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eMedicine Journal
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Emergency Medicine
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Endocrine And Metabolic
Hypomagnesemia Synonyms, Key Words, and Related Terms: hypomagnesemia, low magnesium level, magnesium, electrolytes, parathyroid hormone, magnesium deficiency, magnesium malabsorption, celiac sprue, radiation injury to the bowel, bowel resection, small bowel bypass, chronic diarrhea, laxative abuse, inflammatory bowel disease, neoplasm, malnutrition, diabetes, primary renal disorders, acute tubular necrosis, postobstructive diuresis, renal tubular acidosis, diuretics, cisplatin, pentamidine, fluoride poisoning, primary aldosteronism, hypoparathyroidism, hyperthyroidism, osmotic diuresis, alcoholism, insulin, excessive lactation, hungry bone syndrome, hypokalemia, hypocalcemia, hypophosphatemia, magnesium supplements, ischemic heart disease |
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 | AUTHOR INFORMATION | Section 1 of 11    |
Authored by Nona Novello, MD, Associate Chair, Department of Emergency Medicine, Franklin Square Hospital
Coauthored by Howard A Blumstein, MD, FAAEM, Assistant Professor, Surgery; Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine
Nona Novello, MD, is a member of the following medical societies: American Academy of Emergency Medicine
Edited by Robin R Hemphill, MD, MPH, Associate Professor, Director, Disaster Preparedness, Department of Emergency Medicine, Vanderbilt University Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Jeffrey L Arnold, MD, FACEP, Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
| Author's Email: | Nona Novello, MD |  |
|---|---|---|
| Editor's Email: | Robin R Hemphill, MD, MPH |
eMedicine Journal, January 18 2007, VOLUME 8,
Number 1
| INTRODUCTION | Section 2 of 11  |
Background: Magnesium, the fourth most common cation in the body, has been the recent focus of much clinical and scholarly interest. Previously underappreciated, this ion is now established as a central electrolyte in a large number of cellular metabolic reactions, including DNA and protein synthesis, neurotransmission, and hormone-receptor binding. It is a component of GTPase and a cofactor for Na+/K+–ATPase, adenylate cyclase, and phosphofructokinase. Magnesium also is necessary for the production of parathyroid hormone. Accordingly, magnesium deficiency has an effect on multiple body functions.
Magnesium is present in greatest concentration within the cell and is the second most abundant intracellular cation after potassium. The total body content of magnesium is 2000 mEq. The intracellular concentration of magnesium is 40 mEq/L, while the serum concentration is 1.5-2 mEq/L. Most of the body's magnesium is found in bone. Only 1% of the total body magnesium is extracellular. Of this amount, one half is ionized, and 25-30% is protein bound.
Magnesium, a component of chlorophyll, is absorbed in the small bowel by active and passive transport mechanisms. Absorption of dietary magnesium takes place mainly in the ileum. It is excreted in stool and urine, but regulation of serum magnesium is under renal control. Most renal reabsorption of magnesium occurs in the proximal tubule and the thick ascending limb of the loop of Henle. In hypomagnesemic patients, the kidney may excrete as little as 1 mEq/L of magnesium. Additionally, magnesium may be removed from bone stores in times of deficiency.
Pathophysiology: Clinical effects of hypomagnesemia are greatest in the CNS, neuromuscular, GI, and cardiac systems.
Frequency:
Sex: Incidence is equal in males and females.
| CLINICAL | Section 3 of 11 |
History:
Physical: The primary clinical findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias. The severity of symptoms is not related directly to the magnesium level. The reference range for serum magnesium level is 1.8-3 mEq/L. Usually, patients become symptomatic at 1.8 mEq/L. However, the physical findings may not be present in all cases. In one study of patients who were severely depleted of magnesium, abnormal physical findings were present in only 2 of 21 patients.
Causes: The causes of hypomagnesemia are numerous. Most causes are related to renal and GI losses.
| DIFFERENTIALS | Section 4 of 11 |
| WORKUP | Section 5 of 11 |
Lab Studies:
Other Tests:
| TREATMENT | Section 6 of 11 |
Prehospital Care: Be attentive to the ABCs. At this point, the diagnosis usually is not known; therefore, advanced cardiac life support (ACLS) protocol should be followed. Seizures should be treated with benzodiazepines.
Emergency Department Care:
| MEDICATION | Section 7 of 11 |
Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for mild symptoms, while IV replacement is indicated for severe clinical effects.
