Dott. M. M. Ciammaichella
Dirigente Medico
SC Medicina Interna I° per l'Urgenza
(Direttore: Dott. G. Cerqua)
A.C.O. S. Giovanni – Addolorata, Roma, Italia

KEY-WORDS: Hypermagnesemia

INTRODUCTION
CLINICAL
WORKUP
TREATMENT
MEDICATION
FOLLOW-UP
MISCELLANEOUS
BIBLIOGRAPHY

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INTRODUCTION

Background: Magnesium is a major electrolyte of the body. As the second most common intracellular cation, it acts as a vital part in many cellular metabolic pathways. Magnesium is required for DNA and protein synthesis as well as necessary for most enzymes in phosphorylation reactions. It is also important for parathyroid hormone synthesis. The total body content of this central cation is 2000 mEq or 24 grams. The distribution of magnesium is 67% in bone, 31% intracellularly and a mere 1% extracellularly. The intracellular concentration is 40 mEq/L, while the normal serum concentration is 1.5-2.0 mEq/L. Of this serum component, 25-30% is protein bound, 10-15% complexed and the remaining 50-60% ionized.
Magnesium is absorbed in the ileum and excreted in stool and urine. The daily requirement of magnesium is 300 -350 mg or 15 mmol, which is easily obtainable with normal daily intake of fruits, seeds and vegetables. This is because magnesium is part of chlorophyll.
The kidney acts as the main regulator of magnesium concentrations. Absorption occurs mainly in the proximal tubule and thick ascending limb of the loop of Henle. Hypermagnesemia is a rare electrolyte abnormality because the kidney is so effective in excreting excess.
Pathophysiology: Magnesium excess affects the CNS, neuromuscular and cardiac organ systems. It is most commonly seen in renal insufficiency.
Frequency:

• Levels of 2-4 mEq/L

• Nausea

• Vomiting

• Skin flushing

• Weakness

• Lightheadedness

• High Levels:
  
  Depressed levels of consciousness

• Level of 3.0-4.0 mEq/L:

• Disappearence of deep tendon reflexes

• Muscle weakness

• Level of 5.0-6.0 mEq/L:

• Hypotension

• Vasodilatation

• Level of 8.0-10.0 mEq/L:

• Arrythmias, including atrial fibrillation

• Intraventricular conduction delay

• Levels greater than 10.0 mEq/L:

• Asystole

• Heart block

• Ventilatory failure

• Stupor or coma

• Death

• Elevated levels of magnesium are also associated with delayed thrombin formation and platelet clumping.

• Patients with chronic renal failure who are taking magnesium containing antacids or cathartics commonly develop hypermagnesemia.

• Acute renal failure

• Mothers treated for eclampsia with magnesium infusions

• Infants born to mothers treated with magnesium infusions

• Decreased GI elimination caused by hypomotility and subsequent increased magnesium absorption

• Medications, including narcotics and anticholinergics

• Hypomotility disorders like bowel obstruction and chronic constipation

• Tumor lysis syndrome

• Adrenal insufficiency

• Rhabdomyolysis

• Milk-alkali syndrome

• Hypothyroidism

• Hypoparathyroidism

• Neoplasm with skeletal muscle involvement

• Lithium intoxication
  
  
• Extracellular volume contraction as in DK

• Electrolytes, including potassium, magnesium and calcium
  
  Magnesium is not usually found as an isolated electrolyte abnormality. Hyperkalemia and hypercalcemia are often present concurrently.

• BUN and Creatinine:

• Renal function tests should be ordered and creatinine clearance calculated to ascess the ability of the kidney to excrete magnesium.

• Serum magnesium levels rise when the creatinine clearance is below 30 cc/min.

• Check serum creatinine phosphokinase (CPK) or urine myoglobin in pateints where rhabdomyolysis is suspected.

• An arterial blood gas (ABG) may reveal a respiratory acidosis.

• Hypothyroidism is a rare cause of hypermagnesemia. Check thyroid function tests in the absence of any other good explanation.

• Electrocardiogram (ECG):
  
  An ECG and cardiac monitor may show prolongation of the PR interval or intraventricular conduction delay, which are nonspecific findings.

• Ascess the patient's ABC's and stabilize them.

• Intubate if necessary.

• Treat hypotension with fluids.

• Treat arrythmias as per ACLS protocol or with treatment outlined below, if hypermagnesemia is known.

• Obtain appropriate studies as discussed above.

• A renal consult should be obtained for dialysis if the patient is severely hypermagnesemic.
  
  
• Intensive care unit monitoring should be arranged if the symptoms are severe.

• Consider transfer if a patient with renal failure has a severe elevation of magnesium and no dialysis is available.

• Patients do well upon restoration of normal magnesium levels.

• Information regarding avoidance of medications that cause hypermagnesemia should be given.

• It is not uncommon for the cause of hypermagnesemia to be iatrogenic. Physician education of these problem may help decrease the incidence.