Hyperkalemia

For further information, see CMDT Part 21-05: Hyperkalemia

Essentials of Diagnosis

• Serum potassium > 5.0 mEq/L (> 5.0 mmol/L)

• Hyperkalemia may develop in patients taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and potassium-sparing diuretics, or their combination, even with no or only mild kidney dysfunction

• The ECG may be normal despite life-threatening hyperkalemia

• Measurement of plasma potassium level differentiates potassium leak from blood cells from elevated serum potassium

• Rule out extracellular potassium shift from the cells in acidosis and assess renal potassium excretion

General Considerations

• In acidosis, serum potassium concentration rises about 0.7 mEq/L for every decrease of 0.1 pH unit

• In the absence of acidosis

  • Serum potassium concentration rises about 1 mEq/L when there is a total body potassium excess of 1–4 mEq/kg

  • However, the higher the serum potassium concentration, the smaller the excess necessary to raise the potassium levels further

• Mineralocorticoid deficiency from Addison disease or chronic kidney disease (CKD) is another cause of hyperkalemia with decreased renal excretion of potassium

• Mineralocorticoid resistance due to genetic disorders, interstitial kidney disease, or urinary tract obstruction also leads to hyperkalemia

• The concomitant use ACE inhibitors and ARBs with spironolactone, triamterene, eplerenone, or β-blockers further increases the risk of hyperkalemia

• Thiazide or loop diuretics and sodium bicarbonate may minimize hyperkalemia

• Mild hyperkalemia that occurs in the absence of potassium-sparing drug therapy is usually due to type IV renal tubular acidosis

• Hyperkalemia occurs commonly in AIDS

  • Impaired renal excretion of potassium can be due to use of pentamidine or trimethoprim-sulfamethoxazole or to hyporeninemic hypoaldosteronism

Etiology

• Spurious (Table 21–6)

  • Leakage from erythrocytes, marked thrombocytosis or leukocytosis

  • Repeated fist clenching during phlebotomy

  • Specimen from arm with K⁺ infusion

• Decreased excretion

  • Kidney disease, acute and chronic

  • Renal secretory defects, eg, interstitial nephritis, sickle cell disease

  • Hyporeninemic hypoaldosteronism (type IV renal tubular acidosis), eg, diabetic nephropathy, heparin, AIDS; adrenal insufficiency

  • Drugs that inhibit K⁺ excretion (spironolactone, triamterene, eplerenone, ACE inhibitors, trimethoprim, nonsteroidal anti-inflammatory drugs)

• Potassium shift from within the cell

  • Burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise

  • Metabolic acidosis

  • Hypertonicity (solvent drag)

  • Insulin deficiency

  • Hyperkalemic periodic paralysis

  • Drugs: digitalis toxicity, β-adrenergic antagonists, succinylcholine, arginine

• Excessive intake of K ⁺

  • Ingestion or iatrogenic

Symptoms and Signs

• Frequently asymptomatic

• Muscle weakness, flaccid paralysis, and ileus

• Abdominal distention and diarrhea may occur

Laboratory Tests

• Serum potassium > 5.0 mEq/L (> 5.0 mmol/L)

• Measure plasma potassium rather than serum potassium to confirm that hyperkalemia is genuine

• Obtain serum electrolytes and creatinine

• Consider arterial blood gas

Diagnostic Procedures

• ECG is not a sensitive method for detecting hyperkalemia, since nearly half of patients with a serum potassium level > 6.5 mEq/L will not manifest ECG changes

ECG Changes

• Bradycardia

• PR interval prolongation

• Peaked T waves

• Widening of the QRS complex

• Biphasic QRS–T complexes

• Conduction disturbances, such as bundle branch block and atrioventricular block

• Ventricular fibrillation and cardiac arrest are terminal events

Medications

• Treatment consists of withholding exogenous potassium, identifying the cause, reviewing the patient's medications and dietary potassium intake, and correcting the hyperkalemia

• Emergent treatment of hyperkalemia is indicated when cardiac toxicity or muscle paralysis or severe hyperkalemia (potassium > 6.5 mEq/L) is present, even in the absence of ECG changes

• Insulin, bicarbonate, and β-agonists shift potassium intracellularly within minutes of administration (Table 21–7)

• Intravenous calcium may be given to antagonize the cell membrane effects of potassium, but its use should be restricted to life-threatening hyperkalemia in patients taking digitalis because hypercalcemia may cause digitalis toxicity

• Patiromer

  • Binds potassium in the intestine

  • May be used to treat chronic hyperkalemia in patients with chronic kidney disease who are taking at least one drug that inhibits the renin-angiotensin-aldosterone system

  • May decrease the absorption of orally administered drugs

• Sodium zirconium cyclosilicate powder

  • Binds potassium in the intestine

  • FDA approved for managing hyperkalemia

  • Role in end-stage renal disease is unclear

• Sodium polystyrene

  • Has been widely used for decades although its efficacy and safety have been questioned

  • May not increase potassium excretion above laxatives alone

  • Has been associated with colonic necrosis, both with and without sorbitol coadministration

  • The FDA recommends that sodium polystyrene not be administered in sorbitol, but the mixture remains commonly available

  • Its use should be restricted to patients with life-threatening hyperkalemia when dialysis is not available and other therapies (eg, diuretics) have failed

  • Contraindicated in patients at risk for colonic necrosis: bowel obstruction, ileus, and postoperative state

Therapeutic Procedures

• Hemodialysis may be required to remove potassium in patients with acute kidney injury or chronic kidney disease

Follow-Up

• Monitor potassium frequently (every 1–4 hours) during inpatient therapy for hyperkalemia

Prognosis

• Depends on the underlying condition (chronic kidney disease)

• Drug-induced hyperkalemia is generally readily reversible with therapy

Prevention

• Inhibitors of the renin-angiotensin-aldosterone axis (ie, ACE inhibitors, ARBs, and spironolactone) and potassium-sparing diuretics (eplerenone, triamterene) should be used cautiously in patients with heart failure, liver failure, and kidney disease

• Laboratory monitoring should be performed within 1 week of drug initiation or dosage increase

When to Refer

• Patients with hyperkalemia from kidney disease and reduced renal potassium excretion should be referred to a nephrologist

When to Admit

• Severe hyperkalemia (> 6 mEq/L)

• Any degree of hyperkalemia associated with ECG changes

• Concomitant illness (eg, tumor lysis syndrome, rhabdomyolysis, metabolic acidosis)