C h a p t e r 8
Disorders of Fluid, Electrolyte, and Acid–Base Balance
189
Hypermagnesemia
Hypermagnesemia represents an increase in total body
magnesium and a serum magnesium concentration in
excess of 2.5 mg/dL (1.1 mmol/L).
3
Because of the abil-
ity of the normal kidney to excrete magnesium, hyper-
magnesemia is rare.
When hypermagnesemia does occur, it usually is
related to renal insufficiency and the injudicious use of
magnesium-containing medications such as antacids,
mineral supplements, or laxatives.
3
The elderly are partic-
ularly at risk because they have age-related reductions in
kidney function and tend to consume more magnesium-
containing medications, including antacids and laxa-
tives. Magnesium sulfate is used to treat toxemia of
pregnancy and premature labor; in these cases, careful
monitoring of serum magnesium levels and observation
for signs of hypermagnesemia are essential. Neonatal
hypermagnesemia may also occur, but usually the blood
levels of magnesium are lower in the infant than in the
mother.
52
Manifestations.
The signs and symptoms occur
only when serum magnesium levels exceed 4.0 mg/dL
(2.0 mmol/L).
35,52
Because magnesium tends to sup-
press PTH secretion, hypocalcemia may accompany
hypermagnesemia.
Hypermagnesemia affects neuromuscular and car-
diovascular function
3,50,53
(see Table 8-8). Increased lev-
els of magnesium decrease acetylcholine release at the
myoneural junction, causing hyporeflexia and muscle
weakness. Cardiovascular effects are related to the cal-
cium channel–blocking effects of magnesium. Blood
pressure is decreased, and the ECG shows an increase in
the PR interval, a shortening of the QT interval, T-wave
abnormalities, and prolongation of the QRS and PR
intervals. Severe hypermagnesemia is associated with
muscle and respiratory paralysis, complete heart block,
and cardiac arrest.
Treatment.
The treatment of hypermagnesemia includes
cessation of magnesium administration. Calcium is a
direct antagonist of magnesium, and intravenous admin-
istration of calcium may be used. Peritoneal dialysis or
hemodialysis may be required.
Disorders of Parathyroid Hormone
Both calcium and phosphate homeostasis are impacted
by disorders of PTH. Parathyroid hormone is secreted
by the four parathyroid glands located adjacent to
the thyroid gland in the neck. The hormone is synthe-
sized as a preprohormone, converted to a prohormone
and then to PTH, and finally packaged into secretory
granules for release into the circulation. The domi-
nant regulator of PTH secretion is the serum calcium
concentration (see Fig. 8-13). A unique ECF calcium-
sensing receptor on the parathyroid cell membrane
responds rapidly to changes in serum calcium levels.
1,2
When the serum calcium level is high, the secretion
of PTH is inhibited, and serum calcium is deposited
in the bones. When the level is low, PTH secretion is
increased, and calcium is mobilized from the bones
and released into the blood.
The synthesis and release of PTH from the para-
thyroid gland are also influenced by magnesium.
56
Magnesium serves as a cofactor in the generation of cel-
lular energy and is important in the function of second
messenger systems. Magnesium’s effects on the synthesis
and release of PTH are thought to be mediated through
these mechanisms. Because of its function in regulating
PTH release, severe and prolonged hypomagnesemia
can markedly inhibit PTH levels.
The central function of PTH is to regulate ionized
Ca
++
levels through three target organs: bone, kidney,
and intestine absorption. Parathyroid hormone stimu-
lates the release of calcium from bone; and it increases
calcium reabsorption by the kidney, while increasing the
activation of vitamin D by the kidney; which in turn,
increases the intestinal reabsorption of calcium.
Hypoparathyroidism
Hypoparathyroidism reflects deficient PTH secre-
tion, resulting in low serum levels of ionized calcium.
Parathyroid hormone deficiency may occur because of
a congenital absence of all of the parathyroid glands,
as in DiGeorge syndrome (see Chapter 16), or because
of an acquired disorder due to inadvertent removal
or irreversible damage to the glands during thyroid-
ectomy, parathyroidectomy, or radical neck dissection
for cancer.
35,56,57
A transient form of PTH deficiency
may occur after thyroid surgery owing to parathyroid
gland suppression. Hypoparathyroidism also may have
an autoimmune origin. Antiparathyroid antibodies
have been detected in some persons with hypoparathy-
roidism, particularly those with multiple autoimmune
disorders such as type 1 diabetes mellitus or Graves
disease. Other causes of hypoparathyroidism include
heavy metal damage such as occurs with Wilson dis-
ease and metastatic tumors. Functional impairment
of parathyroid function occurs with magnesium defi-
ciency. Correction of the hypomagnesemia results in
rapid disappearance of the condition.
Manifestations.
Manifestations of acute hypoparathy-
roidism, which result from a decrease in serum calcium,
include tetany with muscle cramps, carpopedal spasm,
and convulsions (see section on hypocalcemia).
56,57
Paresthesias, such as tingling of the circumoral area
and in the hands and feet, are almost always present.
Low calcium levels may cause prolongation of the QT
interval on the ECG, resistance to digitalis, hypotension,
and refractory heart failure. Symptoms of chronic PTH
deficiency include lethargy, an anxiety state, and person-
ality changes. There may be blurring of vision because
of cataracts, which develop over a number of years.
Extrapyramidal signs, such as those seen with Parkinson
disease, may occur because of calcification of the basal
ganglia. Teeth may be defective if the disorder occurs
during childhood.
