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HYPERKALEMIA, a serum potassium level greater than 5. 0 mEq/L. Symptoms often manifest at levels greater than 6. 5 mEq/L and include weakness, paresthesias, areflexia, ascending paralysis, respiratory failure, bradycardia or asystole. Potassium is predominantly located in the skeletal muscle and the serum value represents only 2% of the total body potassium. The serum potassium value is therefore very sensitive to transcellular shifts, and hyperkalemia results with massive cellular efflux of potassium secondary to tissue crush injuries, acidosis, insulin deficiency and hyperkalemic periodic paralysis. Artifactual hyperkalemia is seen with severe leukocytosis, thrombocytosis, hemolysis and poor venipuncture technique. Once artifactual causes and cellular shifts have been excluded, the most common cause of hyperkalemia is impaired renal function. In persons with chronic renal failure, the percent of excreted potassium which is lost in the stool increases to compensate for the impaired ability of the damaged kidneys; therefore, in these persons, constipation is a common cause of hyperkalemia. If the urine pH is consistently above 5.5 consider RTA type IV as a possible etiology for hyperkalemia and in patients with mild renal impairment, hyporeninemic hypoaldosteronism may be the cause. Hyperkalemia is also a potential complication of the tumor lysis syndrome and should be anticipated and screened for in patients with large bulky tumors undergoing chemotherapy.
Current therapies for kidney impairment, congestive heart failure, ascites, and proteinuria include medications associated with potassium retention and therefore these patients may be at risk for hyperkalemia. Medications frequently used for these conditions include ACEI's, ARB's, direct renin inhibitors, beta-adrenergic blocking agents, aldosterone antagonists (spironolactone and eplerenone), and potassium sparing diuretics (amiloride and triamterene). Some protocols even call for combinations of the aforementioned medications which increases the risk of hyperkalemia even more. NSAIDs and heparin usage may also be associated with hyperkalemia.
Electrocardiographic changes include tall peaked T waves (this is the earliest change noted and occurs at a potassium level of approximately 5.7 mEq/L), ST segment depression, loss of p waves, AV block, widening of the QRS interval (widens at a potassium level of 9-11mEq/L) and arrhythmias (bradycardia, asystole or ventricular fibrillation). Electrocardiographic changes consistent with hyperkalemia necessitate immediate treatment.
Long term therapy for mild, asymptomatic hyperkalemia entails discontinuing agents which elevate potassium levels if possible, a low potassium diet, and thiazide or loop diuretics. Hyperkalemia may improve in patients with advanced renal disease and metabolic acidosis with the use of sodium bicarbonate to increase the serum HCO3 to 18 or greater.
Acute treatment for severe or symptomatic hyperkalemia includes cardioprotection, which can be achieved by administering calcium gluconate 10 ml of 10% solution intravenously over 2-5 minutes (protection lasts 15-20 minutes), and lowering the serum potassium level. The latter may be achieved by causing intracellular shifts with sodium bicarbonate (1ampule of 7. 5% solution intravenously over 5 minutes), to induce alkalosis, or glucose and insulin administration (10 units regular insulin with 1 ampule of 50% glucose over 5 minutes) intravenously, or beta-adrenergic agonists (albuterol 20 mg via nebulizer). The above mentioned measures will temporarily reduce the serum potassium value so the patient must be monitored for rebound hyperkalemia. Another more permanent therapy includes the cation exchange resin Kayexalate given orally (15-60 grams in 50-100 ml of 20% sorbitol) or rectally (50-100 grams in 200 ml of 20% sorbitol for 30-60 minutes). Kayexalate may induce hypernatremia as it exchanges 1mEq potassium for 1. 5 mEq sodium. In summary, treatment of symptomatic hyperkalemia or hyperkalemia associated with electrocardiographic changes includes cardioprotection with calcium gluconate therapy,one of the above mentioned rapid but temporary treatments (sodium bicarbonate, insulin with glucose or beta agonist therapy), plus Kayexalate therapy. In patients with end stage renal disease, severe or symptomatic hyperkalemia is an indication for emergent dialysis.