DRG Category: 640

Mean LOS: 5.1 days

Description MEDICAL: Nutritional and Miscellaneous Metabolic Disorders with Major CC

classification section:



Hypomagnesemia occurs when the serum magnesium concentration is less than 1.7 mg/dL (1.4 mEq/L). The normal serum magnesium level is 1.7 to 2.7 mg/dL (1.4 to 2.3 mEq/L). An average-sized adult has approximately 25 g of magnesium in her or his body. About 50% of the body's total magnesium is found in the bones, 1% is located in the extracellular compartment, and the remainder is found within the cells. The body's requirement is met by ingesting foods such as meat, milk, and chlorophyll-containing vegetables and fruits. The risk of hypomagnesemia is 2% in the general population, 10% to 20% in hospitalized patients, 50% to 60% in critically ill patients, 30% to 80% in alcohol-dependent patients, and 5% in diabetic outpatients.

Magnesium is regulated by vitamin D–regulated gastrointestinal (GI) absorption and renal excretion. Magnesium plays an important role in neuromuscular function. It also has a role in several enzyme systems, particularly the metabolism of carbohydrates and proteins, as well as maintenance of normal ionic balance (it triggers the sodium-potassium pump), osmotic pressure, myocardial functioning, and bone metabolism. Deficits of magnesium lead to deficits in calcium, and the two electrolyte imbalances are difficult to differentiate. The hypocalcemia that accompanies hypomagnesemia cannot be corrected unless the magnesium is replaced. Hypomagnesemia is also a stimulus for renin release, which leads to aldosterone production, potassium wasting, and hypokalemia. Because magnesium regulates calcium entry into cells, consequences of magnesium deficiency include ventricular dysrhythmias, an enhanced digitalis toxicity, and sudden cardiac death. Deficits in potassium and calcium potentiate the dysrhythmogenic effect of low magnesium.

The primary sources of magnesium deficit are reduced intestinal absorption and increased renal excretion. Sources of reduced GI absorption include losses from intestinal or biliary fistulae, prolonged nasogastric suction, diarrhea, malabsorption syndrome, and laxative abuse. Decreased oral intake of magnesium also decreases absorption and is caused by malnutrition, chronic alcoholism, starvation, and prolonged administration of magnesium-free parenteral fluids. Increased renal excretion of magnesium occurs because of prolonged diuretic use; the diuretic phase of acute renal failure; acute alcohol intoxication; hyperaldosteronism; syndrome of inappropriate antidiuretic hormone; or medications such as cisplatin, digoxin, tobramycin, gentamicin, cyclosporine, and amphotericin. Other conditions associated with low magnesium include malignancies, diabetic ketoacidosis, hypocalcemia, hypoparathyroidism, acute and chronic pancreatitis, burns, multiple transfusions of stored blood, and toxemia of pregnancy.

There are several heritable syndromes that include hypomagnesemia as a primary feature. Primary hypomagnesemia can be transmitted in an autosomal recessive or dominant pattern and is due to either poor intestinal absorption of magnesium or a defect in renal reabsorption of magnesium. Gitelman's syndrome is a disorder that results in hypokalemic alkalosis, low urinary calcium, and hypomagnesemia. It is transmitted in an autosomal dominant pattern.

Anyone with a chronic illness that causes malabsorption or renal loss of magnesium is susceptible. Pregnant women with toxemia are particularly at risk, as are the elderly who are placed on diuretic therapy and people with cancer who are taking chemotherapy. The incidence and prevalence is the same in men and women, and there are no known ethnic or racial considerations.

Not applicable.

HISTORY. The following conditions put a patient at risk: poor nutrition, diuretics or chemotherapy, pregnancy, old age, or a history of alcohol abuse. Ask about the patient's diet and drinking history, including the amount of alcohol intake on a usual day and an unusual day. Ask the patient to describe bowel patterns, and note if the patient has diarrhea or a history of an eating disorder with laxative abuse. Determine if the patient has experienced irregular heartbeats, lethargy, muscle weakness, tremors, mood alterations, anorexia, nausea, or dizziness.

PHYSICAL EXAM. Observe any signs of muscular changes, such as tetany, spasticity, or tremors. Note the person's affect and mental status because hypomagnesemia can lead to seizures, mood changes, irritability, confusion, hallucinations, psychosis, and depression. The patient's vital signs may reflect hypotension and tachycardia. When you examine the patient's eyes, you may note nystagmus (involuntary cyclical movement of the eyeball) and positive Trousseau's and Chvostek's signs. Trousseau's sign is the development of carpal spasm when a blood pressure cuff is inflated above systolic pressure for 3 minutes; Chvostek's sign is twitching facial muscles when the facial nerve is tapped anterior to the ear.

PSYCHOSOCIAL. The patient may be confused, psychotic, or depressed, which can be relieved with magnesium replacement. If the patient has chronic alcoholism, symptoms may persist beyond treatment of the hypomagnesemia and should be addressed with appropriate consultation and possible rehabilitation. Assess the patient's and significant others' abilities to cope with this sudden illness and any changes in roles that may result.

