Hypomagnesemia refers to a below-normal serum magnesium concentration. The normal serum magnesium level is 1.5 to 2.5 mEq/L (or 1.8–3.0 mg/dL; 0.8–1.2 mmol/L). Approximately one third of serum magnesium is bound to protein; the remain-ing two thirds exists as free cations (Mg ++). Like calcium, it is the ionized fraction that is primarily involved in neuromuscular activity and other physiologic processes. As with calcium levels, magnesium levels should be evaluated in combination with albu-min levels. Low serum albumin levels decrease total magnesium.
Hypomagnesemia is a common yet often overlooked imbalance in acutely and critically ill patients. It may occur with withdrawal from alcohol and administration of tube feedings or parenteral nutrition.
An important route for magnesium loss is the GI tract. Loss of magnesium from the GI tract may occur with nasogastric suc-tion, diarrhea, or fistulas. Because fluid from the lower GI tract has a higher concentration of magnesium (10–14 mEq/L) than fluid from the upper tract (1–2 mEq/L), losses from diarrhea and intestinal fistulas are more likely to induce magnesium deficit than are those from gastric suction. Although magnesium losses are relatively small in nasogastric suction, hypomagnesemia will occur if losses are prolonged and magnesium is not replaced through IV infusion. Because the distal small bowel is the major site of magnesium absorption, any disruption in small bowel function, as in intestinal resection or inflammatory bowel disease, can lead to hypomagnesemia.
Alcoholism is currently the most common cause of sympto-matic hypomagnesemia in the United States. Hypomagnesemia is particularly troublesome during treatment of alcohol withdrawal. Therefore, the serum magnesium level should be measured at least every 2 or 3 days in patients going through withdrawal from alco-hol. The serum magnesium level may be normal on admission but fall as a result of metabolic changes, such as the intracellular shift of magnesium associated with IV glucose administration.
During nutritional repletion, the major cellular electrolytes move from the serum to newly synthesized cells. Thus, if the en-teral or parenteral feeding formula is deficient in magnesium con-tent, serious hypomagnesemia will occur. Because of this, serum magnesium levels should be measured at regular intervals in pa-tients who are receiving parenteral nutrition and enteral feedings, especially those who have undergone a period of starvation. Other causes of hypomagnesemia include the administration of amino-glycosides, cyclosporine, cisplatin, diuretics, digitalis, and am-photericin and the rapid administration of citrated blood, especially to patients with renal or hepatic disease. Magnesium deficiency often occurs in diabetic ketoacidosis, secondary to increased renal excretion during osmotic diuresis and shifting of magnesium into the cells with insulin therapy. Other contributing causes are sep-sis, burns, and hypothermia.
Clinical manifestations of hypomagnesemia are largely confined to the neuromuscular system. Some of the effects are due directly to the low serum magnesium level; others are due to secondary changes in potassium and calcium metabolism. Symptoms do not usually occur until the serum magnesium level is less than 1 mEq/L (0.5 mmol/L).
Among the neuromuscular changes are hyperexcitability with muscle weakness, tremors, and athetoid movements (slow, involuntary twisting and writhing). Others include tetany, gen-eralized tonic-clonic or focal seizures, laryngeal stridor, and pos-itive Chvostek’s and Trousseau’s signs, which occur, in part, because of accompanying hypocalcemia.
Magnesium deficiency can disturb the ECG by prolonging the QRS, depressing the ST segment, and predisposing to cardiac dys-rhythmias, such as premature ventricular contractions, supra-ventricular tachycardia, torsades de pointes (a form of ventricular tachycardia), and ventricular fibrillation. Increased susceptibility to digitalis toxicity is associated with low serum magnesium lev-els. This is important because patients receiving digoxin are also likely to be receiving diuretic therapy, predisposing them to renal loss of magnesium.
Hypomagnesemia may be accompanied by marked alterations in mood. Apathy, depression, apprehension, and extreme agita-tion have been noted, as well as ataxia, dizziness, insomnia, and confusion. At times, delirium, auditory or visual hallucinations, and frank psychoses may occur.
On laboratory analysis, the serum magnesium level is less than 1.5 mEq/L or 1.8 mg/dL (0.75 mmol/L). Hypomagnesemia is frequently associated with hypokalemia and hypocalcemia. About 25% of magnesium is protein-bound, principally to al-bumin. A decreased serum albumin level can, therefore, reduce the measured total magnesium concentration; however, it does not reduce the ionized plasma magnesium concentration. ECG evaluations reflect magnesium, calcium, and potassium deficien-cies, tachydysrhythmias, prolonged PR and QT intervals, wide-ning QRS, ST segment depression, flattened T waves, and a prominent U wave. Torsades de pointes is associated with a low magnesium level. Premature ventricular contractions, parox-ysmal atrial tachycardia, and heart block may also occur. Uri-nary magnesium levels may be helpful in identifying causes of magnesium depletion and are measured after a loading dose of magnesium sulfate is administered. Two newer diagnostic tech-niques (nuclear magnetic resonance spectroscopy and the ion selective electrode) are sensitive and direct means to measure ionized serum magnesium levels.
Mild magnesium deficiency can be corrected by diet alone. Prin-cipal dietary sources of magnesium are green leafy vegetables, nuts, legumes, whole grains, and seafood. Magnesium is also plentiful in peanut butter and chocolate. When necessary, magnesium salts can be administered orally to replace continuous excessive losses. Diarrhea is a common complication of excessive ingestion of mag-nesium. Patients receiving parenteral nutrition require magnesium in the IV solution to prevent hypomagnesemia. IV administrationof magnesium sulfate must be given by an infusion pump and at a rate not to exceed 150 mg/min. A bolus dose of magnesium sul-fate given too rapidly can produce cardiac arrest. Vital signs must be assessed frequently during magnesium administration to detect changes in cardiac rate or rhythm, hypotension, and respiratory distress. Monitoring urine output is essential before, during, and after magnesium administration; the physician is notified if urine volume decreases to less than 100 mL over 4 hours. Calcium glu-conate must be readily available to treat hypocalcemic tetany or hypermagnesemia.
Overt symptoms of hypomagnesemia are treated with paren-teral administration of magnesium. Magnesium sulfate is the most commonly used magnesium salt. Serial magnesium concentra-tions can be used to regulate the dosage.
The nurse should be aware of patients at risk for hypomagne-semia and observe for its signs and symptoms. Patients receiving digitalis are monitored closely because a deficit of magnesium can predispose them to digitalis toxicity. When hypomagnesemia is severe, seizure precautions are implemented. Other safety pre-cautions are instituted, as indicated, if confusion is observed.
Because difficulty in swallowing (dysphagia) may occur in magnesium-depleted patients, the ability to swallow should be tested with water before oral medications or foods are offered. Dysphagia is probably related to the athetoid or choreiform (rapid, involuntary, and irregular jerking) movements asso-ciated with magnesium deficit. To determine neuromuscular irritability, the nurse needs to assess and grade deep tendon re-flexes.
Teaching plays a major role in treating magnesium deficit, particularly that resulting from abuse of diuretic or laxative med-ications. In such cases, the nurse can instruct the patient about the need to consume magnesium-rich foods. For patients experi-encing hypomagnesemia from abuse of alcohol, the nurse can provide teaching, counseling, support, and possible referral to alcohol abstinence programs or other professional help.
Copyright © 2018-2021 BrainKart.com; All Rights Reserved. (BS) Developed by Therithal info, Chennai.