The transcellular shift of potassium after initiation of insulin therapy in children with diabetic ketoacidosis (see Chapter 171) can be dramatic. These patients have reduced total bodypotassium because of urinary losses, but they often have a normal serum potassium level before insulin therapy from a trans-cellular shift into the extracellular space secondary to insulin deficiency and metabolic acidosis. Children receiving aggressive doses of β-adrenergic agonists (albuterol) for asthma can have hypokalemia resulting from the intracellular movement of potassium. Poor intake is an unusual cause of hypokalemia, unless also associated with significant weight loss (anorexia nervosa).
Diarrhea has a high concentration of potassium, and the resulting hypokalemia usually is associated with a metabolic acidosis secondary to stool losses of bicarbonate. With emesis or nasogastric suction, there is gastric loss of potassium, but this is fairly minimal given the low potassium content of gastric fluid (approximately 10 mEq/L). More important is the gastric loss of hydrochloride, leading to a metabolic alkalosis and a state of volume depletion. Metabolic alkalosis and volume depletion increase urinary losses of potassium.
Urinary potassium wasting may be accompanied by a metabolic acidosis (proximal or distal renal tubular acidosis) (see Chapter 37). Loop and thiazide diuretics lead to hypokalemia and a metabolic alkalosis. Bartter syndrome and Gitelman syndrome are autosomal recessive disorders resulting from defects in tubular transporters. Both disorders are associated with hypokalemia and a metabolic alkalosis. Bartter syndrome is usually associated with hypercalciuria, often with nephrocalcinosis; children with Gitelman syndrome have low urinary calcium losses, but hypomagnesemia secondary to urinary losses.
In the presence of a high aldosterone level, there is urinary loss of potassium, hypokalemia, and a metabolic alkalosis. There also is renal retention of sodium, leading to hypertension. A variety of genetic and acquired disorders can cause high aldosterone levels. Liddle syndrome, an autosomal dominant disorder caused by constitutively active sodium channels, has the same clinical features as hyperaldosteronism, but the serum aldosterone level is low.
The heart and skeletal muscle are especially vulnerable to hypokalemia. Electrocardiographic (ECG) changes include a flattened T wave, a depressed ST segment, and the appearance of a U wave, which is located between the T wave (if still visible) and P wave. Ventricular fibrillation and torsades de pointes may occur, although usually only in the context of underlying heart disease. Hypokalemia makes the heart especially susceptible to digitalis-induced arrhythmias.
The clinical consequences in skeletal muscle include muscle weakness and cramps. Paralysis is a possible complication (generally only at potassium levels <2.5 mEq/L). Paralysis usually starts with the legs, followed by the arms. Respiratory paralysis may require mechanical ventilation.
Some hypokalemic patients develop rhabdomyolysis, especially following exercise. Hypokalemia slows gastrointestinal motility; potassium levels less than 2.5 mEq/L may cause an ileus. Hypokalemia impairs bladder function, potentially leading to urinary retention. Hypokalemia causes polyuria by producing secondary nephrogenic diabetes insipidus. Chronic hypokalemia may cause kidney damage, including interstitial nephritis and renal cysts. In children, chronic hypokalemia, as in Bartter syndrome, leads to poor growth.