Diagnostic Highlights

Test	Normal Result	Abnormality with Condition	Explanation
Serum magnesium	1.7–2.7 mg/dL (1.4–2.3 mEq/L)	< 1.7 mg/dL; critical value: < 1.0 mg/dL	Deficit of magnesium ions
Serum calcium: Total calcium, including free ionized calcium and bound calcium	8.6–10.3 mg/dL	< 8.5 mg/dL; critical value: < 6.5 mg/dL	Deficit of calcium below normal levels in the extracellular fluid compartment
Serum ionized calcium: Unbound calcium; level unaffected by albumin level	4.5–5.1 mg/dL	< 4.5 mg/dL; critical value: < 3.5 mg/dL	Ionized calcium is approximately 46%–50% of circulating calcium; calcium available for enzymatic reactions and neuromuscular function
Electrocardiogram (ECG)	Normal PQRST pattern	Prolonged PR and QT intervals; patients on digitalis may have atrial and ventricular dysrhythmias	Magnesium deficit leads to alterations in generation and conduction of the action potential

Other Tests: Serum potassium level, blood urea nitrogen, creatinine, glucose.

DIAGNOSIS. Risk for injury related to muscle weakness, unstable gait

OUTCOMES. Cardiac pump effectiveness; Circulation status; Electrolyte and acid-base balance; Knowledge: Medication; Respiratory status: Ventilation and gas exchange

INTERVENTIONS. Electrolyte management: Hypomagnesemia; Intravenous therapy; Cardiac care: Acute; Emergency care; Medication administration; Medication management

COLLABORATIVE

If the levels are severely low, the patient needs intravenous (IV) or intramuscular magnesium replacement with magnesium sulfate (MgSO₄). Calcium gluconate may be administered with IV magnesium replacement therapy to reduce the risk of sudden reversal to hypermagnesemia. If the patient does not suffer from chronic malabsorption requiring total parenteral nutrition, an increase in dietary intake of magnesium is prescribed. Foods high in magnesium include bananas, chocolate, green leafy vegetables, grapefruit, oranges, nuts, seafood, soy flour, and wheat bran.

Monitor for signs of hypermagnesemia during IV infusions. These symptoms include hypotension, labored respirations, and diminished or absent patellar reflex (knee jerk). If any of these symptoms occurs, stop the infusion and notify the physician immediately. If hypokalemia occurs simultaneously with hypomagnesemia, the magnesium level should be corrected first because magnesium is necessary for the movement of potassium into the cell. Be aware that hypomagnesemia may precipitate digitalis toxicity by enhancing the effects of digitalis, which places the patient at increased risk for digitalis-induced atrial and ventricular dysrhythmias and Mobitz type I atrioventricular (AV) block (Wenckebach). Alkalosis should be avoided or corrected because this condition may precipitate tetany.

Pharmacologic Highlights

Medication or Drug Class	Dosage	Description	Rationale
MgSO4	1–2 g MgSO4 IV over 15 min followed by an infusion of 6 g in 1 L over 24 hours	Electrolyte replacement	Replace magnesium
Magnesium gluconate (Almora)	500 mg/d (27 mg elemental magnesium) PO; oral preparations for mild/chronic hypomagnesemia: 240 mg elemental magnesium PO qd to bid; other preparations: Mag-Ox 400 and Uro-Mag; magnesium-containing antacids containing aluminum hydroxide and magnesium hydroxide (Mylanta or Maalox) if problem was not caused by chronic GI loss (e.g., diarrhea)	Electrolyte replacement	Given when patient is mildly depleted (magnesium > 1 mEq/L and patient is asymptomatic)

INDEPENDENT

The patient's safety is of primary concern. Reorient the patient as necessary, and reassure both the patient and the family that mood changes and the altered level of consciousness are temporary and improve when magnesium levels return to normal. If neurological and muscle status places the patient at risk for injury, evaluate the patient's environment to limit risks for trauma. Symptoms of hypomagnesemia are similar to those of delirium tremens (DTs) in chronic alcoholism; if you suspect the patient of developing either DTs or hypomagnesemia, discuss the symptoms with the physician and monitor the magnesium levels to determine the cause of the symptoms.

Maintain seizure precautions for patients with symptoms and keep environmental stimuli to a minimum. Encourage active range-of-motion (ROM) exercises or perform passive ROM exercises several times a day to help prevent complications of inactivity. Dysphagia may also occur in these patients, and their ability to swallow should be assessed before giving them food or liquids. Encourage the intake of magnesium-enriched foods in small, frequent meals if the patient is suffering from inadequate nutrition. Keep the environment as pleasant as possible. Include the patient and family in meal planning, and request a nutritional consultation if necessary.

• Serum magnesium, potassium, and calcium levels; patency of the IV line

• Vital signs, cardiac rhythm, and ECG strip and interpretation

• Neurological assessment findings: Level of consciousness, orientation, muscle strength and sensation, presence of Chvostek's and Trousseau's signs

• Presence of complications: Respiratory distress, tetany, IV infiltration

• Response to treatment: MgSO₄ or magnesium-containing antacids, calcium gluconate

Teach the patient to eat foods high in magnesium and to eat several small meals. Tell him or her to use any prescribed antiemetics before eating if nausea, vomiting, or diarrhea is a problem. Teach the signs and symptoms of hypomagnesemia (changes in level of consciousness, neuromuscular weakness), and instruct the patient to notify the physician if these return.

Explain any oral magnesium supplements, including the dosage, action, adverse effects, and need for routine laboratory monitoring if hypomagnesemia is a chronic problem. Explain that many of the magnesium-containing antacids may cause diarrhea, and instruct the patient to notify the physician if this occurs. Teach the use of assistive devices (cane or walker). The patient should also be taught muscle-strengthening exercises and may need a home care evaluation before discharge.