Management of Hyperkalemia on the Medicine Ward Aaron Jattan, MD, CCFP Education Director, FM-CTU, St. Boniface Hospital Department of Family Medicine University of Manitoba
No Conflict of Interests to Declare
Learning Objectives 1. Recognize the signs and symptoms of hyperkalemia 2. Recognize and understand possible causes of pseudohyperkalemia 3. Understand the limitations of the EKG in diagnosing hyperkalemia 4. Manage and treat hyperkalemia
Hyperkalemia 1 • Rare and uncommon as the kidneys can excrete large amounts of K+. • However, common complication in renal failure
Why do we care? There is a worry that the first sign of hyperkalemia is – Death Patients without CKD and K+ >6.0 have an adjusted OR of death of 30! 2
Signs and Symptoms • Muscle Weakness
Hyperkalemia • Ask yourself two questions: 1. Is it real? And… 2. Why would they have Hyperkalemia?
1. Is it Real? • Pseudohyperkalemia: Marked elevation of K+ on labs not representative of in vivo potassium values. • Leakage of K+ out of cells contained in a blood sample before it is analyzed • Mechanical Trauma, fist clenching during phlebotomy, use of tourniquets, use of pneumatic tubes for transport 3 • Usually (BUT NOT ALWAYS), hemolysis is reported by the lab • Gentle venipuncture and using a heparinized tube (green) can help the blood from clotting as clotting can result in K+ leakage.
1. Is it Real? • Hyperkalemia is rare as the body is well equipped to deal with elevated levels. • Compensation: Movement of potassium into the intracellular compartment (immediate) • Correction: Excretion of excess potassium by the kidneys • With exercise, K+ levels can spike as high as 8.0 with rapid resolution 4
2. Why do they have hyperkalemia? • 1) Increased intake • 2) Movement out of cells • 3) Decreased renal excretion
Etiology: Increased Intake • Seldom causative in patients without end stage renal disease • Consider IV fluids and TPN as potential sources in hospitalized patients.
Etiology: Movement out of Cells 5 • Cell Death (rhabdomyolysis, tumour lysis syndrome, hypothermia) • Acidosis • Hyperglycemia and Lack of Insulin • B-blockers, Digoxin
Etiology: Impaired Renal Excretion • Renal Failure • Low effective circulating volume • Low Aldosterone States
RAAS System Image from “The Fluid, Electrolyte & Acid - Base Companion” by Faubel and Topf
Aldosterone Image from “The Fluid, Electrolyte & Acid - Base Companion” by Faubel and Topf
Impaired Renal Excretion 5 • Medications • ACEi/ARBs – Hypoaldosteronism • NSAIDs – Inhibit renin release from the kidneys • MRAs – Antagonize Aldosterone • K+-Sparing Diuretics (Amiloride) – block Na reabsorption • Trimethoprim-Sulfa – block Na reabsorption • Adrenal Insufficiency • Primary (Addison’s Dx) – HIV, TB, autoimmune disorders
Diagnosis • Ask yourself: Does it make sense for this patient to have hyperkalemia?
EKG 6 • Hyperkalemia leads to altered cardiac conduction leading to ventricular fibrillation or asystole. • The EKG changes reflects the effect of potassium on myocardial contraction. • Prominent findings: • Peaked T-waves • Increased PR interval • Widening of the QRS complex • Loss of the p-waves • Sinusoidal wave form (late finding)
EKG 6
EKG EKGs are NOT sensitive in diagnosing hyperkalemia 7-8 .
Treatment – First Steps • Rule-out acute urinary obstruction and hyperglycemia • Stop, or hold, offending medications • Consider Calcium
Treatment – Calcium 9 • Calcium is used to stabilize cardiac membranes and prevent dysrhythmias. • If severe hyperkalemia (e.g. EKG changes, potassium greater than 7.0 mEq/L) is present, calcium should be the first medication given • Calcium is given IV as either calcium gluconate or calcium chloride. • Calcium chloride contains 3x the amount of Ca but can only be given through a central line • Calcium works within 1-3 minutes but only lasts 30-60minutes.
