use a modified water deficit formula. I divide 12 (the change in sodium we are looking for) by the target sodium (current sodium minus 12):

12/(174-12) = 0.08 x total body water = 2.0 liters or just over 80 mL/hour


Step three

Calculate the electrolyte free water clearance. The reason the ICU team repeatedly failed to correct the sodium is that they corrected the deficit without accounting for the ongoing water losses. In this case it is renal losses. If you just add the urine volume to the water deficit you will over estimate the amount of water needed because the urine contains sodium and potassium. To account for the electrolyte content of the urine we calculate the free water clearance.

Urine Na + K divided by the serum Na will give the ratio of urinary electrolytes to serum solute. 
56 + 12 / 174 = 39%
The urine has 39% electrolyte content of plasma, another way of thinking about this is that 39% of the urine volume is isotonic and the remainder (61%) is pure water. The 61% is what we are interested in; multiply the urne output by 61% this is the volume of water we need to give the patient to account for his ongoing renal losses. 
Then multiply this by the urine output (2,800) to get the electrolyte free water clearance, 1705 ml. This is another 71 mL/hour

Wrap up

Final fluid orders: 154 mL/hour of water, this can be given as D5W in the IV or preferably oral flushes. This calculation does not insensible losses.


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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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Patient with a Liddle problem

The Set Up

42 year old African American woman presents with muscle weakness and palpitations. Her blood pressure is 180/110. Her hypertension has been documented since age 16.

Her sister has a history of hypokalemia and hypertension. Three of her six kids, all of which are younger than 20 have hypertension.

Na 144
Cl 96
BUN 14

Photo: Creative Commons/Paleontour

K 2.7
Bicarb 42
Cr 0.8

ABG
pH 7.54
pCO2 51
paO2 97

Step one


What is the primary acid-base disturbance.
pH is elevated, so its an alkalosis. The pH, pCO2 and HCO3 are all going up (same direction) so it is a metabolic condition. Metabolic alkalosis.

Step two


Is compensation appropriate.
To find the target pCO2 add two thirds of the delta bicarb to a normal pCO2 of 40 mmHg.

Her bicarb is 42, and the delta (42 – normal bicarb of 24) = 18.
Two thirds of 18 is 12.
40 + 12 = 52 mmHg.

Actual pCO2 is 51, so we are in the house, pCO2 is appropriate for a serum bicarbonate of 42, no second primary disorder affecting compensation.

Step three


What is the differential of hypokalemia, metabolic alkalosis and abnormal blood pressures?

Hypokalemnia and metabolic alkalosis is an important pattern. The first concept that medical students invariably want to lean on is the intracellular exchange of hydrogen and potassium. When there is hypokalemia, potassium flows from the cells. To maintain electroneutrality hydrogen goes into the cells. The certainly is operating in these cases, however a model that looks at changes in total body potassium is much richer.

The reason that metabolic alkalosis and hypokalemia can walk together is that they both are responces to hyperaldosteronism. The increased aldosteronism can be primary, secondary or unusual.

  • Secondary hyperaldosteronism. Patients with GI losses, diuretics or other causes of volume depletion will upregulate their aldosterone. Aldosterone will fight the volume depletion by reabsorbing sodium in the principle cells, flowing down its concentration gradient through the eNAC. Aldosterone increases the number and activity of the eNAC channels (it also increases the number and activity of the potassium channels and the Na-K-ATPase).
    • Volume deficiency
    • Renal artery stenosis decreases renal blood flow and induces a secondary hyperaldosteronism
  • Primary hyperaldosteronism. This is major cause of hypertension. Patients can have metabolic alkalosis and hypokalemia. If your patient has hypokalemia and alkalosis, definatly pursue primary hyperaldo, but do not rule out primary hyperaldo if you don’t have the electrolyte abnormality. Most patients with pimary hyperaldo do not have the typical electrolytes.
  • Unusual: one conditions to remember that cause metabolic alkalosis and hypokalemia:
    • Liddle syndrome. Patients have a mutation at 16p12 that encode the beta and gamma subunits of the eNAC. The eNAC is no longer sodium selective and is always open. The sodium reabsorption causes hypertension. The eNAC channel also increases potassium and hydrogen secretion.
    • The functional opposite of Liddle syndrome is Pseudohypoaldosteronism type 1. Here mutations to the alpha, beta or gamma subunits results in resistance to the effects of aldosterone. Patient have sodium wasting and hyperkalemia. There is an autosomal recessive and autosomal dominant form.
    • Licorice and SAME (Syndrome of Apparent Mineralocorticoid Excess) The structure of cortisol and aldosterone are almost identical and the mineralocorticoid receptors in the principle cells are unable to differentiate between these molecules. This means that cortisol can activate the mineralocorticoid receptors. This is made worse by the fact that cortisol typically is found at concentrations a 1000-fold higher than aldosterone. To prevent cortisol from acivating the mineralocorticoid receptors, cortisol is rapidly metabolised by 11-beta-hydoxysteroid dehydrogenase. If this enzyme is absent (SAME) or inhibited (licorice ingestion) you can get wildly up-regulated mineralocorticoid activity with simultaneous suppression of aldosterone.
  1. Sodium is reabsorbed through the ENaC. Sodium moves
    down its concentration gradient.
  2. The movement of sodium is electrogenic and results in
    a negative charge in the tubule.
  3. Chloride in the tubule can be reabsorbed paracellularly.
    The more chloride that is reabsorbed the less potassium
    is secreted.
  4. Potassium flows down an electrical and chemical gradient into the tubule.

Step four


The family history shows first degree relatives with a similar condition. This suggestes autosomal dominant transmission. This is consistant with Liddle syndrome.

Step five

Next steps in the diagnosis. Though the genetics are suggestive of autosomal dominant transmission, Liddle Syndrome is very uncommon while primary hyperaldosteronism is relatively common. A serum aldosterone level will separate these patients neatly. In Liddle Syndrome the aldosterone is suppressed, while in primary hyperaldosteronism it is up regulated. Genetic testing is available to confirm the diagnosis.

See these posts at the Renal Fellow Network for additional information.

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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!