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A case of severe barium poisoning with typical symptoms was published (Bahlman et al., 2005). Intense potassium supplementation did not correct hypokalemia and clinical symptoms worsened. Veno-venous hemodialysis was started around 15h after barium nitrate ingestion, resulting in clinical improvement, normalization of serum potassium levels and enhanced clearance of barium. This case completes the existing, scanty documentation published so far on the use of hemodialysis in barium intoxication, and it is recommended that hemodialysis is considered in case of barium intoxication which do not rapidly respond to potassium supplementation.

A second case report presented typical features of acute barium poisoning (Payen et al., 2011). The benign outcome can be attributed to prompt and massive potassium supplementation. Acute barium poisonings are medical emergencies. Severe hyperkalemia that occurs within 2 hours post-ingestion is the predominating feature. It is unclear whether mechanisms other than hypokalemia contribute to the neuromuscular and cardiovascular toxic effects of soluble barium compounds. In most cases, recovery is achieved with normalization of kalemia. It is recommended to measure serum phosphate levels when muscular weakness does persist despite normalized kalemia.