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FLUIDS AND ELECTROLYTES are present in the intracellular fluid (ICF) compartment, interstitial spaces, and vascular compartment. Normal fluid and electrolyte balance is critical to maintaining overall normal body functions.
In the previous article in this series, we discussed the normal functions of sodium and potassium. (See "Balancing Act: Sodium and Potassium" in the July issue of Nursing2011.) In this article, we review normal functions of magnesium as well as clinical manifestations and nursing interventions for imbalances of this important electrolyte.
Note: Normal value ranges may vary slightly according to age group, gender, and lab reference values. Always refer to reference lab data to verify normal serum electrolyte ranges used in your institution.
Magnesium is the second most common intracellular cation after potassium. About two-thirds of the body's magnesium is found in bones; most of the rest is found in the ICF compartment. Only about 2% of magnesium is located in extracellular fluid (ECF), which includes the vascular compartment and interstitial spaces. As a result, the normal serum magnesium concentration is relatively low, ranging from 1.5 to 2.5 mg/dL.
About one-third of magnesium in the ECF is bound to protein (albumin), while the remaining two-thirds are free (ionized). It's the ionized portion that's largely involved with neuromuscular activity and other physiologic processes.1
Major sources of magnesium include unprocessed cereal/grain and legumes. It's also found in all green vegetables, dairy products, dried fruit, and fish. It's absorbed by the intestines and excreted through the kidneys.1
Besides its major role in neuromuscular activities, magnesium is a cofactor for over 300 enzymatic processes. Because magnesium works directly at the myoneural junction, it affects neuromuscular irritability and contractility.2 Magnesium is important for
* generation of adenosine triphosphate (ATP).
* proper functioning of the sodium-potassium pump.
* carbohydrate, protein, and fat metabolism.
* secretion of parathyroid hormone, influencing ECF calcium concentrations.
* cardiovascular function because of its vasodilatory effect.3
The following discussion examines the implications for your patient when magnesium levels are out of balance.
Defined as a serum magnesium level less than 1.5 mg/dL, hypomagnesemia is most often associated with conditions that limit dietary magnesium intake (for example, malnutrition), impair intestinal absorption of magnesium (for example, diarrhea), or increase renal losses of magnesium (for example, use of diuretics).1
Chronic alcohol abuse is a major cause of hypomagnesemia for many reasons, including poor dietary intake, acute pancreatitis, and increased urinary excretion.4 Shifts of magnesium from the ECF to the ICF compartment-for example, due to rapid I.V. glucose administration-can also cause a relative hypomagnesemia. A patient receiving parenteral nutrition or enteral feeding may develop hypomagnesemia if the formulas don't contain adequate magnesium replacement or if the patient develops refeeding syndrome. Patients in diabetic ketoacidosis, as well as those with hypokalemia or hypoalbuminemia, may also develop low magnesium levels. Other causes include administration of certain medications, such as diuretics, cyclosporine, and some proton pump inhibitors, or the rapid administration of citrated blood.2,4
The most common signs and symptoms of hypomagnesemia reflect increased neuromuscular excitability. Clinical manifestations may be related directly to low serum magnesium levels or to hypokalemia and hypocalcemia, which are often associated with hypomagnesemia. Signs and symptoms include muscle tremors and weakness, athetoid movements (continuous, slow, involuntary twisting/writhing movements), ataxia, and hyperactive deep tendon reflexes. Patients may exhibit tetany, seizure activity, and laryngeal stridor secondary to laryngospasm; on physical assessment, you may find a positive Chvostek sign and Trousseau sign (which are also possible signs of hypocalcemia).
Mental status changes include mood alterations such as apathy, depression, or apprehension; confusion; hallucinations; delirium; or psychosis. Severe hypomagnesemia may cause coma and death.2
Hypomagnesemia also affects cardiac function. Characteristic ECG changes include progressive QRS complex widening, PR interval prolongation, and flattened T waves. Hypomagnesemia can cause potentially life-threatening cardiac dysrhythmias, including ventricular tachycardia and ventricular fibrillation.
The underlying cause of hypomagnesemia needs to be identified and appropriately treated, along with any other accompanying electrolyte imbalances. Magnesium replacement therapy varies depending upon the severity of the patient's signs and symptoms. For example, a patient without symptoms may be treated with oral magnesium supplements. Encourage the patient to consume magnesium-rich food sources, such as green vegetables, nuts, legumes, bananas, and oranges.
