Magnesium Replacement Calculator

Magnesium replacement is dosed by severity band rather than by a deficit equation, because serum magnesium is a poor census of body stores. An adult carries roughly 24 grams of magnesium, but around 60 percent is locked in bone and most of the remainder is intracellular; barely 1 percent circulates in the extracellular fluid the laboratory samples. The normal serum range is about 1.7 to 2.4 mg/dL, equivalent to 0.7 to 1.0 mmol/L, and a normal value can coexist with substantial total body depletion. Conventional dosing gives 1 to 2 g of magnesium sulfate for a level of 1.5 to 1.8 mg/dL, 2 to 4 g for 1.0 to 1.5, and 4 to 8 g below 1.0, with 1 g of MgSO4 supplying 8.12 mEq or 4.06 mmol of elemental magnesium. Rate matters as much as total dose. Routine infusion is held near 1 g per hour diluted in 100 mL, because a rapid load is largely dumped by the kidney and causes flushing, hypotension and bradycardia; the exception is 2 g pushed over two to five minutes for torsades de pointes. Since the kidney clears 90 percent or more of an administered load, doses are roughly halved at a GFR of 30 to 60 mL/min and cut to about a quarter below 30, where hypermagnesemia can cause respiratory failure. Loss of deep tendon reflexes is the earliest toxicity sign, around 7 to 10 mg/dL. Repleting intracellular stores usually takes repeated dosing over 2 to 5 days, and coexisting hypokalemia and hypocalcemia will not correct until magnesium does.

Magnesium entered clinical practice through obstetrics. Injectable magnesium sulfate was used for tetanus in the early 1900s, and in 1906 the obstetrician Martin Horn reported treating eclamptic convulsions with it. The approach spread in the United States after Lazard described intravenous use in California in the 1920s, and it was standardized by Jack Pritchard, whose intramuscular and intravenous regimens developed at Parkland Hospital in Dallas from the 1950s onward became the reference protocols. Superiority over phenytoin and diazepam was settled by the Eclampsia Trial Collaborative Group in 1995 and by the international MAGPIE trial published in 2002. Recognition of hypomagnesemia as a distinct electrolyte disorder came much later. Reports of deficiency causing tetany and arrhythmia accumulated from the 1930s through the 1960s, but the mechanism behind refractory hypokalemia was explained only after the renal outer medullary potassium channel was cloned in the 1990s and shown to be blocked by intracellular magnesium, so that depletion releases the brake on renal potassium secretion. Magnesium as first-line therapy for torsades de pointes was established by case series in the 1980s, including work by Tzivoni and colleagues, along with the finding that it terminates the arrhythmia whether or not the serum level is low. Routine inclusion of magnesium in hospital chemistry panels is comparatively recent, which is why the deficiency stayed under-recognized for decades.