the Medicine Ward Aaron Jattan, MD, CCFP Education Director, - - PowerPoint PPT Presentation

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

Hyperkalemia1

• 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 transport3

• 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 resolution4

• 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 Cells5

• 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 Excretion5

• 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?

EKG6

• 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)

EKG6

EKG

EKGs are NOT sensitive in diagnosing hyperkalemia7-8

.

Treatment – First Steps

• Rule-out acute urinary obstruction and hyperglycemia
• Stop, or hold, offending medications
• Consider Calcium

Treatment – Calcium9

• 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 – Compensation9

• 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
• ccurs in approximately one hour
• Sodium Bicarbonate
• Slow and more appropriate for cases of chronic hyperkalemia
• b2-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 Correction9

• 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. 5. Reddi AS. (2018). Fluid, electrolyte and acid-base disorders, 2nd ed. Springer Nature: Newark, New Jersey. 6. Martindale J.L., & Brown D.F.M. (2016). A visual guide to ECG interpretation, 2nd edition. Wolters Kleuwer: 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