Hypomagnesemia magnesium therapy

Magnesium plays an important role in the transmission of nerve impulses. It is also important in the activity of many enzyme reactions, for example carbohydrate metabolism. Magnesium sulfate is used as replacement therapy in hypomagnesemia Magnesium sulfate (MgS04) is used in die prevention and control of seizures in obstetric patients with pregnancy-induced hypertension (PIH, also referred to as eclampsia and preeclampsia). It may also be added to TPN mixtures. 

Hypomagnesemia - Magnesium sulfate is used as replacement therapy in magnesium deficiency especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia. In such cases, the serum magnesium (Mg++) level is usually below the lower limit of normal (1.5 to 2.5 or 3 mEq/L) and the serum calcium (Ca++) level is normal (4.3 to 5.3 mEq/L) or elevated. 

Hypocalcemia can result from hypoparathyroidism, chronic renaJ failure, vila-niin D deficiency, and hypomagnesemia. Hypomagnesemia occurs mainly in those with alcoholism so severe as to requite hospitaiization. Magnesium deficiency results in a decline in the responsiveness of osteoclasts to FTH, resulting in interruption of the normal process of bone fumover. In this case, hypocalcemia cannot be effectively corrected unless magnesium therapy is used. 

Parathyroidectomy is a treatment of last resort for sHPT, but should be considered in patients with persistently elevated iPTH levels above 800 pg/mL (800 ng/L) that is refractory to medical therapy to lower serum calcium and/or phosphorus levels.39 A portion or all of the parathyroid tissue may be removed, and in some cases a portion of the parathyroid tissue may be transplanted into another site, usually the forearm. Bone turnover can be disrupted in patients undergoing parathyroidectomy whereby bone production outweighs bone resorption. The syndrome, known as hungry bone syndrome, is characterized by excessive uptake of calcium, phosphorus, and magnesium for bone production, leading to hypocalcemia, hypophosphatemia, and hypomagnesemia. Serum ionized calcium levels should be monitored frequently (every 4 to 6 hours for the first 48 to 72 hours) in patients receiving a parathyroidectomy. Calcium supplementation is usually necessary, administered IV initially, then orally (with vitamin D supplementation) once normal calcium levels are attained for several weeks to months after the procedure. 

L A. Nephrotoxicity is the most common and most serious toxicity associated with amphotericin B administration. This is manifested by azotemia (elevated serum blood urea nitrogen and creatinine), and by renal tubular acidosis, which results in the wasting of potassium and magnesium in the urine (leading to hypokalemia and hypomagnesemia, requiring oral or intravenous replacement therapy). Normochromic normocytic anemia is also seen with long-term amphotericin B administration. Elevation of hver enzymes is not associated with the use of amphotericin B. 

Hjq)onatremia is rare, and persistent hyponatremia very rare in patients taking cisplatin (162). In a detailed description of the biochemical abnormalities that can result from renal tubular dysfunction after cisplatin therapy, it was noted that hypocalciuria is more common than hypomagnesemia, and that there tends to be a state of reduced serum bicarbonate. The most severe renal tubular damage caused by cisplatin is characterized by hypocalciuria, total body magnesium deficiency, and hypokalemic metabolic alkalosis (163). 

The most restrictive adverse effect associated with AmB therapy is its potential to induce nephrotoxicity, manifested as disturbances in both glomerular and tubular function. The clinical manifestations usually include azotemia, renal tubular acidosis, decreased concentrating ability of the kidney, and electrolyte disturbances such as urinary potassium wasting leading to hypokalemia, and magnesium wasting to result in hypomagnesemia [17]. 

In summary, parenteral pentamidine administration for the treatment of PCP can be associated with the development of usually mild, reversible acute kidney injury. Compounding risk factors, of which volume depletion is the most important, are found in the majority of cases of pentamidine nephrotoxicity. There is no convincing evidence that the aerosol route of pentamidine administration for PCP prophylaxis results in nephrotoxicity. Hypocalcemia and hypomagnesemia with renal magnesium wasting, and particularly, hyperkalemia are seen with pentamidine therapy. 

Shah GM, Alvarado P, Kirschenbaum MA. Symptomatic hypocalcemia and hypomagnesemia with renal magnesium wasting associated with pentamidine therapy in a patient with AiDS.The American journal of medicine. 1990 Sep 89(3) 380-2. 

Hypomagnesemia of any cause may be associated with severe symptomatic hypocalcemia that is unresponsive to calcium replacement therapy (see Chap. 50). Reduced serum magnesium concentrations can impair PTH secretion and induce resistance of target organs to the actions of PTH. ° Normalization of serum calcium concentrations in these patients is thus dependent on appropriate replacement of magnesium. 

Once acnte hypocalcemia is corrected by parenteral administration, fnrther treatment modahties shonld be individnalized according to the canse of hypocalcemia. If hypomagnesemia is present, magnesium supplementation is indicated (see Chap. 50). Asymptomatic and chronic hypocalcemia associated with hypoparathyroidism and vitamin D-deflcient states may be managed by oral calcium and vitamin D supplementation (see Tables 44—6 and 44—7). Therapy is begnn with 1 to 3 g/day of elemental calcium. Average maintenance doses range from 2 to 8 g of elemental calcium per day in divided doses. If serum calcium does not normalize, a vitamin D preparation may need to be added. 

Hypomagnesemia Diarrhea, malabsorption, anabolism magnesium-wasting drug therapy Increase magnesium intake... 

Patients undergoing OLT receive a substantial amount of crystalloid and blood products during the operative procedure. This often results in an edematous state in the postoperative period, especially in patients who had ascites preoperatively. The large citrate load from administered blood products has been implicated in causing hypocalcemia (due to citrate binding of ionized calcium) and metabolic alkalosis (due to conversion of citrate to bicarbonate) in the postoperative period. Low serum concentrations of magnesium are common in the postoperative period. Reduced intake from restricted diets and increased urinary excretion secondary to cyclosporine therapy contribute to hypomagnesemia. 

Parenteral used for seizure prevention and control in severe preeclampsia or eclampsia without deleterious CNS depression in the mother, fetus, or newborn as replacement therapy in magnesium deficiency, especially in acute hypomagnesemia accompanied by signs of tetany similar to those observed in hypocalcemia to correct or prevent hypomagnesemia by addition to total parenteral nutrition admixture hypertension, encephalopathy, and convulsions in children with acute nephritis inhibition of premature labor as treatment of life-threatening ventricular arrhythmias for prevention and treatment of nutritional magnesium deficiency and as a laxative. 

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