Treatment • Treatment thresholds vary – rule of thumb would be greater than 6.2 • Goal: Compensate if severe Always Correct
Treatment – Compensation 9 • Insulin and Glucose • 10 U of insulin R and an ampule of D50 (unless hyperglycemia with glucose >13) • This lowers plasma potassium by 0.5 to 1.5 mEq/L and the effect occurs in approximately one hour • Sodium Bicarbonate • Slow and more appropriate for cases of chronic hyperkalemia • b 2- Adrenergic Agents • 20mg of nebulized salbutamol (8 salbutamol nebulizers) • The effect is seen in the first hour • All treatments work within 30minutes and last upwards to 4 hours.
Treatment - Correction • 2 routes for correction: • Kidneys (Preferable) • GI Tract
Treatment – Renal Correction 9 • Loop Diuretics • Lasix 40mg IV to start and monitor for diuresis • Fluid Bolus • Caution if hypervolemic • Fludrocortisone • Often reserved for chronic hyperkalemia • Takes 1-2 days to take effect • Caution in patients in hypertension and congestive heart failure. • Dialysis when all else fails
Treatment – GI Correction • Cation Exchange Resins (Sodium Polystyerene Sulfonate) • Risk of intestinal necrosis (rare) 10 • New potassium binders are entering the market which are better tolerated but difficult to obtain. • Patiromer and Sodium zirconium
Take Home Points • Is it real? – consider pseudohyperkalemia? • If it is real, think about why? • Intake, movement out of cells, decreased renal excretion • EKGs are not sensitive in diagnosing hyperkalemia • With treatment, give calcium readily and often • With treatment, compensate if severe, but always correct
References 1. Faubel S., & Toph J. (1999). The Fluid, Electrolyte & Acid-Base Companion. Alert and Oriented Publishing Company: Chelsea, Michigan. 2. Einhorn, L., Zhan, M., Hsu, V., Walker, L., Moen, M., Seliger , S., … Fink, J. (2009). The Frequency of Hyperkalemia and Its Significance in Chronic Kidney Disease. Archives of Internal Medicine, 169(12), 1156 – 1162. 3. Kellerman, P., & Thornbery, J. (2005). Pseudohyperkalemia Due to Pneumatic Tube Transport in a Leukemic Patient. American Journal of Kidney Diseases, 46(4), 746 – 748. 4. Medbø, J., & Sejersted, O. (1990). Plasma potassium changes with high intensity exercise. The Journal of Physiology, 421, 105 – 122. Reddi AS. (2018). Fluid, electrolyte and acid-base disorders, 2 nd ed. Springer Nature: Newark, New Jersey. 5. Martindale J.L., & Brown D.F.M. (2016). A visual guide to ECG interpretation, 2 nd edition. Wolters Kleuwer: 6. Philadelphia, Pennsylvania. 7. Montague, B., Ouellette, J., Buller, G., & Montague, B. (2008). Retrospective review of the frequency of ECG changes in hyperkalemia. Clinical Journal of the American Society of Nephrology, 3(2), 324 – 330. 8. Aslam, S., Friedman, E., & Ifudu, O. (2002). Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in haemodialysis patients. Nephrology Dialysis Transplantation, 17(9), 1639 – 1642. 9. Kovesdy, C. (2015). Management of Hyperkalemia: An Update for the Internist. The American Journal of Medicine, 128(12), 1281 – 1287 10. Harel, Z., Harel, S., Shah, P., Wald, R., Perl, J., & Bell, C. (2013). Gastrointestinal Adverse Events with Sodium Polystyrene Sulfonate (Kayexalate) Use: A Systematic Review. The American Journal of Medicine, 126(3), 264.e9 – 264.e24
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