Also at risk are patients who receive prolonged parenteral nutrition
undergo prolonged nasogastric suction.
253 Hypomagnesemia may be present in
patients who have increased magnesium requirements, such as pregnant women and
254 Conditions associated with steatorrhea, such as nontropical sprue and
short-bowel syndrome, can result in reduced GI magnesium absorption. Insoluble
magnesium soaps may be formed in the GI tract because of the presence of
255 Hypomagnesemia can also occur in patients with a bowel
257 A rare genetic disorder has also been reported in
patients with defective GI magnesium absorption.
258 An impaired carrier-mediated
magnesium transport system is believed to be responsible for the symptomatic
deficiency, which requires high oral magnesium intake to overcome the defect.
Renal magnesium wasting can be caused by a primary defect or be secondary to
systemic factors. A rare form of renal magnesium wasting is congenital.
drugs can induce hypomagnesemia through increased renal loss: cisplatin,
diuretics can also result in hypomagnesemia, which can be reversed with the
concurrent use of amiloride or triamterene. Magnesium depletion can be associated
chronic ingestion of alcohol will result in increased renal magnesium loss.
Various endocrinologic disorders, such as SIADH,
244 and postparathyroidectomy,
R.J. could be hypomagnesemic for many reasons. His long history of alcohol use,
malnutrition, and malabsorption may all have contributed to his magnesium deficit.
The vomiting and diarrhea that he experienced could have reduced GI magnesium
absorption. Use of furosemide and nasogastric suction while in the hospital could
also have exacerbated his magnesium depletion through renal and GI losses,
CASE 27-13, QUESTION 2: What are the clinical manifestations of hypomagnesemia in R.J.?
Magnesium depletion can result in abnormal function of the neurologic,
neuromuscular, and cardiovascular systems. Hypomagnesemia lowers the threshold
for nerve stimulation, resulting in increased irritability. Typical findings include
Chvostek and Trousseau signs, muscle fasciculation, tremors, muscle spasticity,
generalized convulsions, and possibly tetany. The patient may experience weakness,
anorexia, nausea, and vomiting, as seen in R.J. Hypokalemia, hypocalcemia, and
alkalosis may be present as well. In patients who are moderately depleted, changes
in the ECG include widening of the QRS complex and a peaking T wave.
depletion, a prolonged PR interval and a diminished T wave may be seen.
Ventricular arrhythmias have also been reported in some patients.
CASE 27-13, QUESTION 3: Outline a regimen to replenish the body stores of magnesium for R.J., and
develop a monitoring plan to assess efficacy and potential adverse effects.
The specific regimen for magnesium replenishment depends on the clinical
presentation of the patient. Symptomatic patients require more aggressive parenteral
therapy, whereas oral replacement may suffice for asymptomatic hypomagnesemia.
Patients with life-threatening symptoms, such as seizures and arrhythmias, need
immediate magnesium infusion. Because serum magnesium concentrations do not
reflect total body stores, symptoms are more important determinants of the urgency
and aggressiveness of therapy.
The body stores of magnesium must be replenished slowly. Serum magnesium
concentrations may return to the normal range within the first 24 hours, but total
replenishment of body stores may take several days. Furthermore, approximately
50% of the administered IV dose of magnesium will be excreted in the urine.
Because the threshold for urinary magnesium excretion is low, the abrupt increase in
serum magnesium after an IV dose will result in increased urinary magnesium
excretion despite a total body magnesium deficit. Conversely, in patients with renal
insufficiency, decreased excretion of magnesium will place the patient at risk for
hypermagnesemia. A reduced rate of magnesium administration and frequent
monitoring of serum magnesium concentrations are therefore necessary in patients
Oral replacement of magnesium is indicated for asymptomatic patients with mild
depletion. Magnesium-containing antacids, milk of magnesia, and magnesium oxide
are effective choices for replacement. Sustained-release preparations, such as Slow
(magnesium chloride) or Mag-Tab SR (magnesium lactate), are preferred,
however. With 5 to 7 mEq (2.5–3.5 mmol or 60–84 mg) of magnesium per tablet, six
to eight tablets should be given daily in divided doses for severe magnesium
depletion. For mild and asymptomatic disease, two to four tablets per day may be
274 A diet high in magnesium (cereals, nuts, meat, fruits, fish, legumes, and
vegetables) will also help replenish body stores and prevent depletion.
For patients with symptomatic hypomagnesemia, such as R.J., parenteral
magnesium replacement is indicated. The magnesium deficit in patients with chronic
alcoholism is estimated to be 1 to 2 mEq/kg.
276 Because up to half of the IV
magnesium dose will be excreted in the urine during replacement, approximately 2 to
4 mEq/kg will be needed to replenish R.J.’s body store.
as magnesium sulfate 10% solution, should be administered IV in the first 24 hours.
