Hyperkalemia

Ninety eight percent of the body’s potassium is in the intracellular fluid. Acidosis, hyperosmolarity, or cell lysis all cause potassium to leave cells and cause hyperkalemia. Potassium homoeostasis is mainly governed by regulation of renal potassium excretion, controlled by aldosterone. Delivery of sodium to the distal nephron is needed for potassium excretion. Underlying renal insufficiency, glomerular filtration rate <15-20 ml/min (implicated in 75% of cases) and use of medications that disrupt potassium balance, such as angiotensin-converting enzyme (ACE) inhibitors and potassium-sparing diuretics, are well described risk factors. Spurious hyperkalemia (also called pseudohyperkalemia) occurs when the reported laboratory potassium values do not reflect actual serum concentrations and is typically due to lab draw cell lysis or lab error.

EKG changes due to hyperkalemia include peaked T waves, flattened or absence P waves, widened QRS complexes, and eventually sine waves. EKG changes correlate poorly with the degree of potassium disturbance, as half the patients with serum potassium concentration greater than 6.5 mmol/l do not have EKG changes. Urgent treatment (outlined below) is suggested for potassium levels greater then 5.5-6mmol/L with EKG changes or a serum potassium greater then 6.5 mmol/L. Mild to moderate hyperkalemia, 6-6.5 mmol/L, without EKG changes can be treated as an inpatient with a loop diuretic, pending no renal insufficiency.

Urgent Treatment

  1. Calcium gluconate (10ml 10% solution): stabilizes the cardiac membrane and EKG changes can be seen after 1-3 minutes with effect lasting 30-60 minutes. The infusion can be repeated if no effect is seen within 5-10 minutes. Caution should be exercised when replacing calcium in patients taking digoxin.
  2. Insulin (10 units with 50 ml of 50% dextrose to prevent hypoglycemia): shifts potassium into cells in 20 minutes, and effects peak between 30-60 minutes. Total reduction in serum potassium is 0.6 to 1.0 mmol/L.
  3. Albuterol (10-20 mg in 4 ml of saline): shifts potassium into cells within 30 minutes, with maximum effect at 90–120 minutes. Total reduction in serum potassium is 0.3 to 0.6 mmol/L.
  4. Sodium bicarbonate (500 ml of a 1.26% solution, 75 mmol): benefit is uncertain and routine bicarbonate treatment for hyperkalemia is controversial.
  5. Furosemide (40-80 mg IV): enhances renal potassium excretion by increasing urine flow and sodium delivery to the distal nephron in patients with intact renal function.
  6. Dialysis is the ultimate end point of treatment and is likely needed in patients with renal failure.
  7. Resins (kayexelate) used to bind potassium in the intestine have no good evidence for their use and can be associated with serious side effects including gastrointestinal bleeding and colonic necrosis. The majority of these cases involved concomitant use of sorbitol.

Of note NSAIDS should be avoided in patients with diabetes or renal insufficiency, particularly if they are taking ACE inhibitors or angiotensin-receptor blockers, to prevent worsening renal function and hyperkalemia.

Nyirenda MJ, et al.  Hyperkalaemia. BMJ. 2009 Oct 23;339:b4114. doi: 10.1136/bmj.b4114.
Elliott MJ, et al.  Management of patients with acute hyperkalemia. CMAJ. 2010 Oct 19;182(15):1631-5. Epub 2010 Sep 20.
Sterns RH, et al.  Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol. 2010 May;21(5):733-5. Epub 2010 Feb 18.
About these ads
This entry was posted in Nephrology, Resus. Bookmark the permalink.