Porth's Essentials of Pathophysiology, 4e

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Integrative Body Functions

U N I T 2

renal losses, and it is a common finding in patients in emergency departments and critical care units. Magnesium deficiency can result from insufficient intake, excessive losses, or movement between the ECF and ICF compartments. 3,53,54 It can result from condi- tions that directly limit intake, such as malnutrition, starvation, or prolonged use of magnesium-free par- enteral nutrition. Other conditions, such as diarrhea, malabsorption syndromes, prolonged nasogastric suc- tion, or laxative abuse, decrease intestinal absorption. Another common cause of magnesium deficiency is chronic alcoholism. Many factors contribute to hypo- magnesemia in alcoholism, including low intake and gastrointestinal losses from diarrhea. There also have been recent reports of hypomagnesemia associated with prolonged use of proton-pump inhibitor medications, presumably due to decreased intestinal absorption of magnesium. 55 Although the kidneys are able to defend against hypermagnesemia, they are less able to conserve mag- nesium and prevent hypomagnesemia. Urine losses are increased in diabetic ketoacidosis, hyperparathyroid- ism, and hyperaldosteronism. Some drugs increase renal losses of magnesium, including both loop and thiazide diuretics, nephrotoxic drugs such as aminogly- coside antibiotics, cyclosporine, cisplatin, and ampho- tericin B. 54 Relative hypomagnesemia may also develop in con- ditions that promote movement of magnesium between the ECF and ICF compartments, including rapid admin- istration of glucose, insulin-containing parenteral solu- tions, and alkalosis. Although transient, these conditions can cause serious alterations in body function. Manifestations. Signs of magnesium deficiency are not usually apparent until the serum magnesium is less than 1.0 mEq/L (0.4 mmol/L). 3 Hypomagnesemia is charac- terized by an increase in neuromuscular excitability as evidenced by hyperactive deep tendon reflexes, paresthe- sias (i.e., numbness, pricking, tingling sensation), mus- cle fasciculations, and tetanic muscle contractions 3,50,53 (Table 8-8). A positive Chvostek or Trousseau sign may be present, especially if the abnormal serum magnesium

level is associated with hypocalcemia. Other manifesta- tions may include ataxia, vertigo, disorientation, depres- sion, and psychotic symptoms. Cardiovascular manifestations include tachycardia, hypertension, and ventricular arrhythmias. 51 There may be ECG changes such as widening of the QRS complex, appearance of peaked T waves, prolongation of the PR interval, T-wave inversion, and appearance of U waves. Ventricular arrhythmias, particularly in the presence of digitalis, may be difficult to treat unless magnesium lev- els are normalized. Magnesium deficiency often occurs in conjunc- tion with hypocalcemia and hypokalemia, producing a number of related neurologic and cardiovascular manifestations. Hypocalcemia is typical of severe hypomagnesemia. Most persons with hypomagnesemia- related hypocalcemia have decreased PTH levels, prob- ably as a result of impaired magnesium-dependent mechanisms that control PTH synthesis and release. The resultant hypocalcemia is corrected with cal- cium replacement until the magnesium is normalized. Hypokalemia is also a typical feature of hypomagne- semia. It leads to a reduction in intracellular potas- sium and impairs the ability of the kidneys to conserve potassium. When hypomagnesemia is present, hypo- kalemia remains unresponsive to potassium replace- ment therapy. Treatment. The treatment of hypomagnesemia consists of magnesium replacement. 3,50,54 The route of admin- istration depends on the severity of the condition. Symptomatic moderate to severe magnesium deficiency is treated by parenteral administration. Treatment must be continued for several days to replace stored and serum levels. In conditions of chronic intestinal or renal loss, maintenance support with oral magnesium may be required. Magnesium often is used therapeutically to treat car- diac arrhythmia, myocardial infarct, angina, bronchial asthma, and pregnancy complicated by preeclampsia or eclampsia. Caution is needed to prevent hypermag- nesemia in persons with any degree of chronic kidney disease.

Manifestations of Hypomagnesemia and Hypermagnesemia

TABLE 8-8

Hypomagnesemia

Hypermagnesemia

LaboratoryValues

LaboratoryValues

Serum magnesium <1.3 mg/dL (0.65 mmol/L) Neural and Muscle Effects (increased)

Serum magnesium >2.1 mg/dL (1.1 mmol/L) Neural and Muscle Effects (decreased)

Paresthesias

Lethargy

Ataxia, dizziness,

Hyporeflexia

Muscle fasiculations, tetany Confusion, disorientation

Confusion

Coma

Cardiovascular Effects

Cardiovascular Effects

Tachycardia Hypertension

Hypotension

Cardiac arrhythmias

Cardiac arrhythmias

Cardiac arrest (severe hypomagnesemia)