Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content + Download Section PDF Listen ++ For further information, see CMDT Part 21-04: Hypokalemia + Key Features Download Section PDF Listen +++ +++ Essentials of Diagnosis ++ Serum K+ < 3.5 mEq/L (< 3.5 mmol/L) Severe hypokalemia may induce arrhythmias and rhabdomyolysis Assessment of urine potassium excretion (urine potassium to creatinine ratio) can distinguish renal from non-renal loss of potassium +++ General Considerations ++ Hypokalemia can result from Insufficient dietary potassium intake Intracellular shifting of potassium from the extracellular space Potassium loss (renal or extra-renal) A low dietary potassium intake is usually not sufficient to cause hypokalemia because the kidneys can lower urine potassium excretion to very low levels (< 15 mEq/L) Shift of potassium into cells is increased by insulin and beta-adrenergic stimulation Excess potassium excretion by the kidneys is usually due to increased aldosterone action in the setting of preserved delivery of sodium to the distal nephron Magnesium An important regulator of potassium handling Low levels lead to persistent renal excretion of potassium; hypokalemia is often refractory to treatment until the magnesium deficiency is corrected Loop diuretics (eg, furosemide) cause substantial renal potassium and magnesium losses + Clinical Findings Download Section PDF Listen +++ ++ Usually asymptomatic When severe, may lead to muscle weakness and cardiac arrhythmias Involvement of gastrointestinal smooth muscle may result in constipation or ileus Rhabdomyolysis with associated acute kidney injury may occur with potassium levels < 2.5 mEq/L May additionally present as polyuria and polydipsia due to diminished concentrating ability of the kidney (nephrogenic DI) Chronic hypokalemia can lead to kidney disease (tubulointerstitial nephritis) + Diagnosis Download Section PDF Listen +++ +++ Laboratory Tests ++ Transient hypokalemia is generally secondary to intracellular shift, while sustained hypokalemia is secondary to potassium wasting or rarely inadequate intake Assessment of renal potassium excretion can help distinguish renal from non-renal causes A 24-hour urine collection is the most accurate method for assessing renal handling of potassium, with a level < 25 mEq/day compatible with appropriate renal potassium retention, and higher values corresponding to renal potassium wasting A more immediate assessment can be made by measuring a urine potassium to creatinine ratio (UK/UCr) on a spot urine sample In the setting of hypokalemia, a UK/UCr ratio < 13 mEq/g (or 1.5 mEq/mmol) is suggestive of a nonrenal etiology, most commonly gastrointestinal losses, intracellular potassium shifts, or inadequate dietary intake; higher values imply renal potassium wasting +++ Diagnostic Procedures ++ Characteristic progression of electrocardiogram (ECG) changes as the hypokalemia becomes more severe: initially T wave flattening, subsequently ST depressions and T wave inversions, ultimately U waves Typical ECG patterns may be not be observed in all patients + Treatment Download Section PDF Listen +++ ++ Any underlying conditions should be treated and causative drugs discontinued Magnesium deficiency should be corrected, particularly in refractory hypokalemia Oral potassium supplementation Safest for mild to moderate deficiency However, may cause gastrointestinal upset Dosages 20 mEq/day is generally sufficient to prevent hypokalemia In cases of established hypokalemia, 40–100 mEq/day over a period of days to weeks may be needed to treat hypokalemia and fully replete potassium stores Intravenous potassium Reserved for severe hypokalemia (< 3.0 mEq/L) Requires careful monitoring due to the risk of transient hyperkalemia Potassium chloride May be given through a peripheral intravenous line at rates up to 10–15 mEq/h diluted in 0.5% or 0.9% normal saline Higher rates (up to 20 mEq/h) require central access due to the risk of peripheral vein irritation In cases of concurrent metabolic acidosis, potassium repletion should take precedence over alkali administration because correction of the acidosis results in intracellular shift of potassium, further decreasing extracellular potassium concentration Similarly, potassium should be given in a saline, rather than dextrose solution since dextrose would stimulate insulin release and hence, intracellular shift + Outcome Download Section PDF Listen +++ +++ Follow-Up ++ Monitor ECG continuously when infusing intravenous potassium for severe hypokalemia Check serum potassium level every 3–6 hours +++ Complications ++ Hypokalemia increases the likelihood of digitalis toxicity In patients with heart disease, hypokalemia induced by beta-2-adrenergic agonists and diuretics may impose a substantial risk +++ Prognosis ++ Most hypokalemia will correct with replacement after 24–72 h +++ When to Refer ++ Patients with unexplained hypokalemia, refractory hyperkalemia, or clinical features suggesting alternative diagnoses (eg, aldosteronism or hypokalemic periodic paralysis) should be referred for endocrinology or nephrology consultation +++ When to Admit ++ Patients with symptomatic or severe hypokalemia, especially with cardiac manifestations, require cardiac monitoring, frequent laboratory testing, and potassium supplementation + References Download Section PDF Listen +++ + +Gumz ML et al. An integrated view of potassium homeostasis. N Engl J Med. 2015 Jul 2;373(1):60–72. Erratum in: N Engl J Med. 2015 Sep 24;373(13):1281. [PubMed: 26132942] + +Palmer BF et al. Physiology and pathophysiology of potassium homeostasis: Core Curriculum 2019. Am J Kidney Dis. 2019 Nov;74(5):682–95. [PubMed: 31227226] + +Wu KL et al. Identification of the causes for chronic hypokalemia: importance of urinary sodium and chloride excretion. Am J Med. 2017 Jul;130(7):846–55. [PubMed: 28213045]