Heliyon (Sep 2024)

Rare electrocardiographic findings in a young woman with acute barium poisoning: A case report

  • Yubin Zhang,
  • Xi Huang,
  • Yiru Han,
  • Ren Yan

Journal volume & issue
Vol. 10, no. 17
p. e37136

Abstract

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Background: Barium, as a heavy divalent alkaline earth metal, can be found in various products such as rodenticides, insecticides, depilatories, and fireworks. Barium can be highly toxic upon both acute and chronic exposure. The toxicity of barium compounds is dependent on their solubility. Both suicidal and accidental exposures to soluble barium can cause toxicity. Case summary: We report a case characterized by two different wide QRS complex tachycardia in a patient with acute barium poisoning, one due to barium-induced ventricular tachycardia (VT) under hypokalemia and, subsequently, sino-ventricular conduction with intraventricular conduction delay due to hyperkalemia after aggressive potassium supplementation. The latter may be misdiagnosed as VT for the history of acute barium poisoning and the absence of peaked T wave in hyperkalemia. Of note, another hemodynamically unstable VT and profound hypokalemia occurred during the potassium-lowering therapy, which, in addition to barium poisoning, may also be due to the iatrogenic hypokalemia. We also observed the prominent T-U waves at serum potassium of 4.6 mM 12 hours after admission, which may indicate that barium had not been completely cleared from the plasma at that moment. There are some parallels to the Andersen-Tawil syndrome with prominent T-U waves and risk of ventricular tachycardias. To our knowledge, this is the first case report of conversion from hypokalemia to hyperkalemia, and in a short moment, from hyperkalemia to hypokalemia, in acute barium poisoning. Conclusion: In addition to profound hypokalemia secondary to acute barium poisoning, hyperkalemia may also occur after aggressive potassium supplementation. A more careful rather than too aggressive potassium supplementation may be suitable in these cases of hypokalemia due to an intracellular shift of potassium. And a iatrogenic hypokalemia risk in the treatment of rebound hyperkalemia in barium poisoning must be considered.

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