Heparin-Induced Hyperkalemia in a Patient Diagnosed with Thyroid Storm

Abstract

To describe a case of heparin-induced hyperkalemia and the role for transtubular potassium gradient (TTKG) to guide fludrocortisone therapy. A 52-year-old white male developed hyperkalemia after receiving intravenous unfractionated heparin (UFH) for atrial fibrillation during thyroid storm. Admission laboratory results were noteworthy for normal potassium levels, undetectable thyroid-stimulating hormone, and mild transaminitis. Treatment for thyroid storm was initiated but UFH was stopped because the international normalized ratio was subsequently found to be elevated. Rising potassium levels developed just 24 hours after UFH discontinuation, without exogenous potassium supplementation, renal dysfunction, or acidosis. A TTKG was low, reflecting a hypoaldosterone state. In addition, the Naranjo probability scale indicated probable medication-associated hyperkalemia. Heparin-induced hyperkalemia (HIH) was suspected and oral fludrocortisone 0.2 mg was given daily alongside serial TTKG measurements. TTKG and hyperkalemia normalized with 2 days of treatment. UFH is commonly used; therefore, clinicians must be cautious of hyperkalemia. Although HIH usually resolves after discontinuation of heparin, it may persist despite discontinuation of the drug, as highlighted by this case. In this setting, a TTKG should be determined, which can be used to guide fludrocortisone therapy. HIH can occur despite discontinuation of heparin, and TTKG can be helpful in guiding fludrocortisone treatment in this circumstance.