Hypokalemia refers to a condition in which the serum potassium concentration is below 3.5 mmol/L.
Etiology
The main causes include:
- Insufficient potassium intake caused by gastrointestinal obstructions, prolonged fasting, coma, or anorexia nervosa.
- Significant potassium loss through the gastrointestinal tract, seen in cases of severe vomiting, diarrhea, continuous gastrointestinal decompression, or intestinal fistulas.
- Excessive renal potassium excretion due to prolonged use of loop diuretics like furosemide or thiazide diuretics, renal tubular acidosis, the polyuric phase of acute renal failure, or hyperaldosteronism.
- Long-term infusion of potassium-free solutions or insufficient potassium supplementation in parenteral nutrition.
- Redistribution of potassium into tissues, which may occur after infusion of large amounts of glucose and insulin or in cases of metabolic or respiratory alkalosis.
Clinical Manifestations
The earliest clinical manifestation is muscle weakness, initially presenting as weakness in the limbs, which may eventually extend to the trunk and respiratory muscles. Flaccid paralysis, diminished or absent tendon reflexes, and intestinal paralysis (manifested as anorexia, nausea, vomiting, abdominal distension, and absence of bowel sounds) may occur. Cardiac involvement primarily manifests as sinus tachycardia, conduction block, and arrhythmias.
Characteristic electrocardiogram (ECG) changes in hypokalemia include early findings of ST segment depression, reduced amplitude, widening, or inversion of T waves, followed by prolonged QT intervals and the appearance of U waves. Severe cases may show increased P wave amplitude, widened QRS complexes, supraventricular or ventricular tachycardia, or atrial fibrillation. However, not all patients exhibit these ECG changes, and therefore hypokalemia should not be diagnosed solely based on ECG abnormalities.
In certain cases, hypokalemia may present with subtle or nonspecific symptoms, especially when combined with severe extracellular fluid depletion, where dehydration- and sodium deficiency-related symptoms predominate. However, after dehydration is corrected, further dilution of potassium concentration can lead to the manifestation of hypokalemia symptoms.
Diagnosis
The diagnosis of hypokalemia can be made by combining detailed patient history, clinical manifestations, and laboratory tests. A potassium concentration below 3.5 mmol/L is diagnostic, and an ECG can serve as an auxiliary diagnostic tool.
Treatment
Addressing the underlying cause of hypokalemia is critical and often allows for its quick correction. Potassium supplementation depends on serum potassium levels, the presence of hypokalemia symptoms and signs, and whether there is ongoing potassium loss.
Mild hypokalemia cases can benefit from increased consumption of potassium-rich foods, such as oranges, bananas, or coffee, or through oral potassium chloride administration.
For patients unable to consume food, intravenous potassium supplementation may be required. The supplementation dosage, which is determined based on the degree of potassium reduction, typically ranges from 40 to 80 mmol per day. One gram of potassium chloride is approximately equivalent to 13.4 mmol of potassium, so daily potassium chloride supplementation typically ranges from 3 to 6 grams. Intravenous supplementation has specific concentration and infusion rate limitations. The potassium concentration in the intravenous solution should not exceed 40 mmol/L (approximately 3 grams of potassium chloride), and the infusion rate should generally be kept below 20 mmol/h.
Rapid infusion of potassium-containing solutions may cause a dangerous and potentially fatal rapid increase in serum potassium concentration. In rare cases where life-threatening arrhythmias or paralysis occur, a higher concentration and faster infusion rate may be employed, but this must be done via a central vein using an infusion pump under strict monitoring of serum potassium levels, muscle tone, and continuous ECG monitoring. Once the critical condition is stabilized, the infusion rate should be reduced.
In cases of hypokalemia accompanied by shock, blood volume should be restored promptly, and potassium supplementation should be initiated only after urine output exceeds 40 ml/h.
It is important to note that the rise in serum potassium concentration following potassium supplementation is often temporary, as most of the supplemented potassium is taken up by cells to replenish intracellular potassium deficits. As a result, close monitoring of serum potassium levels is necessary throughout the supplementation process.