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Magnesium Hypomagnesemia

Fhtients with hypomagnesemia (low magnesium plasma levels) are at increased risk for digitalis toxicity. If low magnesium levels are detected, die primary care provider may prescribe magnesium replacement dierapy. [Pg.364]

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. [Pg.640]

Other electrolytes of importance include calcium (especially if the patient is receiving a calcium channel blocker, such as nicardipine) and magnesium, as hypomagnesemia may predispose the patient to seizures, further complicating the ICP management. If the patient received intravenous iodinated contrast as part of their stroke evaluation, then careful monitoring of the blood urea nitrogen (BUN) and creatinine levels is necessary to detect contrast nephropathy. [Pg.166]

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. [Pg.389]

Although severe hypomagnesemia has been associated with VF/PVT, clinical trials have not demonstrated any benefit with routine administration of magnesium during a cardiac arrest. Because two observation trials showed improvement in ROSC in patients with arrests associated with torsade de pointes, magnesium administration should be limited to these patients. [Pg.93]

Hypomagnesemia is usually associated with disorders of the intestinal tract or kidneys. Drugs (e.g., aminoglycosides, amphotericin B, cyclosporine, diuretics, digitalis, cisplatin) or conditions that interfere with intestinal absorption or increase renal excretion of magnesium can cause hypomagnesemia. [Pg.906]

The severity of magnesium depletion and presence of symptoms dictate the route of magnesium supplementation (Table 78-7). Intramuscular magnesium is painful and should be reserved for patients with severe hypomagnesemia and limited venous access. IV bolus injection is associated with flushing, sweating, and a sensation of warmth. [Pg.908]

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. [Pg.23]

Total parenteral nutrition Total parenteral nutrition patients may develop hypomagnesemia (less than 1.5 mEq/L) without supplementation. Magnesium is added to correct or prevent hypomagnesemia. [Pg.23]

Electrolyte disorders In patients with hypokalemia or hypomagnesemia, toxicity may occur despite serum digoxin concentrations less than 2 ng/mL, because potassium or magnesium depletion sensitizes the myocardium to digoxin. Therefore, it is desirable to maintain normal serum potassium and magnesium concentrations in patients being treated with digoxin. [Pg.407]

Hypomagnesemia Loop diuretics increase the urinary excretion of magnesium. Hypocalcemia Serum calcium levels may be lowered (rare cases of tetany have occurred). [Pg.690]

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. [Pg.603]

Pharmacological issues (i) Renal handhng of magnesium . (ii) Metabolic effects of diuretics , (iii) Myocardial infraction , (iv) Hypomagnesemia, (v) Central nervous system injury . [Pg.268]


See other pages where Magnesium Hypomagnesemia is mentioned: [Pg.411]    [Pg.411]    [Pg.256]    [Pg.639]    [Pg.642]    [Pg.342]    [Pg.167]    [Pg.221]    [Pg.45]    [Pg.50]    [Pg.130]    [Pg.415]    [Pg.537]    [Pg.841]    [Pg.1217]    [Pg.1508]    [Pg.1508]    [Pg.1524]    [Pg.729]    [Pg.85]    [Pg.901]    [Pg.679]    [Pg.380]    [Pg.384]    [Pg.606]    [Pg.598]    [Pg.293]    [Pg.380]    [Pg.384]    [Pg.954]    [Pg.267]    [Pg.299]    [Pg.324]    [Pg.341]    [Pg.458]    [Pg.407]   
See also in sourсe #XX -- [ Pg.177 ]




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