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The disturbances of magnesium (Mg+2) and calcium (Ca+2) are closely interrelated. Calcium disorders are discussed in Chapter 78.


  1. Definition. Normal serum levels for Mg+2 are typically given as 0.5–1.0 mmol/L (1.2–2.6 mg/dL). Hypomagnesemia is usually seen as any value <0.66 mmol/L (1.6 mg/dL); however, clinical signs do not manifest until levels have dropped <0.5 mmol/L (1.2 mg/dL).

  2. Incidence. True incidence in neonates is not well characterized, but neonates appear to be more predisposed than other groups of patients.

  3. Pathophysiology. Mg+2 is a key trace element for maintaining skeletal integrity, and it acts as a catalyst for intracellular enzymes for adenosine triphosphate (ATP) activation in skeletal and myocardial contractility. It is also integral to protein synthesis, vitamin D metabolism, parathyroid function, and calcium homeostasis.

  4. Risk factors

      1. Hypocalcemia.

      1. Inadequate intake of Mg+2.

      1. Infant of diabetic mother reflecting maternal Mg+2 deficiency secondary to gestational diabetes.

      1. Intrauterine growth restriction, especially if the mother had preeclampsia.

      1. Inherited renal wasting.

      1. Hypoparathyroidism.

      1. Associated hypocalciuria and nephrocalcinosis.

      1. Secondary to furosemide- or gentamicin-induced loss.

      1. Citrated blood exchange transfusions.

  5. Clinical presentation

      1. Same as in hypocalcemia (Chapter 78, Section V); may also present as seizures.

      1. May be masked as hypocalcemia but with symptoms that persist after adequate calcium gluconate therapy.

  6. Diagnosis. Laboratory testing to establish serum levels as noted earlier.

      1. Serum magnesium levels.

      1. Total and ionized calcium levels.

  7. Management. Acute hypomagnesemia should be treated with intravenous magnesium sulfate. See Chapter 132 for dosing information. Infusion must be monitored closely for cardiac arrhythmias and hypotension. Maintenance Mg+2 can be by parenteral nutrition solutions or by oral feeds with a fivefold dilution of Mg+2 salt solution.

  8. Prognosis. Hypomagnesemia generally has a good outcome if diagnosed promptly and treated adequately. The exception is a clinical presentation that includes hypomagnesemia-induced seizures with follow-up studies suggesting ≥20% incidence of neurologic abnormalities.


  1. Definition. Reference levels of serum Mg+2 signifying hypermagnesemia vary from >1.15 mmol/L (2.3 mg/dL) to >1.5 mmol/L (3.0 mg/dL). Hypermagnesemia is uncommon in a NICU population of patients, but in certain circumstances it must be recognized.

  2. Incidence. Occurs rarely except in infants whose mothers were treated with Mg+2 sulfate, where it occurs more frequently.

  3. Pathophysiology. Increased serum Mg+2 levels depress the central nervous system and decrease skeletal muscle contractility.

  4. Risk factors

      1. Increased maternal serum levels following Mg+2 sulfate therapy for pregnancy-related hypertension or preeclampsia (most common cause).

      1. Excessive Mg+2 sulfate administration to an infant for hypomagnesemia (iatrogenic medication error) or following administration of Mg+2 containing antacid; especially if hydration and urine output are low. Hypermagnesemia can also be caused by magnesium sulfate enemas, which are contraindicated in neonates.

  5. Clinical presentation

      1. Birth depression, hypotonia, hypotension, hyporeflexia.

      1. Respiratory depression, apnea.

      1. Poor suck, decreased gastrointestinal motility, increased gastric aspirates, abdominal distention, and delayed meconium passage.

      1. Meconium plug syndrome, intestinal perforation.

      1. Urinary retention.

      1. Symptoms may mimic hypercalcemia.

      1. Paradoxically, hypermagnesemia may be asymptomatic despite appreciable Mg+2 levels.

  6. Diagnosis

      1. Laboratory studies

          1. Serum Mg+2 determination.

          1. Serum calcium levels. Always determine calcium levels with Mg+2 abnormalities.

      1. Electrocardiogram may reveal ...

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