Half of this amount is given in the first 3 hours, and the remaining half is infused over
the course of the rest of the day. This dose may be repeated to keep the serum
magnesium concentration greater than 1.0 mg/dL.
magnesium may be replenished daily for up to 4 additional days.
be given IM as 50% solution, but the injections are painful and potentially sclerosing,
and multiple administrations are needed. Therefore, the IV route is the preferred
mode of parenteral administration. For patients with symptomatic hypomagnesemia
who are unstable, such as those experiencing seizures or life-threatening arrhythmias,
16 mEq of magnesium sulfate may be administered as a short IV infusion over the
course of 2 minutes, followed by 16 mEq over the course of 20 minutes, then 16 to 24
mEq over the course of 2 to 4 hours.
After IV magnesium administration, the patient should remain in a supine position
to avoid hypotension. He should be monitored carefully for marked suppression of
deep tendon reflexes (magnesium, 4–7 mEq/L); ECG, BP, and respiration changes;
and high serum magnesium levels. Facial flushing, a sensation of warmth, and
sweatiness may result from vasodilation secondary to a rapid magnesium infusion.
Particular caution is warranted in patients with renal impairment, in whom the rate of
magnesium should be reduced. These patients should be monitored frequently to
avoid toxicities related to hypermagnesemia. IV magnesium should also be
administered cautiously in patients with severe atrioventricular heart block or
bifascicular blocks because magnesium possesses pharmacologic properties similar
In patients who exhibit hypomagnesemia secondary to a thiazide or loop diuretic,
amiloride may be added to reduce renal magnesium loss by increasing reabsorption
in the cortical collecting tubule.
CASE 27-13, QUESTION 4: For the initial 2 days of hospitalization, R.J. received 3 mEq/kg of IV
have contributed to the lack of favorable response to the magnesium therapy?
The total amount of magnesium administered to R.J. during the past 2 days was
higher than the usual recommended rate (4–5 days) of magnesium replenishment,
leading to renal excretion of a large portion of the dose.
nasogastric suction and furosemide have increased the magnesium loss during the
replacement period, and hypokalemia may have reduced the effectiveness of
magnesium replacement. In a patient whose serum magnesium concentration does not
increase after appropriate magnesium therapy, a 24-hour urine collection to assess
magnesium renal excretion can be helpful. A low urinary magnesium concentration is
consistent with magnesium depletion, whereas high urinary magnesium excretion in
the presence of hypomagnesemia suggests renal magnesium wasting.
and depressed deep tendon reflexes. The ECG reveals prolonged PR and QRS intervals. The serum
magnesium concentration is 6.5 mEq/dL. What is the most likely cause of hypermagnesemia in J.O.?
Because the kidney is the primary route of magnesium elimination, renal
impairment is a virtual requisite for hypermagnesemia (see Chapter 28, Chronic
renal function, including older adults. When a patient with renal failure, such as J.O.,
takes magnesium-containing medications, the serum magnesium concentration can
increase substantially, resulting in toxicities. Hypermagnesemia may be seen when
the creatinine clearance drops to less than 30 mL/minute; an inverse relationship is
observed between the serum magnesium concentrations and the creatinine
281 Hypermagnesemia is also seen in patients with acute renal failure
during the oliguric phase, but not the diuretic phase.
hypermagnesemia include adrenal insufficiency,
magnesium citrate used as a cathartic for drug overdose,
CASE 27-14, QUESTION 2: Describe the usual clinical presentation of a patient with hypermagnesemia.
An elevated magnesium serum concentration alters the normal function of the
neurologic, neuromuscular, and cardiovascular systems. When the serum magnesium
concentration is greater than 4 mEq/L, deep tendon reflexes are depressed; they are
usually lost at greater than 6 mEq/L. Flaccid quadriplegia can develop when the
concentration is greater than 8 to 10 mEq/L. Respiratory paralysis, hypotension, and
difficulty in talking and swallowing may also be present. Changes in the ECG may
include a prolonged PR interval and widening of the QRS complex. Complete heart
block may be seen at concentrations of approximately 15 mEq/L. In mild
hypermagnesemia, the patient may experience nausea and vomiting.
Drowsiness, lethargy, diaphoresis, and altered consciousness may be present at
higher serum magnesium concentrations. J.O.’s increasing weakness, hypotension,
depressed deep tendon reflexes, and ECG findings are consistent with
CASE 27-14, QUESTION 3: How should J.O.’s hypermagnesemia be treated?
If magnesium-containing medications are discontinued in patients with
hypermagnesemia, the serum magnesium concentration will usually return to the
normal range through renal elimination. When potentially life-threatening
complications are present, as in J.O., 5 to 10 mEq of IV calcium should be
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