By Shawna Kopchu RN
Hypomagnesemia is a common imbalance in critically ill patients; yet it is frequently overlooked. (Perhaps one reason is that it is easily mistaken for potassium deficit, a condition with which it is often associated.) Magnesium deficit also occurs in less acutely ill individuals, such as those experiencing withdrawal from alcohol and those receiving nourishment after a period of starvation (as in tube feedings or total parental nutrition). Indeed, there are a number of clinical situations associated with hypomagnesemia; some of the more common etiological factors are described below.
An important route for magnesium loss is the gastrointestinal tract. Losses may take the form of drainage from nasogastric suction, diarrhea, or fistulas. Since fluid from the lower gastrointestinal tract is richer (10mEq-14mEq/Liter) than is fluid from the upper tract (1mEq-2mEq/Liter), losses from diarrhea and intestinal fistulas are more likely to induce magnesium deficit than are those from gastric suction. One should be aware that even though magnesium losses are relatively low in nasogastric suction, hypomagnesemia will occur if losses are prolonged and parenteral fluids are magnesium-free.
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. One study reported that 15 of 42 patients with malabsorption syndromes had subnormal serum magnesium levels; the degree of hypomagnesemia showed a rough correlation with the degree of steatorrhea, it is thought that magnesium ions are excreted in the stool in the form of magnesium soaps.
Alcoholism is currently the most common cause of symptomatic magnesium deficiency in the United States. In one study, it was found that 30% of all alcoholics and 86% of patients with delirium tremens had hypomagnesemia during the first one to two days of hospitalization. Although there are no convincing data to indicate that hypomagnesemia causes delirium tremens, it is likely that magnesium deficiency aggravates alcohol withdrawal. For this reason, it is recommended that the serum magnesium level be measured every two or three days in hospitalized alcoholic patients going through withdrawal. While the serum magnesium level may be normal on admission, it can fall as a result of metabolic changes associated with therapy (such as intracellular shift of magnesium associated with intravenous glucose administration).
Decreased dietary intake of magnesium is a major factor in the development of hypomagnesemia in alcoholics. Other factors include increased gastrointestinal losses (due to episodic emesis and diarrhea) and intestinal malabsorption. In addition, alcohol ingestion is thought to increase magnesium excretion in the urine.
Renal losses from primary renal disorders or secondary causes like drugs, hormones or osmotic load may result in magnesium wasting and subsequent hypomagnesemia. Primary renal disorders cause hypomagnesemia by decreased tubular reabsorption of magnesium by the damaged kidneys. This occurs in the diuretic phase of acute tubular necrosis, post obstructive diuresis, renal tubular acidosis. Drugs may cause magnesium wasting. Offenders include thiazide and loop diuretics. Diuretics decrease the renal threshold for magnesium reabsorption in addition to wasting of potassium and calcium. Cisplatin causes dose dependent kidney damage in 100% of patients receiving this drug. Pentamidine and some antibiotics also cause renal magnesium wasting. Flouride poisoning similarly causes hypomagnesemia.
Refeeding After Starvation
In the catabolic state, the protein structure of cells is metabolized as energy sources; as a result, intracellular ions are lost, and total body concentrations of these ions (magnesium, potassium, and phosphate) are decreased. Conversely, during nutritional repletion, these electrolytes are taken from the serum and deposited into newly synthesized cells. Thus, if the enteral or parenteral feeding formula is deficient in magnesium content, serious hypomagnesemia will occur. Serum levels of these primarily intracellular ions should be measured at regular intervals during the administration of IV total parenteral nutrition and even during enteral feedings, especially in patients who have undergone a period of starvation.
Drugs Disrupting Magnesium Homeostasis
Agents that induce osmotic diuresis can cause large amounts of magnesium to be lost in the urine; some of these include mannitol, urea, and glucose. Furosemide and other diuretics that act in the thick ascending limb of Henle’s loop can cause large magnesium losses. Gentamicin and cisplatin therapy have been noted to result in symptomatic hypomagnesemia because of renal magnesium wasting. In a recent study it was found that 38% of 55 patients receiving amino glycoside antibiotics developed hypomagnesemia associated with renal magnesium wasting.
Recall that citrate is a preservative added to collected blood to prolong its longevity. Rapid administration of citrated blood can temporarily drop the ionized magnesium level because citrate chelates circulating magnesium ions (and calcium ions). This is most likely to occur when citrate clearance is diminished by renal or hepatic disease or by hypothermia.
Hypercalcemic states induced by excessive doses of Vitamin D or Calcium supplements can result in increased renal magnesium excretion.
