History
Symptoms of hypermagnesemia are nonspecific at lower levels (2-4 mg/dL) and may include the following:
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Nausea
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Vomiting
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Flushing
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Lethargy
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Weakness
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Dizziness
Higher levels may lead to a depressed sensorium, and cardiopulmonary arrest may occur at extreme levels (>10-15 mg/dL).
Physical
Hypermagnesemia results in loss of deep-tendon reflexes at levels of 4-6 mg/dL. At magnesium levels of more than 5 mg/dL, CNS depression, which may range from drowsiness to coma, begins. Although concentrations of magnesium of more than 10 mg/dL lead to respiratory depression in adults, this may occur at much lower levels in the newborn.
Hypermagnesemia has a negative effect on heart rate. [8] Beginning with magnesium serum levels of 4.5 mg/dL, depression of sinoatrial node activity and atrial fibrillation may occur. Higher magnesium levels increase the P-R interval, widen the QRS complex, and can cause intraventricular conduction delays. Serum magnesium concentrations greater than 15 mg/dL can lead to complete heart block and asystole.
At varying levels (5-8 mg/dL), hypermagnesemia may produce vasodepression of vascular smooth muscle leading to systemic hypotension.
Although the absolute serum levels are important, the rate of rise is even more significant. For instance, a fast rise in serum level can produce cardiovascular symptoms more readily than can a slower rise in serum levels.
Causes
Major predisposing factors for the development of hypermagnesemia include the following:
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Renal failure (acute or chronic)
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Iatrogenic over administration of magnesium (eg, antacids, cathartics)
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Neonates born to mothers treated with magnesium sulfate for eclampsia
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(A) Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. FHHNC = Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. ADH = autosomal dominant hypocalcemia. FHH/NSHPT = Familial hypomagnesemia/neonatal severe hyperparathyroidism. (B) Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. HSH = Hypomagnesemia with secondary hypocalcemia. GS = Gitelman syndrome. IDH = Isolated dominant hypomagnesemia. Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.
