Hypokalemia: pathophysiology, diagnosis and clinical management

Abstract

Hypokalemia is a commonly encountered electrolyte disturbance in clinical practice. As the predominant intracellular cation, potassium homeostasis ensures optimum cell functionality. Transient reductions in plasma potassium concentration depend on dietary intake and potassium excretion. An acceptable lower limit for serum potassium (K+) is 3.5 mmol/L. Although hypokalemia is well tolerated in healthy individuals, its severe cases can cause serious repercussions. The clinical manifestation of hypokalemia varies depending on the severity and duration of potassium loss from the body. Symptoms include heart palpitations, fatigue, muscle spasm, numbness, muscle twitches, and in severe cases cardiac arrhythmias and heart failure. The main route of K+ excretion is urine (90%) whereas a small amount (10%) is removed by GIT. External potassium losses are exacerbated in individuals with chronic diarrhea and prolonged sweating. Clinical history and examination are often sufficient to rule out the cause of hypokalemia. The overarching principle of hypokalemia therapy requires reducing potassium deficit, replenishing potassium reserves, and diagnosis and alleviation of causative factors to avoid future reoccurrences. Optimum recovery is reported in the majority of cases when underlying factors are eliminated. Potassium supplementation is paramount in all cases. The route of potassium administration should be based on the severity of the disease. The scope of this work is to provide a critical review of the pathophysiology, clinical diagnosis, and management of hypokalemia.