K 3.5 - 5.0 LOW

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HYPOKALEMIA, a serum potassium value less than 3. 5 mEq/L. This abnormality occurs in up to 30% of hospitalized patients and the frequency increases to 50% in acutely ill patients at the time of admission. Potassium is predominantly located in skeletal muscle and the serum value represents only 2% of the total body potassium. Therefore, the serum potassium value is very sensitive to cellular influx or efflux of potassium. Hypokalemia will result when influx of potassium occurs. Common conditions which enhance cellular influx include alkalosis, glucose loads and insulin administration. Common medications which induce hypokalemia include diuretics (thiazide, loop and carbonic anhydrase inhibitors), insulin and beta agonists. Iatrogenic hypokalemia is common and medications should always be suspect as the etiology. If cellular shifts and medications have been eliminated as the cause, then the etiology is generally the result of increased renal or gastrointestinal potassium loss. If the etiology is elusive after a thorough intial intake, then determination of the 24 hour urine potassium helps determine whether the etiology is increased renal loss versus gastrointestinal loss. If the 24 hour urine potassium level is greater than 15 mmol/day in a hypokalemic patient, then increased renal potassium wasting is present.  Conversely, if the 24 hour urine potassium is less than 15 mmol/day, a gastrointestinal etiology should be suspected.

Diarrhea is a common cause of gastrointestinal hypokalemia. Profound hypokalemia in the presence of chronic diarrhea should raise concern about the possibility of a villous adenoma or non-beta-cell pancreatic islet cell tumors (vipoma, gastrinoma).

Conditions associated with renal potassium wasting include RTA, vomiting, diuretic use, Bartters syndrome, acute myelocytic leukemias and hypomagnesemia. In patients with renal hypokalemia, measuring the urinary pH is helpful as a persistently elevated level greater than 6 is suggestive of type 1 RTA. When hypokalemia is associated with hypertension, secondary causes of hypertension including renal artery stenosis, Cushings syndrome, primary aldosteronism and pheochromocytoma should be considered as possible underlying etiologies. A less common cause is excessive licorice ingestion.  Licorice contains glycyrrhizic acid, a substance which inhibits 11-betahydroxy steroid dehydrogenase thus causing increased levels of renal cortisol which then activate mineralocorticoid receptors (aldosterone-like effect) and cause renal potassium wasting.

Symptoms of hypokalemia usually manifest at levels less than 2. 5 mEq/L and include malaise, fatigue, weakness, hyporeflexia, paresthesias, cramps, paralysis, polyuria, rhabdomyolysis, constipation or ileus. In patients with underlying cardiovascular disease, hypokalemia increases the incidence of arrhythmias along with morbidity and mortality. Characteristic electrocardiographic changes include depression of the ST segment, flattening or inversion of the T waves and the presence of U waves. Digitalis toxicity is markedly potentiated by low serum potassium levels.

Hypomagnesemia is a common cause of hypokalemia, and if the low magnesium level is not corrected, hypokalemia will be resistant to treatment. Therefore, a serum magnesium level should be determined in all hypokalemic patients prior to an extensive work-up. Therapy for hypokalemia is with oral (potassium chloride, potassium phosphate or potassium bicarbonate) or intravenous potassium chloride. In outpatients whose hypokalemia is secondary to diuretic use, the addition of a potassium sparing diuretic (amiloride, spironolactone or triamterene), an ACEI, an ARB, or other medications known to increase the serum potassium may prove effective for long term management.