Jou Da Hye, Kim Su In, Choi In Hong, Song Su Hyun, Oh Tae Ryom, Suh Sang Heon, Choi Hong Sang, Kim Chang Seong, Kim Soo Wan, Bae Eun Hui, Ma Seong Kwon
Department of Internal Medicine, Chonnam National University Medical School and Chonnam National University Hospital, Gwangju, Republic of Korea.
Electrolyte Blood Press. 2023 Dec;21(2):66-71. doi: 10.5049/EBP.2023.21.2.66. Epub 2023 Dec 18.
Hypermagnesemia is a rare but potentially fatal electrolyte disorder often overlooked because of its unfamiliarity. Magnesium is regulated through a balance of bone, intestinal absorption, and renal excretion. Hypermagnesemia typically arises from excessive magnesium intake or reduced renal excretion; however, it also occurs in patients with normal kidney function. Herein, we report two cases of hypermagnesemia in patients taking magnesium hydroxide for constipation. The first case involved an 82-year-old woman with end-stage renal disease who developed metabolic encephalopathy due to hypermagnesemia, after taking 3,000 mg of magnesium hydroxide daily for constipation. Her magnesium level was 9.9 mg/dL. Her treatment involved discontinuing magnesium hydroxide and continuing hemodialysis, which led to her recovery. In the second case, a 50-year-old woman with a history of cerebral hemorrhage and mental retardation developed hypermagnesemia despite having normal renal function. She was also taking magnesium hydroxide for constipation, and her magnesium level was 11.0 mg/dL. She experienced cardiac arrest while preparing for continuous renal replacement therapy (CRRT). After achieving return of spontaneous circulation, CRRT was initiated, and her magnesium level showed a decreasing trend. However, vital signs and lactate levels did not recover, leading to death. These cases highlight the importance of prompt diagnosis and intervention for hypermagnesemia and the need to regularly monitor magnesium levels in individuals receiving magnesium-containing preparations, especially those with impaired kidney function.
高镁血症是一种罕见但可能致命的电解质紊乱，常因不为人熟悉而被忽视。镁通过骨骼、肠道吸收和肾脏排泄之间的平衡来调节。高镁血症通常源于镁摄入过多或肾脏排泄减少；然而，在肾功能正常的患者中也会发生。在此，我们报告两例因服用氢氧化镁治疗便秘而发生高镁血症的病例。第一例涉及一名82岁的终末期肾病女性，她因便秘每天服用3000毫克氢氧化镁后，因高镁血症发展为代谢性脑病。她的镁水平为9.9毫克/分升。她的治疗包括停用氢氧化镁并继续进行血液透析，这使她得以康复。第二例，一名有脑出血和智力障碍病史的50岁女性，尽管肾功能正常，但仍发生了高镁血症。她也因便秘服用氢氧化镁，她的镁水平为11.0毫克/分升。她在准备进行连续性肾脏替代治疗（CRRT）时发生心脏骤停。在实现自主循环恢复后，开始进行CRRT，她的镁水平呈下降趋势。然而，生命体征和乳酸水平未恢复，导致死亡。这些病例凸显了对高镁血症进行及时诊断和干预的重要性，以及对接受含镁制剂的个体，尤其是肾功能受损者定期监测镁水平的必要性。