Drug Category: Electrolyte supplement -- These agents are used to replace an existing magnesium deficit.
| Drug Name | Magnesium gluconate (Almora) -- Oral supplementation should be given when patient is mildly depleted of magnesium (ie, magnesium level > 1 mEq/L and patient is asymptomatic). Other oral supplements (eg, magnesium oxide, magnesium hydroxide) may be used. |
|---|---|
| Adult Dose | 500 mg/d (27 mg elemental magnesium) PO |
| Pediatric Dose | 3-6 mg elemental magnesium/kg/d PO divided tid/qid; not to exceed 400 mg in 24 h |
| Contraindications | Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis |
| Interactions | Concurrent nifedipine may cause hypotension and neuromuscular blockade; may worsen neuromuscular blockade seen with aminoglycosides, tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and ritodrine |
| Pregnancy | A - Safe in pregnancy |
| Precautions | Impaired renal function may increase toxicity; diarrhea is most common adverse effect |
| Drug Name | Magnesium sulfate -- Supplementation via IV infusion should be given to patients with moderately severe to severe depletion. |
|---|---|
| Adult Dose | 2-4 g of 50% magnesium sulfate (16.6-33.3 mEq) diluted in saline or dextrose IV over 30-60 min In cases of life-threatening arrhythmias, give same amount IV push |
| Pediatric Dose | 1 mEq/kg IV on day 1; 0.5 mEq/kg/d over next 3 d |
| Contraindications | Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis |
| Interactions | Concurrent nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants and betamethasone and cardiotoxicity of ritodrine |
| Pregnancy | A - Safe in pregnancy |
| Precautions | May alter cardiac conduction, leading to heart block in digitalized patients; respiratory rate, deep tendon reflexes, and renal function should be monitored when administered parenterally; caution when administering magnesium dose since may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL of 10% solution IV, can be given as antidote for clinically significant hypermagnesemia |
| FOLLOW-UP | Section 8 of 11 |
Further Inpatient Care:
In/Out Patient Meds:
Deterrence/Prevention:
Prognosis:
Patient Education:
| MISCELLANEOUS | Section 9 of 11 |
Special Concerns:
| TEST QUESTIONS | Section 10 of 11 |
CME Question 1: A 40-year-old alcoholic man presents with diaphoresis, combativeness, and vomiting. He then proceeds to seize. What electrolyte abnormality may account for the seizure?
A: Hypomagnesemia
B: Hypocalcemia
C: Hypoglycemia
D: Hypophosphatemia
E: A, B, and C
The correct answer is E: All of these disturbances may lead to seizures. Alcoholics are at risk of developing hypomagnesemia because of their poor nutritional status and the osmotic wasting of magnesium. Hypomagnesemia may lead to hypocalcemia.
CME Question 2: In a patient with healthy kidney function, which test is the best means of determining magnesium depletion?
A: Serum magnesium level
B: 24-hour urinary excretion of magnesium
C: Albumin level
D: ECG
E: All of the above
The correct answer is B: Since magnesium is mostly intracellular, the serum magnesium level may be in the reference range despite whole-body magnesium depletion. A 24-hour urinary excretion of magnesium is the best indicator of magnesium status. However, a low serum magnesium level indicates a deficiency.
Pearl Question 1 (T/F): The preferred route of replacement in the treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects.
The correct answer is True: Oral replacement is appropriate for mild symptoms, while intravenous replacement is indicated for severe clinical effects.
Pearl Question 2 (T/F): Patients with hypomagnesemia may present with primarily neurologic signs and symptoms.
The correct answer is True: Altered mental status may be present in severe cases. Less severe cases may result in vertigo, ataxia, depression, and seizure activity.
Pearl Question 3 (T/F): The severity of symptoms of hypomagnesemia is not related directly to the magnesium level.
The correct answer is True: Usually, patients become symptomatic at a magnesium level of 1.8 mEq/L or less. (Reference range for serum magnesium level is 1.8-3 mEq/L.) However, clinical findings may not be present in all cases of hypomagnesemia. The primary findings are neuromuscular irritability, CNS hyperexcitability, and cardiac arrhythmias.
Pearl Question 4 (T/F): Patients with hypomagnesemia have a poor prognosis.
The correct answer is False: Patients with hypomagnesemia have an excellent prognosis once the deficiency is corrected. For the most part, the symptoms are reversible with treatment.
| BIBLIOGRAPHY | Section 11 of 11 |
| NOTE: |
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| Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER |
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