Hyperkalemia is a serum potassium concentration > 5.5 mEq/L, usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There are usually several simultaneous contributing factors, including increased potassium intake, drugs that impair renal potassium excretion, and acute kidney injury or chronic kidney disease. Hyperkalemia 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 potassium. Treatment may involve decreasing potassium intake, adjusting drugs, giving a cation exchange resin and, in emergencies, calcium gluconate, insulin, and dialysis.
(See also Overview of Disorders of Potassium Concentration.)
A common cause of increased serum potassium concentration is probably pseudohyperkalemia, which is most often caused by hemolysis of RBCs in the blood sample. This can also occur from prolonged application of a tourniquet or excessive fist clenching when drawing venous blood. Thrombocytosis can cause pseudohyperkalemia in serum (platelet potassium is released during clotting), as can extreme leukocytosis.
Normal kidneys eventually excrete potassium loads, so sustained, nonartifactual hyperkalemia usually implies diminished renal potassium excretion. However, other factors usually contribute. They can include increased potassium intake, increased potassium release from cells, or both (see Table: Factors Contributing to Hyperkalemia). When sufficient potassium chloride is rapidly ingested or given parenterally, severe hyperkalemia may result even when renal function is normal, but this is usually temporary.
Factors Contributing to Hyperkalemia
Hyperkalemia due to total body potassium 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 potassium intake is excessive.
Hyperkalemia (serum potassium > 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 potassium-sparing diuretics.
Pseudohyperkalemia should be considered in patients without risk factors or ECG abnormalities. Hemolysis may be reported by the laboratory. When pseudohyperkalemia is suspected, potassium concentration should be repeated, taking measures to avoid hemolysis of the sample (such as avoiding small-gauge needles or tourniquet use and limited fist clenching) and blood should be promptly processed by the laboratory.
ECG should be done on patients with hyperkalemia. ECG changes (see Figure: ECG patterns in hypokalemia and hyperkalemia.) are frequently visible when serum potassium 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. Potassium > 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 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.
Patients with serum potassium < 6 mEq/L and no ECG abnormalities may respond to diminished potassium intake or stopping potassium-elevating drugs. The addition of a loop diuretic enhances renal potassium excretion as long as volume depletion is not present.
Sodium 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 potassium 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 potassium in patients with ileus. Enemas should not be used if acute abdomen is suspected. About 1 mEq of potassium is removed per gram of resin given. Resin therapy is slow and often fails to lower serum potassium significantly in hypercatabolic states. Because sodium is exchanged for potassium when sodium polystyrene sulfonate is used, sodium overload may occur, particularly in oliguric patients with preexisting volume overload.
In patients with recurrent hyperkalemia, avoidance of drugs that can induce hyperkalemia (see Table: Factors Contributing to Hyperkalemia) is generally all that is needed. In patients who need ACE inhibitors and angiotensin receptor blocking agents (eg. patients with chronic heart failure or diabetic nephropathy), newly available polymer resin patiromer can be taken daily to help decrease gut absorption of potassium and prevent hyperkalemia.
Serum potassium 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 potassium measurements are needed to ensure that the hyperkalemia has been successfully treated. If serum potassium 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 potassium 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% calcium gluconate (or 5 to 10 mL 22% calcium gluceptate) is given IV over 5 to 10 min. Calcium antagonizes the effect of hyperkalemia on cardiac muscle. Calcium 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, calcium gluconate may be given more rapidly (5 to 10 mL IV over 2 min). Calcium chloride can also be used but can be irritating to peripheral veins and cause tissue necrosis if extravasated. Calcium chloride should be given only through a correctly positioned central venous catheter. The benefits of calcium occur within minutes but last only 20 to 30 min. Calcium 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 beta 2-agonist, such as albuterol 10 to 20 mg inhaled over 10 min (5 mg/mL concentration), can lower serum potassium by 0.5 to 1.5 mEq/L and may be a helpful adjunct. The peak effect occurs in 90 min. However, beta 2-agonists are contraindicated in patients with unstable angina or acute myocardial infarction.
Administration of IV sodium bicarbonate (NaHCO3) is controversial. It may lower serum potassium over several hours. Reduction may result from alkalinization or the hypertonicity due to the concentrated sodium in the preparation. The amount of sodium that it contains may be harmful for dialysis patients who also may have volume overload. Another possible complication of IV sodium bicarbonate is to acutely lower ionized calcium concentration which would further enhance the cardiotoxicity of hyperkalemia. When given, the typical dose is 3 ampules of 7.5% sodium bicarbonate in one liter 5% D/W infused over 2 to 4 h. Bicarbonate 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 potassium by shifting it into cells, maneuvers to remove potassium from the body should also be done early in the treatment of severe or symptomatic hyperkalemia. Potassium can be removed via the GI tract by administration of sodium polystyrene sulfonate (see Mild hyperkalemia), but because the rate of potassium removal is somewhat unpredictable, close monitoring is needed. Patiromer is not recommended for use as an emergency treatment to acutely lower potassium because of its delayed onset of action.
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 potassium acutely.
Common causes of hyperkalemia include potassium-retaining drugs, renal insufficiency, adrenal insufficiency, and disorders involving cellular breakdown (eg, rhabdomyolysis, burns, bleeding into soft tissue or the GI tract).
Hyperkalemia is usually asymptomatic until cardiac toxicity develops, although some patients have weakness.
ECG changes begin with an increased PR interval, shortening of the QT interval, and tall, symmetric, peaked T waves; with potassium > 6.5 mEq/L, QRS interval widens, and P wave disappears; ultimately, the QRS complex degenerates into a sine wave pattern, and ventricular fibrillation or asystole ensues.
Give sodium polystyrene sulfonate for mild hyperkalemia.
Give IV insulin, glucose, and calcium, and possibly an inhaled beta 2-agonist for moderate to severe hyperkalemia.
Use hemodialysis for patients with chronic kidney disease and those with significant ECG changes.