Increases in plasma [Mg2+] are nearly always due to excessive intake (magnesium-containing antacids or laxatives), renal impairment (GFR < 30 mL/min), or both. Less common causes include adrenalinsufficiency, hypothyroidism, rhabdomyolysis, and lithium administration. Magnesium sulfate therapy for preeclampsia and eclampsia can cause hyperma-gnesemia in the mother as well as in the fetus.
Symptomatic hypermagnesemia typically presents with neurological, neuromuscular, and cardiac manifestations, including hyporeflexia, sedation, muscle weakness, and respiratory depression. Vasodilation, bradycardia, and myocardial depres-sion may cause hypotension. ECG signs may include prolongation of the P–R interval and widening of the QRS complex. Marked hyper-magnesemia can lead to respiratory andcardiac arrest.
With relatively mild hypermagnesemia, all that is usually necessary is to discontinue source(s) of magnesium intake (most often antacids). In cases of relatively high [Mg2+], and especially in the pres-ence of clinical signs of magnesium toxicity, intra-venous calcium can temporarily antagonize most of the effects of clinical toxicity. A loop diuretic in conjunction with intravenous fluid replacement enhances urinary magnesium excretion in patients with adequate renal function. When diuretic administration with intravenous infusion is used to enhance magnesium excretion, serial measure-ments of [Ca2+] and [Mg2+] should be obtained,urinary catheter is required, and goal-directed hemodynamic and fluid management should be considered. Dialysis may be necessary in patients with marked renal impairment. In cases of severe magnesium toxicity, ventilatory or circulatory support, or both, may be necessary.
Hypermagnesemia requires close monitoring of the ECG, blood pressure, and neuromuscular function. Potentiation of the vasodilatory and negative inotropic properties of anesthetics should be expected. Dosages of nondepolarizing NMBs should be reduced.
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