{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,25]],"date-time":"2026-04-25T09:47:57Z","timestamp":1777110477077,"version":"3.51.4"},"reference-count":12,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2002,3,15]],"date-time":"2002-03-15T00:00:00Z","timestamp":1016150400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J Industrial Med"],"published-print":{"date-parts":[[2002,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Acute barium poisoning is most often the result of accidental or suicidal ingestion of the rodenticide, barium carbonate. We describe a trauma patient whose condition was complicated by severe acute barium toxicity from an explosion of the propellant, barium styphnate. In addition to critical injuries, the patient manifested classic signs of barium toxicity including repeated profound hypokalemia, cardiac arrhythmias, respiratory failure, prolonged gastrointestinal dysfunction, paralysis, myoclonus, hypertension, and profound lactic acidosis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The patient required lidocaine for ventricular bigeminy, massive infusions of potassium, prolonged ventilatory support, and parenteral nutrition to manage the effects of barium toxicity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>He is the first reported case to demonstrate recurrent profound hypokalemia as an effect of blood transfusions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Considering the paucity of information concerning management of this life\u2010threatening problem, the pathophysiology of barium toxicity, including the transfusion related hypokalemia, and its management is reviewed. Am. J. Ind. 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