Thread by @medrants

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Hypokalemic quadriparesis (or severe hypokalemia)
39 yo Egyptian admitted with quadriparesis &K = 1.3
Spend #5goodminutes reading how #KashlakChief conceptualizes &teaches this electrolyte disorder. hope @thecurbsiders and @CPSolvers enjoy & @kidney_boy appropriately critiques

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Step 1 determine the acid-base status. Patients can get severe hypokalemia and have normal gap acidosis, normal acid-base or metabolic alkalosis. I am not certain about increased anion gap acidosis, but suspect that some DKA patients have severe hypokalemia.

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Let's first understand the normal gap acidosis hypokalemia. There are two major possibilities - distal RTA (Type 1) or diarrhea. We diagnose distal RTA when we have a normal gap acidosis and an elevated urine pH.

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Sjogren's syndrome seems the most often reported distal RTA with severe hypokalemia. Other associated rheumatologic diseases can present with this.

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Diarrhea - from infections or other secretory causes or surreptitious laxative use - can present with this combination. You can often distinguish between distal RTA and diarrhea with the urine anion gap en.wikipedia.org/wiki/Urine_ani…

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Quick summary - normal gap acidosis - check urine pH and consider urine anion gap to help with diagnosis

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Now lack of an acid-base disorder - hypokalemic periodic paralysis - perhaps more common in men of Asian descent and with hyperthyroidism. These patients will often have recurrent episodes.

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Finally, we get to our patient who had a bicarbonate of 37 and a very low K.
When I see hypokalemic metabolic alkalosis, in addition to a careful history, I check urine chloride and serum magnesium.

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The urine chloride often helps separate between volume contraction states (protracted UGI losses or diuretic use) and an increased aldosterone effect. Our patient denied vomiting and had a high urine chloride. So now we need to consider the aldo differential

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First, we must consider the possibility of an aldosterone producing adenoma. I have had such a patient. Check an aldo/renin ratio. These patients usually have significant hypertension and a long such history. The patient in consideration today did not have that history.

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He was not taking Fludrocortisone. His magnesium was normal. We consider Bartter's, Gittleman's and Liddle's but none of these fit in this patient. We ask him about licorice. "Liquorice contains glycyrrhizinc acid (GZA),"

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To learn more about these diagnoses - Elizabeth Mumford, Robert J Unwin, Stephen B Walsh; Liquorice, Liddle, Bartter or Gitelman—how to differentiate?, Nephrology Dialysis Transplantation, Volume 34, Issue 1, 1 January 2019, Pages 38–39, doi.org/10.1093/ndt/gf…

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Our patient freely admitted licorice oil use. Reports of this syndrome include "true" licorice candies, licorice oil and swallowing the spit from chewing tobaccos flavored with licorice.

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He told his physicians that during Ramadan he flavored his water with licorice oil to suppress his appetite. Potassium repletion quickly treated him.

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I hope that when presented with severe hyperkalemia, you understand the differential diagnosis and how the acid-base status can direct your other diagnostic evaluation.

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Oops hypokalemia