Magnesium deficiency is often seen in patients with diabetic ketoacidosis. It is primarily the result of increased renal excretion of magnesium during osmotic diuresis (caused by the high glucose load) and of the shifting of magnesium into cells that occurs with insulin therapy.
Hyperaldosteronism, as occurs in heart failure or cirrhosis, increases the urinary and fecal excretion of magnesium by increasing intravascular volume. Hypomagnesemia may also occur in thyrotoxicosis and is the result of both renal magnesium wasting and thyroid hormone-induced shifting of magnesium into the cells. Hyperparathyroidism can cause renal magnesium wasting and thus induce hypomagnesemia.
Some causes of renal disease, such as glomerulonephritis, pyelonephritis, and renal tubular acidosis, may produce hypomagnesemia by impairing renal magnesium reabsorption. However, it is important to remember that with advanced renal disease (GFR less than 10ml to 25ml/hr), hypermagnesemia usually results from impaired renal magnesium excretion.
Pancreatitis may cause hypomagnesemia in much the same way it causes hypocalcemia. In addition, any condition associated with hypercalcemia, such as excessive doses of vitamin D or calcium supplements, may result in renal magnesium loss. It should be noted that magnesium and calcium share a common route of absorption in the intestinal tract and appear to have a mutually suppressive effect; thus, if calcium intake is unusually high, calcium will be absorbed in preference to magnesium and vice versa.
Magnesium deficiency has also been described in burn patients and is possibly related to loss of magnesium during debridement and bathing of denuded skin. Other conditions thought to predispose to hypomagnesemia are sepsis and hypothermia.
Administration of magnesium-free, sodium rich IV fluids to induce extracellular fluid expansion can cause hypomagnesemia. In fact, any condition predisposing to excessive calcium or sodium in the urine can augment renal excretion of magnesium since magnesium is normally reabsorbed in the kidney with calcium and sodium.
Excessive lactation may create a significant amount of magnesium loss.
Hungry bone syndrome may lead to lower serum magnesium concentrations
Pregnant women have been found to be magnesium depleted, especially those who experience preterm labor.
Defining characteristics resulting from magnesium deficiency are largely confined to the neuromuscular system. Some of the effects of hypomagnesemia are due directly to the low serum magnesium level, others are due to secondary changes in potassium and calcium metabolism. One must remember that hypomagnesemia can cause hypocalcemia because it interferes with the calcium-elevating effects of parathyroid hormone (PTH); it may also cause hypokalemia (Low Potassium).
Below you will find some of the symptoms of hypomagnesemia
- Neuromuscular Irritability
- Hyperactive deep tendon reflexes
- Muscle cramps
- Trousseau’s and Chovstek’s signs
- Dysphagia (difficulty swallowing) from esophageal dysmotility
- Irritability and combativeness
At levels less than 1 mEq/L, one may see;
- Cardiac arrythmias may be caused by hypomagnesemia alone or the concomittant hypokalemia resulting from decreased activity of ATPase.
- Paroxysmal atrial and ventricular disrrhythmias.
- Repolarization alternans
Lab Studies for Hypomagnesemia
Electrolytes, including magnesium, calcium, potassium and phosphorus.
The serum magnesium level is not a reliable way for determining total body magnesium depletion because of the minimal extracellular concentration. If the level is low, there is clearly a deficiency. However, the total body may be markedly depleted before the serum level drops. In one study, alcoholics were found to be total body magnesium depleted by 24-hour urine excretion of magnesium but had normal serum levels. In addition, some of the extracellular magnesium is protein bound, making the protein status of the patient important. Hypomagnesemia contributes to hypokalemia. This may be due to defective membrane ATPase or urinary losses of potassium.
Hypocalcemia is caused by magnesium depletion but the reason is not clearly known.
Some studies link decreased parathyroid hormone to hypomagnesemia as well as end-organ resistence to parathyroid hormone from hypomagnesemia.
There is also some alteration in vitamin D metabolism that may contribute to hypocalcemia.
Hypophosphatemia has been found in patients with hypomagnesemia.
BUN and creatinine
RBC Serum Magnesium Level
24 hour Urine
Other Tests that should be done
Electrocardiogoram (ECG) and Cardiac Monitor: Findings in hypomagnesemia are nonspecific. They include ST segment depression, tall peaked T waves, flat T waves or depression in the precordium, U waves, loss of voltage, PR prolongation and widened QRS.
Once the deficiency is corrected, patients have and excellent prognosis. The symptoms are for the most part completely reversible with treatment.Print This Post