The prize for the most extreme hypokalemia ever is not awarded solely for the magnitude of the hypokalemia. It is much more impressive when the potassium refuses to rise above 2.5 despite more than 160mmol of potassium being given per day for 5 days, as in the case of a lady in her mid 80s who had come in for an EVAR.

Her operation was uneventful. Day 1 post operatively, her potassium sank to 2.6 and never rose above this value till the day this post was written some 6 days later.

Why?

The causes of any serum electrolyte depletion can be split into inadequate intake, intracellular shift and excess losses.

Our patient was getting about 160mmol of potassium a day. Her intake was clearly more than sufficient.

Intracellular shift of potassium is usually caused by one of three things:

• insulin (as in refeeding syndrome, the best condition ever)
• a beta-adrenoreceptor agonist like salbutamol
• alkalosis

Our patient was having some occasional salbutamol for recently feeling SOB, but nowhere near enough to cause K of 2.2 as it was yesterday morning. A venous bicarbonate was 23.

So she must have been she losing it from somewhere…

GI fluid is potassium rich, but post operatively there had been no diarrhoea or vomiting. A CT Abdomen showed no anastomic leak. She was on no laxitives.

What about urine?

She was on no diuretics. That said, her magnesium was 0.4-0.5 since the operation. Her electrolytes seemed to worsen when she had her fortisips resumed. I was thinking of refeeding syndrome, which as you may be starting to realise, is fast becoming my favourite thing ever (her phosphate was low-normal).

The team initially wanted to treat her magnesium cautiously, with oral supplements. However, the magnesium barely budged on this for 5 days. In fact, reading the BNF will reveal that oral magnesium is only for preventing recurrence of the deficit, not for correction of a deficit. I decided to switch to IV magnesium after 5 days of this, on the grounds that hypomagnesemia can make hypokalemia impossible to correct. I also discussed the case with the endocrine registrar, who suggested adding urine U&Es to determine if the kidneys are to blame.

Why exactly does a lack of magnesium lead to persistently low potassium?

See this review. The gist is that there are magnesium-inhibited ROMK channels in the late distal tubule/collecting duct that let potassium into the urine. If you lose the magnesium, those channels go into freeflow mode.

What were the results of the urine U&Es, and how did you interperate them?

The fractional Na excretion was about 1.2%, which is normal for a euvolemic patient. <1% would go with pre-renal failure, or a normal response to hypovolemia as the kidneys try to preserve sodium. Anthing above 2% is suggestive of a problem with sodium reabsorption, and as most reabsorption happens in the tubules this suggests a tubular problem, like acute tubular necrosis.

The normal bicarbonate pushes us away from renal tubular acidosis as a cause for the hypokalemia, although does not rule it out.

So what’s your conclusion?

In our patient’s case, the amount of potassium lost was inappropriate for the serum level of potassium, so this suggested the cause of the hypokalemia was renal. In light of the generally OK function of the tubules as suggested by the fractional Na excretion, and the lack of acidosis as suggested by the bicarbonate (though I do appreciate a normal bicarbonate is not proof of normal pH), this was not a tubular problem, and in particular not renal tubular acidosis. Something was selectively letting potassium leak through the kidneys.

My money is on low magnesium helping K to leak via the ROMK channel. I corrected the magnesium intravenously yesterday, and the magnesium level was back to normal this morning, with a K of 2.8. I’ll post what happens to the K tomorrow. If it’s still abnormal, we’ll have to call the endocrine gods.