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Abstract
Barium poisoning is uncommon. Barium salts are used in a number of industries, including mining, ceramics, plastics, and adhesives and as a green coloring in fireworks. It is also a rodenticide. In poisoning, it blocks passive efflux potassium channels without affecting the Na/K-ATPase pump resulting in an increase in intracellular potassium and extracellular hypokalemia. A 44-year-old man self-presented to hospital six hours following deliberately ingesting 10 g of barium carbonate with suicidal intention. On presentation, he had profuse vomiting with decreased power globally and hyporeflexia in his upper and lower limbs. His ECG was in sinus rhythm with first-degree heart block and diffuse T wave flattening and U wave formation. He had severe hypokalemia with a potassium concentration of 2.4 mmol/L. He was managed supportively with antiemetics and supplemental potassium, receiving 80 mmol of intravenous potassium chloride in total. He was discharged home 24 hours post-ingestion. Soluble barium salts are highly toxic and clinical effects include hypokalemia, flaccid paralysis, cardiac arrest and death. Management of barium toxicity is largely supportive, focusing on the correction of hypokalemia. Oral sulfate salts may prevent absorption through precipitating insoluble barium sulfate in the gastrointestinal tract. Hemodialysis increases elimination and can be considered in severe poisoning.
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