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HYPERKALEMIA


A. Note symptoms of hyperkalemia such as anorexia, nausea, vomiting, and weakness. Identify predisposing factors such as renal disease, metabolic acidosis (diabetic ketoacidosis or aspirin intoxication), acute hemolysis, or acute rhabdomyolysis. Consider excessive intravenous administration of potassium in patients receiving intravenous fluids.

B. Note Vital signs and assess the circulatory status (skin color, capillary refill). Suspect congenital adrenal hyperplasia in infants with ambiguous genitalia. Addison’s disease is associated with a characteristic slate-gray skin color. Note the signs of diabetic ketoacidosis (dehydration, Kussmaul respirations, acetone breath).

C. ECG findings in hyperkalemia include peaked T waves, which may progress to widening of the QRS complex, decreased P-wave amplitude, and increased P-R interval. Serum potassium concentrations above 6 mEq/L may produce bradycardia, dysrhythmias, and cardiac arrest.

D. Since potassium is the major intracellular cation, any significant cellular damage (acute hemolysis, or acute rhabdomyolysis) may elevate serum potassium levels. Consider the possibility that hemolysis of red blood cells during blood sampling is responsible for a false elevation of serum potassium. Metabolic acidosis elevates serum potassium as a result of displacement of potassium from within the cell by hydrogen ions.

E. When serum potassium levels are more than 7 mEq/L and ECG changes are present, administer: sodium bicarbonate, 1 to 2 mEq/kg intravenously over 10 to 15 minutes; calcium gluconate, 50 to 100 mg/kg by slow intravenous drip over 5 to 10 minutes, with a maximum single dose of 1 g; and/or glucose D25, 2 cc/kg with insulin 0.2 units/kg intravenous over 10 to 15 minutes. Treat less urgent situations with D5 or D10 isotonic solution, 20 cc/kg per hour, and consider Lasix. When adrenal disorders are suspected, give hydrocortisone (Solucortef), 10 mg/kg intravenous stat, and the same dosage on a daily basis divided into four equal doses to be given each 6 hours. At the same time, give oral Florinef 0.1 mg. In addition, lower potassium with a potassium-binding resin, kayexalate 1 g/kg by rectum as an enema. Serum potassium may be expected to decrease by 0.5 to 2.0 mEq/L with each enema. This may be repeated 2 or 3 times per day. In life-threatening situations, consider peritoneal dialysis and/or hemodialysis.

F. Defects in mineralocorticoid secretion or action may result in excessive sodium excretion and potassium retention. Causes of a deficiency of mineralocorticoid (desoxycorticosterone or aldosterone) include deficiencies in enzymes (20, 22 desmolase, 3-beta-al dehydrogenase, 21-hydroxylase, 18-hydroxylase). A defect in the 20, 22 desmolase enzyme results in an accumulation of cholesterol in the adrenal gland (lipoid hyperplasia), which is usually fatal in early infancy. Defects in 3-beta-ol dehydrogenase and 21-hydroxylase produce adrenal hyperplasia due to the excessive ACTH secretion that accompanies decreased cortisol production. A defect in enzyme 11-dehydrogenase decreases aldosterone production but does not result in hyperkalemia since desoxycorticosterone has significant mineralocorticoid effect. Adrenal failure (Addison’s disease) caused by adrenal injury or autoantibodies presents with mineralocorticoid and glucocorticoid deficiencies. Additional causes of hyperkalemia include end-organ unresponsiveness to aldosterone and congenital adrenal hypoplasia, a rare embryologic deficiency of the adrenal gland.