Hypokalemia
المؤلف:
Marcello Ciaccio
المصدر:
Clinical and Laboratory Medicine Textbook 2021
الجزء والصفحة:
p277-279
2025-08-27
360
Hypokalemia is defined as a plasma potassium concentration <3.5 mmol/L. It is mild when serum potassium values are between 3 and 3.4 mmol/L; it is severe when serum potassium values are less than 3 mmol/L.
The causes of hypokalemia can be distinguished into three classes:
• Reduced dietary intake
• Passage of potassium into the intracellular compartment
• Increased renal or extrarenal leakage
Table 1 summarizes the main causes of hypokalemia.
Table1. Causes of hypokalemia
Reduced dietary potassium intake is a rare cause because it can be compensated by reduced renal potassium excretion. Commonly, dietary potassium intake exceeds the amount excreted in the urine. Several causes of hypokalemia due to renal potassium loss lead to excess aldosterone (primary and secondary hyperaldosteronism) or, in general, excess mineralocorticoid and glucocorticoid hormones.
From a clinical point of view, the symptoms of hypokalemia rarely appear unless the potassium concentration is less than 3 mmol/L. Symptoms are related to alterations in muscular system (muscular asthenia, myalgia, muscle cramps), the cardiovascular system (palpitations, tachycardia, electrocardiographic changes), nervous system (mental confusion, depression), urinary system (polyuria, renal morphological damage), gastrointestinal system (dysphagia, constipation, nausea, vomiting), and metabolism (reduced protidosynthesis, reduced glucose tolerance, metabolic alkalosis).
Diagnosis and Therapy
Hypokalemia is often asymptomatic. Evaluation begins by looking for signs and symptoms that require urgent treatment, such as asthenia or palpitations, electrocardiogram (ECG) changes, severe hypokalemia, rapid onset of hypokalemia, underlying heart disease, or cirrhosis. Identification and treatment of concurrent hypomagnesemia is critical because magnesium depletion often prevents potassium correction and may exacerbate hypokalemia-induced heart rhythm alterations.
In most cases, an accurate history allows to identify the K+ depletion etiology. Diuretic or laxative abuse as well as induced vomiting, although difficult to ascertain, should be excluded. In patients with marked leukocytosis (e.g., in acute myeloid leukemia) and normokalemia, plasma potassium concentration may be reduced due to a laboratory artifact related to the ability of leukocytes to capture K+ at room temperature. This pseudohypokalemia can be avoided by separating plasma (or serum) from cells immediately after collection.
A history of paralysis, hyperthyroidism, or the use of insulin or beta-agonists suggests a possible transcellular shift leading to redistribution-related hypokalemia (passage of K+ within cells).
After ruling out reduced dietary intake or transcellular displacement of K+, the evaluation of renal response can help detect the hypokalemia cause. Hypokalemia with mini mal urinary potassium excretion 15 mmol/day) suggests the renal potassium loss. ECF volume status, blood pressure, and acid–base balance alterations may identify the cause of excessive renal potassium loss (Fig. 1).
Fig1. Diagnostic algorithm of hypokalemia. (Copyright EDISES 2021. Reproduced with permission)
Therapy aims to increase potassium levels, minimize ongoing losses, and treat the underlying disease to prevent complications. KCl administration (potassium chloride) is the choice therapy. KCl results in a rapid increase in plasma potassium concentration. In addition, the persistence of the Cl− ion in ECF limits the initial potassium entry into the cells, thus promoting an increase in plasma potassium. Finally, chloride supports metabolic alkalosis, often associated with hypokalemia. In cases of mild hypokalemia, KCl is administered orally or intravenously, in more severe cases.
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