Hyperkalemia is serum K concentration > 5.5 mEq/L resulting from excess total body K stores or abnormal movement of K out of cells. There are usually several simultaneous contributing factors, including increased K intake, drugs that impair renal K excretion, and acute or chronic kidney disease. It can also occur in metabolic acidosis as in diabetic ketoacidosis. Clinical manifestations are generally neuromuscular, resulting in muscle weakness and cardiac toxicity that, when severe, can degenerate to ventricular fibrillation or asystole. Diagnosis is by measuring serum K. Treatment may involve decreasing K intake, adjusting drugs, giving a cation exchange resin and, in emergencies, Ca gluconate, insulin, and dialysis.
The most common cause of increased serum K concentration is probably pseudohyperkalemia caused by hemolysis of RBCs in the blood sample. Normal kidneys eventually excrete K loads, so sustained, nonartifactual hyperkalemia usually implies diminished renal K excretion. However, other factors usually contribute. They can include increased K intake, increased K release from cells, or both (see Table 6: Factors Contributing to Hyperkalemia). When sufficient KCl is ingested or given parenterally, severe hyperkalemia may result even when renal function is normal but is usually temporary.
Hyperkalemia due to total body K excess is particularly common in oliguric states (especially acute kidney injury) and with rhabdomyolysis, burns, bleeding into soft tissue or the GI tract, and adrenal insufficiency. In chronic kidney disease, hyperkalemia is uncommon until the GFR falls to < 10 to 15 mL/min unless dietary or IV K intake is excessive.
Symptoms and Signs
Although flaccid paralysis occasionally occurs, hyperkalemia is usually asymptomatic until cardiac toxicity develops.
In the rare disorder hyperkalemic familial periodic paralysis, weakness frequently develops during attacks and can progress to frank paralysis.
Hyperkalemia (serum K > 5.5 mEq/L) may be found on routine serum electrolyte measurement. It should be suspected in patients with typical changes on an ECG or patients at high risk, such as those with renal failure, advanced heart failure, or urinary obstruction, or treated with ACE inhibitors and K-sparing diuretics.
ECG should be done on patients with hyperkalemia. ECG changes (see Fig. 1: ECG patterns in hypokalemia and hyperkalemia.) are frequently visible when serum K is > 5.5 mEq/L. Slowing of conduction characterized by an increased PR interval and shortening of the QT interval as well as tall, symmetric, peaked T waves are visible initially. K > 6.5 mEq/L causes further slowing of conduction with widening of the QRS interval, disappearance of the P wave, and nodal and escape ventricular arrhythmias. Finally, the QRS complex degenerates into a sine wave pattern, and ventricular fibrillation or asystole ensues.
Diagnosis of cause:
Pseudohyperkalemia should be considered in patients without risk factors or ECG abnormalities. Hemolysis may be reported by the laboratory. When pseudohyperkalemia is suspected, K concentration should be repeated, taking measures to avoid hemolysis of the sample.
Diagnosis of the cause of hyperkalemia requires a detailed history, including a review of drugs, a physical examination with emphasis on volume status, and measurement of electrolytes, BUN, and creatinine. In cases in which renal failure is present, additional tests, including renal ultrasonography to exclude obstruction, are needed (see Diagnosis).
Patients with serum K < 6 mEq/L and no ECG abnormalities may respond to diminished K intake or stopping K-elevating drugs. The addition of a loop diuretic enhances renal K excretion as long as volume depletion is not present.
Na polystyrene sulfonate in sorbitol can be given (15 to 30 g in 30 to 70 mL of 70% sorbitol po q 4 to 6 h). It acts as a cation exchange resin and removes K through the GI mucosa. Sorbitol is administered with the resin to ensure passage through the GI tract. Patients unable to take drugs orally because of nausea or other reasons may be given similar doses by enema. Enemas are not as effective at lowering K in patients with ileus. Enemas should not be used if acute abdomen is suspected. About 1 mEq of K is removed per gram of resin given. Resin therapy is slow and often fails to lower serum K significantly in hypercatabolic states. Because Na is exchanged for K when Na polystyrene sulfonate is used, Na overload may occur, particularly in oliguric patients with preexisting volume overload.
Moderate to severe hyperkalemia:
Serum K between 6 and 6.5 mEq/L needs prompt attention, but the actual treatment depends on the clinical situation. If no ECG changes are present and renal function is intact, maneuvers as for mild hyperkalemia are usually effective. Follow-up serum K measurements are needed to ensure that the hyperkalemia has been successfully treated. If serum K is > 6.5 mEq/L, more aggressive therapy is required. Administration of regular insulin 5 to 10 units IV is followed immediately by or administered simultaneously with rapid infusion of 50 mL 50% glucose. Infusion of 10% D/W should follow at 50 mL/h to prevent hypoglycemia. The effect on serum K peaks in 1 h and lasts for several hours.
If ECG changes include the loss of P-wave or widening of the QRS complex, treatment with IV Ca as well as insulin and glucose is indicated; 10 to 20 mL 10% Ca gluconate (or 5 to 10 mL 22% Ca gluceptate) is given IV over 5 to 10 min. Ca antagonizes the effect of hyperkalemia on cardiac muscle. Ca should be given with caution to patients taking digoxin because of the risk of precipitating hypokalemia-related arrhythmias. If the ECG shows a sine wave pattern or asystole, Ca gluconate may be given more rapidly (5 to 10 mL IV over 2 min). CaCl can also be used but can be irritating to peripheral veins and cause tissue necrosis if extravasated. CaCl should be given only through a correctly positioned central venous catheter. The benefits of Ca occur within minutes but last only 20 to 30 min. Ca infusion is a temporizing measure while awaiting the effects of other treatments or initiation of hemodialysis and may need to be repeated.
A high-dose β2-agonist, such as albuterol 10 to 20 mg inhaled over 10 min (5 mg/mL concentration), can lower serum K by 0.5 to 1.5 mEq/L and may be a helpful adjunct. The peak effect occurs in 90 min. However, β2-agonists are contraindicated in patients with unstable angina or acute MI.
Administration of IV NaHCO3 is controversial. It may lower serum K over several hours. Reduction may result from alkalinization or the hypertonicity due to the concentrated Na in the preparation. The hypertonic Na that it contains may be harmful for dialysis patients who also may have volume overload. When given, the usual dose is 45 mEq (1 ampule of 7.5% NaHCO3) infused over 5 min and repeated in 30 min. HCO3 therapy has little effect when used by itself in patients with severe renal insufficiency unless acidemia is also present.
In addition to strategies for lowering K by shifting it into cells, maneuvers to remove K from the body should also be done early in the treatment of severe or symptomatic hyperkalemia. K can be removed via the GI tract by administration of Na polystyrene sulfonate (see Mild hyperkalemia) or by hemodialysis. Hemodialysis should be instituted promptly after emergency measures in patients with renal failure or when emergency treatment is ineffective. Dialysis should be considered early in patients with end-stage renal disease and hyperkalemia because they are at increased risk of progression to more severe hyperkalemia and serious cardiac arrhythmias. Peritoneal dialysis is relatively inefficient at removing K.
Last full review/revision March 2013 by James L. Lewis, III, MD
Content last modified October 2013