Abstract: TH-PO353
Rebound Hyperkalemia in Thyrotoxicosis: A Case Report
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Author
- Ragasa, Richard Raymund Reyes, University of the Philippines System, Manila, Philippines
Introduction
Thyroid hormones play a significant role in potassium homeostasis through increasing expression of the Na/K ATPase pump. This increases the complexity of repleting potassium in patients with hyperthyroidism. This is a case of unexpected rebound hyperkalemia after potassium repletion in a patient with thyroid storm.
Case Description
A 57-year-old woman with multinodular toxic goiter presented with hematochezia, tachycardia, seizure, and jaundice. Initial workup showed thyrotoxicosis (FT4 55 pmol/L) associated with hypercoagulability (INR 6.0) with subdural hematoma, and cholestatic jaundice. Potassium level on admission was 2.3 mEq/L, which was attributed to intracellular shifting of potassium from thyrotoxicosis and low magnesium at 0.6 mmol/L. Thyroid storm was managed in the ICU with propylthiouracil, hydrocortisone, and potassium iodide. Cryoprecipitate was transfused with resolution of hypercoagulability and bleeding. Patient also underwent hematoma evacuation with neurosurgery. Postoperatively, potassium ranged from 2.6 to 4.7 mEq/L, magnesium at 0.65 to 0.99 mmol/L, and were repleted as necessary. On hospital day 18, potassium was found to be low at 1.8 mEq/L with normal magnesium. EKG showed sinus bradycardia with prominent u waves. Continuous intravenous potassium repletion was started at 8-10 mEq/h on top of oral repletion. Urine K/Crea was found to be <13 mEq/g suggesting intracellular potassium shift. Several hours after around 220 mEq repleted, patient was noted to have wide complex tachycardia and went into cardiopulmonary arrest. Advanced cardiac life support was performed without return of spontaneous circulation. Blood chemistry sent minutes prior to the arrhythmia showed serum potassium of 7.7 mEq/L confirmed by plasma potassium of 7.4 mEq/L. It was unexpected that the repletion resulted in disproportionate and precipitous rise in serum levels.
Discussion
In the thyrotoxic state, intracellular redistribution of potassium decreases serum potassium without changing total body potassium. In about 1 of 4 patients with thyrotoxicosis, paradoxical hypokalemia is observed even with repletion and this was associated with higher thyroxine levels and more pronounced rebound hyperkalemia. This phenomenon makes it difficult to anticipate response to repletion. Potassium repletion in these situations, particularly through the intravenous route, should be done cautiously under close monitoring.