Increases in plasma magnesium are often due to excessive intake (magnesium-containing antacids or laxatives) and/or renal impairment. Iatrogenic hypermagnesemia can also occur during magnesium sulfate therapy for gestational hypertension in the mother as well as the fetus. Less common causes include adrenal insufficiency, hypothyroidism, rhabdomyolysis, and lithium administration.
Clinical manifestations typically are hyporeflexia, sedation, nausea, vomiting, flushing, urinary retention, ileus and skeletal muscle weakness. Hypermagnesemia appears to impair the release of acetylcholine and decreases motor end-plate sensitivity to acetylcholine in muscle. Vasodilation, bradycardia, and myocardial depression can lead to hypotension at levels > 10 mmol/dL (> 24 mg/dL). ECG signs are inconsistent but often include prolongation of the P–R interval and widening of the QRS complex. Marked hypermagnesemia can lead to respiratory arrest.
Although mild hypermagnesemia in the setting of normal renal function can be treated with supportive care and withdrawal of the cause, in some cases dialysis is necessary. All sources of magnesium intake (most often antacids) should be stopped. Intravenous calcium can temporarily antagonize most of the effects of hypermagnesemia. A loop diuretic along with an infusion of ½-normal saline in 5% dextrose enhances urinary magnesium excretion. Diuresis with normal saline is generally not recommended to decrease the likelihood of iatrogenic hypocalcemia, because the latter potentiates the effects of hypermagnesemia. Hypermagnesemia requires close monitoring of the ECG, blood pressure, and neuromuscular function. Potentiation of the vasodilating and negative inotropic properties of anesthetics should be expected. Dosages of NMBAs should be reduced by 25–50%. A urinary catheter is required when diuretic and saline infusions are used to enhance magnesium excretion (see above). Serial measurements of [Ca2+] and [Mg2+] may be useful.