188
U N I T 2
Integrative Body Functions
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.
TABLE 8-8
Manifestations of Hypomagnesemia and Hypermagnesemia
Hypomagnesemia
Hypermagnesemia
LaboratoryValues
LaboratoryValues
Serum magnesium <1.3 mg/dL (0.65 mmol/L)
Serum magnesium >2.1 mg/dL (1.1 mmol/L)
Neural and Muscle Effects (increased)
Neural and Muscle Effects (decreased)
Paresthesias
Lethargy
Ataxia, dizziness,
Hyporeflexia
Muscle fasiculations, tetany
Confusion
Confusion, disorientation
Coma
Cardiovascular Effects
Cardiovascular Effects
Tachycardia
Hypotension
Hypertension
Cardiac arrhythmias
Cardiac arrhythmias
Cardiac arrest (severe hypomagnesemia)
