Linking To And Excerpting From The Curbsiders’ “#537 Hyperkalemia and Hypokalemia”

Today, I review, link to, and excerpt from The Curbsiders“#537 Hyperkalemia and Hypokalemia”.

All that follows is from the above resource.

Transcript available via YouTube

I’m Going Bananas for This One!

Learn how to formulate a framework while dealing with potassium disorders in patients with varying levels of kidney disease.We’re joined by Dr Joel Topf, (@kidney_boy) to explore how to navigate potassium disorders, develop etiology frameworks, and treat these patients.

Claim CME for this episode at curbsiders.vcuhealth.org!

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Show Segments

  • Intro
  • Rapid fire questions/Picks of the Week
  • Case 1: Hyperkalemia
  • How to Approach Patients with Hyperkalemia
  • Treatment Options for Hyperkalemia
  • Case 2: Hypokalemia
  • How to Approach Patients With Hypokalemia
  • Treatment Options for Hypokalemia
  • Case 3: Hyperkalemia in ESKD patients
  • How To Approach the Management in ESKD patients
  • Take Home Points
  • Outro

Disclosures

Dr. Topf reports the following conflicts of interests: Advisor-Travere Therapeutics, Advisor-Otsuka, Advisor-Vera Therapeutics, Advisor-Novartis, Advisor-Vertex Therapeutics

The Curbsiders report no relevant financial disclosures.

CME Partner: VCU Health CE

The Curbsiders are partnering with VCU Health Continuing Education to offer continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit.

Hyperkalemia and Hypokalemia Pearls

  1. In a case of hyperkalemia, the first step is to rule out any cause of pseudohyperkalemia: such as hemolyzed samples
  2. Hyperglycemia can cause hyperkalemia due to solute drag; if the sugars can be controlled, then that will aid in the control of hyperkalemia.
  3. Medications can also lead to hyperkalemia so it’s important to do a thorough medication check.
  4. The potassium switch manages high potassium through inactivation of a sodium-chloride transporter, causing a thiazide-like effect of distal sodium delivery and increased excretion of sodium and potassium
  5. Even in dialysis patients who have hyperkalemia, there are roles for potassium binders
  6. Proton pump inhibitors often cause hypomagnesemia and related hypokalemia; with repletion of magnesium, the potassium should improve.

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How is rhabdomyolysis diagnosed?

AI Overview
Rhabdomyolysis is diagnosed primarily through a blood test that measures high levels of creatine kinase (CK), a protein released into the blood when muscle tissue is damaged. [1]
Doctors combine this blood test with a review of your medical history, recent physical activity, and physical examination. [1, 2]
Common Symptoms
Doctors look for signs of severe muscle injury. The classic signs include: [1]
  • Muscle pain or severe aches (especially in the thighs, shoulders, calves, or lower back)
  • Muscle weakness or trouble moving your arms and legs
  • Dark urine that looks like tea or cola [1, 2]
Note: Not everyone has all three symptoms. Some people only feel tired, stiff, or sore.
Key Diagnostic Tests
  • Creatine Kinase (CK) Blood Test: This is the most important test. A CK level that is five times higher than normal (or over 1,000 to 5,000 IU/L) strongly points to rhabdomyolysis. [1, 2]
  • Urine Test (Urinalysis): Doctors check your urine for myoglobin, a muscle protein that turns urine dark. A urine dipstick might show a false positive for blood, but a microscope will show no actual red blood cells. [1, 2]
  • Kidney Function Tests: Blood tests for creatinine and blood urea nitrogen (BUN) check if muscle breakdown products have started to harm your kidneys. [1, 2]
  • Electrolyte Tests: Blood tests check for dangerous shifts in potassium, calcium, and phosphorus. [1, 2]
  • ECG (Electrocardiogram): This heart test checks for irregular heart rhythms caused by high potassium levels. [1, 2]
You can read more about these signs on the CDC Rhabdomyolysis Page or review a comprehensive overview at the Cleveland Clinic Rhabdomyolysis Guide.
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What is TLS in hyperkalemia:

“In the context of hyperkalemia, TLS stands for Tumor Lysis Syndrome, a life-threatening oncological emergency where rapid breakdown of cancer cells floods the bloodstream with intracellular contents, including large amounts of potassium.”

Overview of TLS
  • Definition: A group of metabolic disturbances that happens when a massive number of cancer cells die at once.
  • Timing: It usually occurs within 24 to 72 hours after starting chemotherapy, but it can also happen spontaneously in fast-growing cancers like leukemia or lymphoma. [1, 2, 3, 4, 5]
The Metabolic Tetrad
TLS is characterized by four major electrolyte and chemical imbalances: [1]
  • Hyperkalemia: High blood potassium (released from inside the destroyed cells), which can cause fatal heart rhythms.
  • Hyperphosphatemia: High blood phosphorus from cell destruction.
  • Hypocalcemia: Low blood calcium, which happens because the excess phosphorus binds to calcium.
  • Hyperuricemia: High uric acid from the breakdown of nucleic acids, which can lead to kidney injury. [1, 2, 3, 4, 5]

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Resuming The Curbsiders#537 Hyperkalemia and Hypokalemia:

Hyperkalemia and Hypokalemia-Show Notes

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