Bittern is made by extracting the salt from marine water, and it contains various amounts of electrolyte components, such as magnesium and calcium. The excess consumption of bittern can therefore lead to electrolyte imbalances. We report a case in which a bittern overdose induced hypermagnesemia and hypercalcemia complicated by cardiopulmonary arrest. A 21-year-old Japanese female was transported to our emergency room approximately 8 hours after ingesting a bottle of bittern. On arrival, she could speak, but cardiopulmonary arrest suddenly occurred. Her initial blood chemistry showed hypermagnesemia and hypercalcemia. We immediately initiated hemodialysis. The serum concentrations of magnesium and calcium gradually decreased after the initiation of hemodialysis, and they had normalized by hospital day 3. Electrolyte monitoring and the early initiation of hemodialysis are useful for treating a bittern overdose. As hypermagnesemia can induce not only cardiopulmonary arrest, but also a systemic hemorrhage tendency, multimodal management is very important.

The buttonhole puncture technique was used in a 70-year-old female dialysis patient to reduce the puncture pain associated with dialysis. However, her venous pressure increased 10 minutes after dialysis was started, and it was speculated that the side lumens of the painless needle used in the procedure had caused the increase in venous pressure. After using the non-side lumens of the painless needle, the patient’s venous pressure fell. This is considered to be an informative case, which will be helpful for facilities that are considering the introduction of the buttonhole puncture technique.

Upper gastrointestinal bleeding is a common complication in patients undergoing maintenance hemodialysis. However, bleeding due to esophagitis and/or esophageal ulcers involving the whole circumference of the esophagus is rare. We report a case of hematemesis due to esophagitis and esophageal ulcers involving the whole circumference of the esophagus in a hemodialysis patient, despite the regular use of a proton pump inhibitor and a gastric mucosa-protecting agent. A 69-year-old female hemodialysis patient suddenly became nauseous and then vomited blood during hemodialysis therapy. Urgent upper gastrointestinal endoscopy was performed, which revealed mucosal edema and erosive lesions. The lesions covered the whole circumference of the esophagus, and active hemorrhaging was seen from isolated ulcers, which was suggestive of esophagitis and esophageal ulceration. The bleeding lesions were successfully treated with endoscopic clipping. After the endoscopic hemostasis, conservative treatment was employed. On the 11th hospital day, the patient was discharged without recurrent bleeding or symptoms. We concluded that the bleeding in this case was caused by an acute esophageal mucosal lesion associated with microcirculatory insufficiency.