A patient with serious signs and symptoms such as ventricular dysrhythmias may require I.V. magnesium sulfate given slowly with careful monitoring. Closely monitor the patient for signs of hypermagnesemia, which can occur with magnesium administration.1
Assess patients for complications associated with a low magnesium level. Patients receiving magnesium should be placed on a cardiac monitor because magnesium administration can cause a prolonged PR interval and widening of the QRS complex, which may lead to dysrhythmias. Magnesium toxicity can depress or cause the loss of deep tendon reflexes, so routinely assess for this warning sign.1
Assess vital signs (including the apical pulse for greater accuracy) and monitor for mood changes. Implement safety measures and monitor lab values for trends in magnesium, potassium, and calcium levels.
Maintain accurate records of intake and output to assess kidney function. Instruct the patient and family to inform you about any discomfort at the I.V. site.
Educate the patient about diet and medications, and about signs and symptoms that should be reported immediately, such as chest discomfort. If appropriate, offer resources for treating chronic alcohol abuse.
Defined as a serum level above 2.5 mg/dL, hypermagnesemia is much less common than hypomagnesemia because normally functioning kidneys easily excrete magnesium.1 It's most likely to occur in patients with renal failure or renal insufficiency who have a glomerular filtration rate (GFR) of less than 30 mL/minute/1.73 m2. Other causes include excessive use of magnesium-containing laxatives or antacids, Addison disease (adrenal insufficiency), and overcorrection of hypomagnesemia. Diabetic ketoacidosis and tumor lysis syndrome may also cause hypermagnesemia. Falsely high magnesium levels may occur when an excessively tight tourniquet is used during a blood draw or when blood specimens hemolyze before analysis.2
Mild hypermagnesemia is usually asymptomatic. With higher levels, the patient may begin to experience signs and symptoms of neuromuscular depression, such as lethargy and respiratory depression. Severe hypotension, concurrent with nausea and vomiting, is a key characteristic of hypermagnesemia. The patient may also develop muscle weakness, paralysis, and hyporeflexia or areflexia. ECG changes include prolonged QT interval, bradycardia, and heart blocks. Severe hypermagnesemia may cause paralysis of the voluntary muscles, coma, and cardiac or respiratory arrest.3
Preventing hypermagnesemia is the first line of defense. Avoid giving magnesium-containing medications to patients with renal failure, and carefully monitor patients receiving I.V. magnesium for any reason.5
If a patient develops hypermagnesemia, causes of the imbalance should be promptly identified and appropriately treated. If the patient's renal function is normal, magnesium levels usually return to normal quickly when magnesium therapy is halted. If renal function is impaired, however, the patient may require peritoneal dialysis or hemodialysis. To treat severe symptoms, the healthcare provider may prescribe I.V. calcium, which acts as a magnesium antagonist.5 Administer I.V. fluids as prescribed to treat hypotension.
Place the patient on continuous cardiac monitoring, initiate safety precautions as appropriate, and monitor vital signs, including the apical pulse. Watch for hypotension, bradycardia, and respiratory depression. Assess neuromuscular function and level of consciousness regularly. Also meticulously document intake and output, and monitor other indicators of renal function, such as urine specific gravity, blood urea nitrogen, creatinine, and GFR.6
Instruct the patient/family to call for assistance before the patient gets up to ambulate from a lying or sitting position. Before discharge, educate the patient regarding the proper use of laxatives and antacids containing magnesium.
1. Porth CM. Essentials of Pathophysiology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011. [Context Link]
2. Ignatavicius D, Workman ML, eds. Medical-surgical Nursing: Patient-centered Collaborative Care. 6th ed. St. Louis, MO: Saunders Elsevier; 2010. [Context Link]
3. Alexander M, Corrigan A, Gorski L, Hankins J, Perucca R, eds. Infusion Nurses Society: Infusion Nursing, an Evidence-based Approach. 3rd ed. St. Louis, MO: Saunders Elsevier; 2010. [Context Link]
4. Agus ZS. Causes of hypomagnesemia. UpToDate; 2011. http://www.uptodate.com. [Context Link]
5. Agus ZS. Causes and treatment of hypermagnesemia. UpToDate; 2011. http://www.uptodate.com. [Context Link]
6. LeMone P, Burke K. Medical-surgical Nursing: Critical Thinking in Nursing Care. 4th ed. Upper Saddle River, NJ: Pearson Education; 2008. [Context Link]
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