Definition, Etiology, PathogenesisTop
Hyperkalemia is defined as a serum [K+] >5.5 mmol/L.
1) Excessive potassium intake in patients with impaired renal function or with impaired transport of potassium into cells.
2) Impaired renal excretion of potassium due to acute or chronic renal failure, aldosterone or glucocorticoid deficiency (congenital or acquired), hyporeninemic hypoaldosteronism (in patients with diabetic, lupus, analgesic-induced, or HIV-associated nephropathy), or resistance of renal tubules to aldosterone (pseudohypoaldosteronism type I, II, or III).
3) Drug-induced hyperkalemia due to angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), aldosterone receptor antagonists (spironolactone, eplerenone), renin inhibitors, potassium supplements, nonsteroidal anti-inflammatory drugs (NSAIDs), amiloride, triamterene, trimethoprim, cyclosporine (INN ciclosporin), tacrolimus, heparin, or digoxin.
4) Impaired transport of potassium into cells due to nonrespiratory acidosis, beta2-adrenergic receptor blockade, insulin deficiency, aldosterone deficiency, or blockade of the renin-angiotensin-aldosterone (RAA) system.
5) Excessive release of potassium from cells due to rhabdomyolysis, tumor lysis syndrome, nonrespiratory acidosis, sepsis, hyperkalemic periodic paralysis, too rapid correction of hypothermia, or malignant hyperthermia.
Common causes of hyperkalemia include drugs such as ACEIs, ARBs, or aldosterone receptor antagonists and acute or chronic renal failure.
Pseudohyperkalemia is a laboratory artifact caused by the release of potassium from blood cells in a blood sample due to hemolysis, thrombocytosis (>900×109/L), or leukocytosis (>70×109/L).
The presence and severity of clinical manifestations are not consistently correlated with the severity of hyperkalemia. Patients with slowly increasing serum [K+] are usually asymptomatic despite severe hyperkalemia (>7.0 mmol/L).
Hyperkalemia decreases the resting potential of cell membranes and therefore impairs the generation and propagation of stimuli. Dysfunction of myocytes and neurons is manifested by skeletal muscle weakness or paralysis, hyporeflexia, cardiac arrhythmias (bradycardia, asystole, ventricular fibrillation), decreased stroke volume, electrocardiography (ECG) changes that include widened QRS complexes and peaked T waves, paresthesia, and altered mental status (confusion).
The clinical presentation of hyperkalemia may be dominated by features of the underlying condition.
The diagnosis of hyperkalemia is based on measurement of serum [K+] (>5.5 mmol/L; exclude pseudohyperkalemia). History may indicate the underlying condition. Take a thorough history of medications, including over-the-counter drugs and herbal remedies. Assess renal function and acid-base homeostasis. While previously in common use, the transtubular potassium gradient (TTKG) has been demonstrated to be invalid and should not be used for diagnosis of hyperkalemia.Evidence 1Strong recommendation (downsides clearly outweigh benefits; right action for all or almost all patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness (majority of evidence coming from animal studies). Kamel KS, Halperin ML. Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: an hypothesis with clinical implications. Curr Opin Nephrol Hypertens. 2011 Sep;20(5):547-54. doi: 10.1097/MNH.0b013e328349b8f9. Review. PubMed PMID: 21788894.
1. Try to control the cause of hyperkalemia.
2. Restrict potassium intake (fruit, fruit juices, plant products).
3. Monitor ECG and vital signs, especially if [K+] is >6.3 mmol/L.
4. If the patient develops ECG features of hyperkalemia or arrhythmia, immediately administer 10 to 20 mL of 10% calcium gluconate IV or calcium chloride (use with particular caution in patients treated with digitalis) and 25 to 50 mL of 50% glucose (dextrose) IV and 5 to 10 units of short-acting insulin. If acidosis is present, add 50 mL of 8.4% NaHCO3. A temporary shift of potassium into cells may be achieved by administering a beta2-agonist, for instance, nebulized salbutamol 2.5 mg every 15 minutes even up to a dose of 10 to 20 mg, or 0.5 mg IV. A smaller dose may be delivered through multiple inhalations of salbutamol using a metered-dose inhaler (MDI). Watch for tachycardia and limit the dose as required.
5. At the same time, start treatment to remove excess potassium from the body:
1) A loop diuretic in patients with normal urine output, for instance, IV furosemide 20 to 40 mg, which may be repeated after 6 to 8 hours. Loss of fluids due to increased urine output should be corrected with 0.9% NaCl infusion.
2) Oral or rectal polystyrene sulfonate 30 g in 150 mL water or 10% glucose (dextrose). This acts as an ion-exchanger in the gastrointestinal tract and causes a decrease of 0.5 to 1.0 mmol/L in serum potassium levels within 4 to 6 hours.
3) Hemodialysis (rarely peritoneal dialysis) in life-threatening hyperkalemia refractory to medical management and in patients with severe renal failure.
6. In patients with diabetes mellitus and hyporeninemic hypoaldosteronism, start by discontinuing drugs known to increase serum potassium levels (beta-blockers, ACEIs, ARBs, mineralocorticoid receptor antagonists, NSAIDs). If serum [K+] continues to be >6.5 mmol/L, administer oral fludrocortisone 0.5 mg/d. Maintain the target serum [K+] in a range <5.5 mmol/L.
7. In patients with suspected adrenal insufficiency, start IV glucocorticoids (see Primary Adrenal Insufficiency).