bubble_chart Overview

The human body relies entirely on external intake for potassium, with approximately 50–100 mmol of potassium ingested daily from food, 90% of which is absorbed by the small intestine. The kidneys are the primary organs responsible for potassium excretion and balance regulation. The potassium in the glomerular filtrate is first completely reabsorbed in the proximal tubules, after which the distal tubule cells and collecting duct cells secrete excess potassium, which is then excreted in the urine to maintain potassium balance in the body. However, when potassium intake is insufficient, the kidneys cannot significantly reduce potassium excretion to retain potassium in the body, making potassium deficiency more likely. The serum potassium concentration ranges from 3.5 to 5.5 mmol/L, with an average of 4.2 mmol/L. Typically, a serum potassium level below 3.5 mmol/L is referred to as hypokalemia. However, a decrease in serum potassium does not necessarily indicate a deficiency of potassium in the body; it only reflects the potassium concentration in the extracellular fluid. Conversely, whole-body potassium deficiency may not always result in reduced serum potassium levels. Therefore, clinical judgment should be based on a combination of medical history and clinical manifestations.

bubble_chart Etiology

There are many causes of potassium deficiency or hypokalemia, the common ones include: a. Insufficient potassium intake, such as prolonged inadequate food intake, failure to provide potassium-containing fluids during intravenous rehydration for patients, or insufficient potassium supplementation in nutritional support solutions; b. Excessive potassium loss, such as vomiting, diarrhea, gastrointestinal decompression, and digestive fistulas leading to significant loss of digestive fluids, long-term use of diuretics like furosemide and ethacrynic acid, or corticosteroids causing excessive renal potassium excretion; c. Abnormal distribution of potassium in the body, such as massive infusion of glucose combined with insulin, or alkalosis, which can cause a large amount of potassium to shift into cells, resulting in hypokalemia.

bubble_chart Clinical Manifestations

The clinical manifestations are related to the severity of intracellular and extracellular potassium deficiency, but more importantly, they depend on the speed at which hypokalemia occurs. Symptoms are more severe when serum K⁺ is <2.5 mmol/L. If potassium deficiency occurs over a short period, symptoms appear rapidly and may even lead to sudden death.

(1) Neuromuscular System: Manifested as decreased excitability of nerves and muscles. When serum K⁺ is <3.0 mmol/L, weakness in the limbs may occur. If it falls below 2.5 mmol/L, flaccid paralysis may develop, most notably in the limb muscles, with diminished or absent tendon reflexes. When respiratory muscles are affected, it can lead to dyspnea. Central nervous system symptoms include depression, fatigue, apathy, drowsiness, confusion, and even unconsciousness.

(2) Digestive System: Potassium deficiency can weaken intestinal motility. Mild cases may present with poor appetite, nausea, and constipation, while severe hypokalemia can cause abdominal distension and fullness, as well as paralytic ileus.

(3) Cardiovascular System: Hypokalemia generally increases myocardial excitability, leading to palpitations and arrhythmias. In severe cases, atrioventricular block, ventricular tachycardia, and ventricular fibrillation may occur, eventually causing the heart to arrest in systole. Additionally, it can reduce myocardial tension, lead to cardiac enlargement, peripheral vasodilation, and hypotension.

(4) Urinary System: Chronic hypokalemia can result in potassium-deficient nephropathy and renal dysfunction, impairing the kidney's concentrating ability and causing polyuria with low specific gravity, particularly increased nocturia. This may be due to damage to the distal renal tubular cells, reducing their response to antidiuretic hormone and impairing water reabsorption. Furthermore, decreased smooth muscle tension in the bladder due to potassium deficiency can lead to urinary retention, often predisposing patients to pyelonephritis.

(5) Acid-Base Imbalance: Hypokalemia can lead to metabolic alkalosis.

bubble_chart Diagnosis

The diagnosis is primarily based on medical history and clinical manifestations. When serum potassium levels (K⁺

) are <3.5 mmol/L and symptoms are present, a diagnosis can be made. However, in cases of dehydration or acidosis, serum K⁺ may not show a decrease. Additionally, electrocardiogram (ECG) testing can often sensitively reflect hypokalemia. The main ECG manifestations include prolonged Q-T interval, S-T segment depression, flattened, widened, biphasic, or inverted T waves, or the appearance of U waves.

bubble_chart Treatment Measures

(1) Generally, oral potassium is administered. The preventive dose for adults is 30–40 ml/d of 10% potassium chloride (each gram of potassium chloride contains 13.4 mmol of potassium). Potassium chloride taken orally may cause gastrointestinal reactions, so potassium citrate is preferable (1 g of potassium citrate contains 4.5 mmol of potassium).

(2) Intravenous infusion of potassium chloride is used for patients who cannot take oral medication or have severe potassium deficiency. The usual concentration is 10–20 ml of 10% potassium chloride added to 1.0 L of 5% glucose solution. Each gram of potassium chloride must be evenly infused over at least 30–40 minutes and should never be administered by intravenous push. The amount of potassium supplementation depends on the condition. For prevention, adults usually receive 3–4 g/d of potassium chloride; for treatment, 4–6 g or more may be required.

(3) Key points for potassium supplementation: a. Potassium supplementation should only be considered if urine output exceeds 30 ml/h; otherwise, hyperkalemia may occur. b. For patients with acidosis, hyperchloremia, or impaired liver function, potassium glutamate may be considered. Each 6.3 g vial contains 34 mmol of potassium and can be added to 0.5 L of glucose solution for intravenous infusion. c. Excessively high concentrations of potassium chloride in intravenous infusions can irritate veins, causing pain or even venous spasm and thrombosis. d. Avoid overly rapid infusion, as a sudden increase in serum potassium concentration may lead to cardiac arrest. e. K⁺

enters cells very slowly, taking about 15 hours to achieve intra- and extracellular balance. In cases of impaired cellular function, such as hypoxia or acidosis, the time required for potassium balance is even longer—approximately one week or more. Therefore, correcting potassium deficiency takes several days, and the process should not be rushed or interrupted prematurely. f. If hypocalcemia coexists with hypokalemia, calcium supplementation should also be considered, as symptoms of hypocalcemia are often masked by hypokalemia. Once hypokalemia is corrected, hypocalcemic convulsions may occur. g. During short-term high-dose potassium supplementation or long-term potassium therapy, regular monitoring of serum potassium levels and electrocardiograms is necessary to prevent hyperkalemia.

bubble_chart Prevention

The emphasis is on prevention. First, promptly remove the causes of disease. Second, for those at risk of potassium deficiency, such as patients who have been fasting for a long time or have lost significant bodily fluids, potassium should be supplemented in a timely manner.