hyperkalemia

Etiology

• pseudohyperkalemia
  • excessively long tourniquet application before phlebotomy cause K+ to leak from muscle distal to the tourniquet
  • hemolysis of specimen during or after phlebotomy
  • thrombocytosis > 1E06/mm3 or leukocytosis > 100,000/mm3
    • lysis of platelets or leukocytes during clot formation & retraction
    • determine K+ from plasma rather than serum
• massive influx of K+ into plasma
  • intravenous K+ salts
  • oral potassium
    • dietary excess
    • salt substitutes
    • prescribed K+ replacements
• hemolysis
• rhabdomyolysis
• redistribution of K+ from within cells to plasma
  • pharmacologic agents
    • succinylcholine
    • digitalis overdose
    • beta-adrenergic receptor antagonists
    • alpha-adrenergic receptor agonists
    • arginine & lysine from hyperalimentation
  • hyperosmolar states especially hyperglycemia
    • insulin-deficiency
  • metabolic acidosis with normal anion gap
    • a decrease in pH of 0.1 increases K+ 0.6 meq/L
  • hyperkalemic periodic paralysis
    • may result in hyperkalemia or hypokalemia
• inadequate renal excretion
  • adrenal disorders
    • hyporeninemic hypoaldosteronism
      • renal tubular acidosis (RTA) IV
    • Addison's disease
  • defects in tubular secretion
    • systemic lupus erythematosus (SLE)
    • obstructive uropathy
    • sickle cell disease
    • renal transplant
  • renal failure (acute renal failure & chronic renal failure)
    • special considerations in dialysis patients
      • extrarenal mechanism of K+ elimination dominate
        • constipation diminishes GI K+ elimination
        • fasting diminishes basal insulin levels
  • pharmacologic agents:
    • potassium-sparing diuretics
      • amiloride
      • triamterene
      • spironolactone
    • agents that inhibit secretion of aldosterone
      • ACE inhibitors, ARBs
      • non-steroidal anti-inflammatory drugs (NSAIDs)
      • heparin
    • beta-blockers
    • cytotoxic drugs
    • cyclosporine A
    • lithium
    • trimethoprim (Bactrim, Septra)
    • pentamidine
  • diminished effective plasma volume (low urine flow state)
    • CHF
    • cirrhosis
    • potassium intake from salt substitute in connection with dehydration
• risk factors
  • advanced age
  • diabetes mellitus
    • insulin secretion which results in translocation of K+ intracellularly is the body's major safegaurd against acute hyperkalemia
• pseudohyperkalemia
  • mechanical release of K+ from cells during phlebotomy or during specimen processing
  • marked leukocytosis & thrombocytosis
  • electrocardiogram is normal

Pathology

• defect in renal tubular potassium secretion
  • defect in the renin-angiotensin-aldosterone axis
  • GFR < 20 mL/min/1.73 m2

Clinical manifestations

• ascending muscle weakness
• perioral paresthesias
• symptoms inconsistently present

Laboratory

• serum chemistries
  • serum potassium: hyperkalemia
  • serum creatinine: assess renal function
  • serum urea nitrogen: obtain BUN/creatinine ratio
  • serum glucose:
    • hyperglycemia with insulin deficiency
  • serum creatine kinase to assess rhabdomyolysis
• plasma potassium if leukocytosis (> 100,000/uL) or thrombocythemia*
• see ARUP consult

* lysis of platelets or leukocytes during clot formation & retraction

Diagnostic procedures

• electrocardiogram
  • peaked T waves especially in precordial leads*
  • shortening of QT interval*
  • prolongation of PR interval
  • loss of P wave
  • widening of QRS complex
    • late change
    • degeneration into sine wave before patient arrest
      • ventricular fibrillation
      • asystole

* earliest changes

* only the EKG, not serum potassium can assess effect of hyperkalemia on the cardiac membrane

Complications

• ventricular arrhythmias
• cardiac conduction defects
• cardiac arrest

• disease interaction(s) of hyperkalemia with systolic heart failure

Management

• serum K+ < 6.5 meq/L & no EKG changes or peaked T waves only
  • identify & correct underlying etiology
    • 10-30 mL of 10% calcium gluconate* IV push if peaked T waves (NEJM)
  • loop diuretics
    • for patients with hypervolemia without advanced renal failure
    • tubular defects
  • thiazide diuretic for chronic hyperkalemia in patients with RTA-4, type 2 diabetes, hypertension & peripheral edema
    • do not change loop diuretic to thiazide diuretic for hyperkalemia in patients with hyperkalemia & systolic heart failure
  • hyporeninemic hypoaldosteronism - fludrocortisone (Florinef)
  • oral NaHCO3
    • useful if metabolic acidosis
    • enhances Na+ delivery to the distal tubules & K+ excretion
  • patiromer or sodium zirconium cyclosilicate (Lokelma)
  • dietary potassium restriction
• serum K+ > 8 meq/L or EKG changes beyond peaked T waves
  • continuous EKG monitoring
  • IV access
  • 10-30 mL of 10% calcium gluconate* IV push
    • transiently stabilizes myocardial cells
    • does not lower serum K+
    • onset: minutes; duration: 1/2 hour
  • IV glucose + insulin
    • 200 to 500 mL of 10% dextrose
    • 10 units of insulin IV or SC
    • over 30 minutes
    • may repeat several times
  • dialysis
    • hemodialysis, peritoneal dialysis
    • never the 1st step because of delay in initiation
  • NaHCO3 drip (may not be effective in dialysis patients)
  • beta 2 adrenergic receptor agonists
    • albuterol
  • continuing influx of K+ into plasma from rhabdomyolysis or tissue necrosis mandates aggressive treatment of hyperkalemia
• removal of potassium from body
  • patiromer & sodium zirconium cyclosilicate can increase GI excretion
  • loop diurectics can increase urinary excretion of potassium
  • hemodialysis treatment of choice with oliguria
• drugs probably not useful, may be harmful
  • avoid, discontinue or decrease dosage of drugs that inhibit K+ excretion; threshold for action 5.5 meq/L
  • discontinue potassium supplementation if potassium at or above upper end of reference interval
  • spironolactone increases serum potassium ~0.3 mEq/L (average)
  • ACE inhibitors & ARBs increase serum K+ by inhibiting production of aldosterone, thus switching from ACE inhibitor to ARB is not useful
  • discontinuation of ACE inhibitor or ARB may be associated with higher mortality
    • continuation of ACE inhibitor or ARB may be facilitated by
      • frequent monitoring of serum potassium, patiromer, discontinuation of beta-blockers
      • increasing dose of loop diuretic (NEJM)
    • use hydralazine/isosorbide dinitrate (Bidil) if vasodilator is indicated
  • patiromer or sodium zirconium cyclosilicate recommended if serum potassium excess threshold for action
  • 25-50 g of Kayexalate with 1 mL of 70% sorbitol/g Kayexalate
    • peak effect seen in 4 hours
    • use is controversial; benefit/risk ratio unfavorable
• low potassium diet (if other measures fail)
• GLP-1 agonists & SGLT-2 inhibitors diminish risk of hyperkalemia in patients with diabetes mellitus type-2 taking ACE-inhibitors or ARBs

* calcium chloride cannot be given through a peripheral IV because extravasation may cause local tissue necrosis 10]

More general terms

• electrolyte disorder
• sign/symptom

Additional terms

• potassium (K+) in serum/plasma
• renal tubular acidosis (RTA) type IV (distal RTA)

Patient information

hyperkalemia patient information