Hyperkalemia in Adults: Review of a Common Electrolyte Imbalance

THERAPY

Emergent

Emergent treatment is needed for severe hyperkalemia (see Figure 4). Any hyperkalemia-inciting medications or potassium supplements should be immediately discontinued.³⁹ IV access and cardiac telemetry monitoring should be promptly applied.²⁶

In cases of severe hyperkalemia that involve cardiac arrhythmias, manifestations on ECG, or risk for arrhythmias, calcium gluconate (10 mL IV over 10 min) should be urgently administered, followed by IV insulin in conjunction with dextrose.²⁶ Calcium chloride should be utilized for hyperkalemia in the context of the advanced cardiac life support (ACLS) protocol for cardiac arrest.²⁶ The patient should remain on cardiac telemetry during this treatment to monitor for ventricular fibrillation or other arrhythmias.¹⁵ IV calcium does not lower serum potassium but rather antagonizes the effects of potassium on the cardiac cell membranes, helping to prevent or terminate arrhythmias.^15,34 It should be noted, however, that firstline treatment for patients who develop hyperkalemia in the setting of digoxin toxicity involves administration of digoxin-specific antibody, while calcium infusion may be utilized later.³⁴ Alternatively, if the patient is dialysis-dependent with ESRD, dialysis may be considered as a prompt initial treatment, with nephrologist consultation.

Administration of 10 U of regular insulin plus 25 g of 50% dextrose via IV will shift potassium intracellularly (see Figure 4). The dextrose will offset the resultant hypoglycemia.^31,34 Of note, this treatment is often firstline for moderate to severe hyperkalemia in patients with a stable cardiac rhythm and ECG. Blood glucose should be monitored with a fingerstick within 30 to 60 minutes of infusion and every hour thereafter for up to six hours following insulin administration.³⁴ Potassium levels should be checked every one to two hours after this treatment step until the serum potassium level stabilizes. Thereafter, recheck the levels every four to six hours to gauge whether further treatment is needed.³⁴

Adjunctive

After performing firstline treatment strategies for severe hyperkalemia, there are alternate therapies to consider that can help lower total body potassium. Nebulized al­buterol may be used, which pushes potassium into cells; this works in synergy with insulin and glucose.^26,33 Sodium bicarbonate may be effective in cases in which the ABG analysis or labs show metabolic acidosis, as this infusion shifts potassium into cells by increasing the blood pH.³³

In patients with dehydration, sepsis, TLS, or rhabdomyolysis, administration of IV fluids to maintain appropriate vascular volume is important. However, excessive fluid resuscitation can result in fluid overload, inducing complications such as respiratory failure and worsened renal function.⁴⁰ A Foley catheter may be placed for strict intake and output monitoring.

The patient’s volume status must be carefully assessed. Hyperkalemia may pre­sent in association with heart failure exacerbation or ascites, which are usually hypervolemic states. Loop diuretics may be used to compensate for volume overload and to help remove potassium from the body, but these medications are contraindicated in anuric patients.^13,41

Removing total body potassium

After emergent therapy is carried out, potassium may need to be removed from the body through diuresis, hemodialysis, or potassium binders. Loop diuretics or potassium binders may be used to treat mild to moderate hyperkalemia or to continue to stabilize the potassium level after emergent therapy is carried out. If severe hyperkalemia persists with kidney injury or with absence of urine output, hemodialysis is the therapy of choice.¹³

The potassium binder sodium polystyrene sulfonate (SPS) exchanges sodium for potassium in the intestine.⁴² This agent is contraindicated if the patient has intestinal obstruction. SPS’s slow onset of action (two to six hours) makes it ineffective as firstline therapy for severe hyperkalemia.³ In addition, SPS has serious but rare adverse effects, more commonly seen in patients who have uremia after kidney transplant or who have had recent abdominal surgery, bowel injury, or intestinal perforation.⁴¹ Adverse effects of SPS include aspiration pneumonitis, upper gastrointestinal injury, colonic necrosis, and rectal stenosis.⁴¹ However, there have been documented events of colonic necrosis due to SPS in patients without ESRD who have not had abdominal surgery.^43,44 In 2009, the FDA advised against concomitant administration of sorbitol with SPS. However, this drug preparation continues to be the only one stocked by many hospital pharmacies.⁴⁴ Because SPS has potentially harmful adverse effects and generally is not effective in promptly lowering serum potassium, it is prudent for clinicians to implement other management strategies first.⁴⁴

MONITORING AT-RISK PATIENTS

Patients with a GFR < 45 mL/min/1.73 m² and a baseline serum potassium level > 4.5 mEq/L are at risk for hyperkalemia while taking an ACEi or an ARB and should be advised to adhere to a potassium-restrictive diet with frequent laboratory checkups.²² Depending on the serum potassium and GFR levels at checkups, these medication doses may need to be reduced or discontinued altogether.