hypermagnesemia complications

  • related: Nephrology
  • tags: #literature #nephrology

This patient has developed hypermagnesemia, likely from excessive use of Epsom salts for his chronic constipation. Epsom salts are magnesium sulfate, deriving the name from the town of Epsom in Surrey, England, where it was originally discovered. People sometimes consume them by dissolving the salt in water and drinking it to treat constipation, insomnia, and fibromyalgia. Others soak in Epsom baths. Magnesium is excreted in urine, and the kidney is vital in maintaining normal magnesium levels, so in addition to ingesting Epsom salts, acute renal failure likely also contributed to his elevated magnesium level.

Hypermagnesemia is uncommon and considerably less common than hypomagnesemia. In addition to renal dysfunction, other potential contributors to hypermagnesemia include massive oral ingestion and GI disorders that increase absorption of magnesium (active ulcers, gastritis, colitis). Hypermagnesemia can also occur with administration to treat preterm labor or preeclampsia in pregnant women. Clinical symptoms can be divided into three categories—neuromuscular effects, cardiovascular effects, and hypocalcemia—and do not usually manifest unless the magnesium level is above 4.8 mg/dL (1.97 mmol/L). Neuromuscular effects include diminished and then absent deep tendon reflexes, somnolence, and muscle paralysis leading to flaccid quadriplegia and even potentially respiratory dysfunction and apnea. Smooth muscle may also be affected. Magnesium acts as a calcium channel blocker at high serum levels. Hypotension, cardiac conduction defects, and bradycardia appear at moderate levels of hypermagnesemia, followed by ECG changes at higher levels, including prolonged PR interval, increased QRS duration, and increased QT interval. At severe levels of hypermagnesemia, complete heart block and cardiac arrest can occur. Moderate hypermagnesemia can inhibit the release of parathyroid hormone, leading to hypocalcemia. Although usually asymptomatic and transient, hypocalcemia can occasionally result in ECG abnormalities.

Treatment of hypermagnesemia depends on renal function, level of hypermagnesemia, and severity of illness. Mild hypermagnesemia with normal renal function likely will correct with removal of exogenous magnesium. In patients with moderate renal impairment or acute kidney injury, initial therapy entails IV isotonic fluids and a loop diuretic. However, in patients with severe renal impairment, those with severe neurological manifestations, or those in whom initial treatment with IV isotonic fluids and loop diuretic fails to lower the magnesium level, hemodialysis should be initiated. Although this patient only has mild renal impairment, the failure of fluids and diuretics to reasonably lower the magnesium level, combined with the severe neurological manifestations, should prompt hemodialysis. Given the results of the first attempt, repeating isotonic fluids and increasing the dose of loop diuretic is unlikely to rapidly correct the problem.

2,3-dimercaptosuccinic acid (DMSA) and deferoxamine are both chelating agents. DMSA is used to chelate lead or arsenic. Deferoxamine is used to chelate iron in patients with hemoglobinopathies and iron overload from recurrent transfusions. Magnesium is highly water soluble and is easily dialyzed. There is no role for chelation therapy in the treatment of hypermagnesemia.1234

Footnotes

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  2. Bokhari SR, Siriki R, Teran FJ, et al. Fatal hypermagnesemia due to laxative use. Am J Med Sci. 2018;355(4):390-395. PubMed ↩

  3. Felsenfeld AJ, Levine BS, Rodriguez M. Pathophysiology of calcium, phosphorus, and magnesium dysregulation in chronic kidney disease. Semin Dial. 2015;28(6):564-577. PubMed ↩

  4. Nishikawa M, Shimada N, Kanzaki M, et al. The characteristics of patients with hypermagnesemia who underwent emergency hemodialysis. Acute Med Surg. 2018;5(3):222-229. PubMed ↩