Hyperkalemia

Essentials of Diagnosis

• Serum potassium level > 5.2 mEq/L (5.2 mmol/L)

• Check medications carefully; hyperkalemia may develop from angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers and potassium-sparing diuretics, most commonly in patients with kidney dysfunction

• ECG may be normal despite life-threatening hyperkalemia

• Rule out pseudohyperkalemia and extracellular potassium shift from cells

General Considerations

• Hyperkalemia is a rare occurrence in healthy individuals due to adaptive mechanisms designed to prevent accumulation of potassium in the extracellular fluid, mainly via rapid urinary excretion

• Persistent hyperkalemia generally requires an impairment in renal potassium excretion due to

  • Impaired secretion of or hyporesponsiveness to aldosterone

  • Impaired delivery of sodium and water to the distal nephron

  • Kidney disease (acute or chronic)

• Transient hyperkalemia suggests shift of potassium from inside cells into the extracellular fluid, which can occur in the context of

  • Tissue damage (rhabdomyolysis, tumor lysis, massive hemolysis, and trauma)

  • Metabolic acidosis

• Pseudohyperkalemia is a laboratory artifact in which there is an elevation in serum potassium levels in the absence of true electrolyte imbalance as a result of

  • Tourniquet application or fist clenching during blood draw

  • Improper transport or processing of venous samples in patients with marked thrombocytosis or leukocytosis

Symptoms and Signs

• Symptoms of hyperkalemia are a consequence of impaired neuromuscular transmission

• Potassium concentrations above 7 mEq/L may cause cardiac conduction abnormalities and neuromuscular manifestations, such as muscle weakness, which may be profound

• Hyperkalemic period paralysis

  • Rare genetic disorder

  • Characterized by episodes of painless muscle weakness precipitated by potassium ingestion, rest after heavy exercise, and cold exposure

• Hyperkalemia additionally impairs urinary ammonium excretion and may lead to metabolic acidosis

Laboratory Tests

• The diagnosis should be confirmed by repeat laboratory testing to rule out spurious hyperkalemia, especially in the absence of medications that cause hyperkalemia or in patients without kidney disease

Diagnostic Procedures

• Electrocardiography is an unreliable method for detecting hyperkalemia with clinical studies showing poor correlation between serum potassium levels and cardiac manifestations

ECG Changes

• The rapidity in development of hyperkalemia may correlate with the development of ECG changes

• Typical sequential changes

  • Peaking of the T waves

  • ST-segment depression

  • Widening of the PR and QRS intervals

• As the QRS continues to widen, sine waves may develop, which are concerning for imminent ventricular fibrillation and ultimately asystole

Medications

• Exogenous sources of potassium should be eliminated

• Medications that can impair potassium excretion should be discontinued

• Volume depletion should be corrected

• Metabolic acidosis, if present, should be improved

• Treatment of hyperkalemia is outlined in Table 21–5

• In emergency situations (cardiac toxicity, muscle weakness or potassium > 6.5 mEq/L), initial therapy should be

  • Intravenous calcium gluconate to stabilize the myocardium in order to protect against arrhythmias, followed by therapies to shift potassium into cells

    • Insulin and beta-agonists shift potassium intracellularly within 10–15 minutes of administration but have a short duration of action (1–2 hours)

    • Sodium bicarbonate may be helpful to shift potassium into cells in patients with a concurrent metabolic acidosis

• Once the patient is stabilized, therapies are focused on potassium excretion

• Potassium excretion may be enhanced with the use of loop diuretics

• Patiromer and sodium zirconium cyclosilicate

  • May be used to treat chronic hyperkalemia

  • Well tolerated and efficacious in patients with hyperkalemia who have either chronic kidney disease or heart failure and take at least one medication that inhibits the renin-angiotensin-aldosterone system

• Sodium polystyrene (Kayexalate)

  • Widely used for decades, although its efficacy and safety have been questioned

  • May not increase potassium excretion greater than laxatives alone

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

  • Contraindicated in patients with risk factors for colonic necrosis, such as 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, particularly in patients who are oliguric

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

When to Refer

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

• Transplant patients may need adjustment of their immunosuppression regimen by transplant specialists

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)