Fatal Hypermagnesemia in Patients Taking Magnesium Hydroxide.

Q3 Medicine
Electrolyte and Blood Pressure Pub Date : 2023-12-01 Epub Date: 2023-12-18 DOI:10.5049/EBP.2023.21.2.66
Da Hye Jou, Su In Kim, In Hong Choi, Su Hyun Song, Tae Ryom Oh, Sang Heon Suh, Hong Sang Choi, Chang Seong Kim, Soo Wan Kim, Eun Hui Bae, Seong Kwon Ma
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Abstract

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.

服用氢氧化镁的患者出现致命的高镁血症。
高镁血症是一种罕见但有潜在致命危险的电解质紊乱,因其陌生而经常被忽视。镁通过骨骼、肠道吸收和肾脏排泄的平衡进行调节。高镁血症通常是由于镁摄入过多或肾脏排泄减少引起的,但肾功能正常的患者也会出现高镁血症。在此,我们报告了两例服用氢氧化镁治疗便秘的高镁血症患者。第一个病例涉及一名患有终末期肾病的 82 岁妇女,她在每天服用 3000 毫克氢氧化镁治疗便秘后,因高镁血症引发了代谢性脑病。她的血镁水平为 9.9 毫克/分升。她的治疗包括停用氢氧化镁和继续进行血液透析,最终她康复了。在第二个病例中,一名有脑出血和智力迟钝病史的 50 岁女性出现了高镁血症,尽管她的肾功能正常。她还在服用氢氧化镁治疗便秘,镁含量为 11.0 毫克/分升。在准备接受持续肾脏替代疗法(CRRT)时,她的心脏骤停。自主循环恢复后,CRRT 启动,她的血镁水平呈下降趋势。然而,生命体征和乳酸水平并未恢复,最终导致死亡。这些病例强调了及时诊断和干预高镁血症的重要性,以及定期监测接受含镁制剂治疗的患者(尤其是肾功能受损的患者)体内镁水平的必要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Electrolyte and Blood Pressure
Electrolyte and Blood Pressure Medicine-Internal Medicine
CiteScore
2.10
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0.00%
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