A Teenager Presents With Hypokalemia and Metabolic Alkalosis

Hypokalemia is one of the most common electrolyte disorders in hospitalized patient. Causes of hypokalemia include impaired renal potassium (K+) excretion, gastrointestinal losses or transcelluar shifts. Assessments of urinary K+ excretion, acid-base status, and blood pressure are three major components to the causes of hypokalemia. A random urine K+-to-creatinine (K+/Cr) less than 13 mEq/g Cr (<1.5 mEq/mmol) in a patient with hypokalemic metabolic alkalosis suggests poor intake, surreptitious vomiting, congenital pyloric stenosis, a shift of K+ from extracellular fluid into the cells, laxative abuse, familial or sporadic periodic paralysis. In the setting of hypertension, urine K/Cr >1.5 mEq/mmol indicates primary and secondary hyperaldosteronism, Liddle syndrome, or apparent mineralocorticoid excess. By contrast, in the absence of hypertension, a urine K+ /Cr>1.5, is usually suggestive of surreptitious use of diuretic, Bartter syndrome or Gitelman syndrome. Measurements of the plasma renin activity and plasma aldosterone concentration are necessary to differentiate these conditions from one another. Severe or symptomatic hypokalemia, if not recognized early or treated appropriately can lead to significant mortality and morbidity. In this article the basic principles of normal K+ homeostasis and the pathophysiology that can disturb this balance are discussed. A selected case report focusing on the essential aspect of patient’s presentation, signs and laboratory data followed by series of questions with particular attention to the diagnosis and management of hypokalemia needed to assist in the differential diagnosis and treatment are also discussed. Each question is followed by detailed discussion and reviews the recent publications that are useful at the bedside.