Neonatal Hypocalcemia

15/9/2015
Neonatal hypocalcemia
Official reprint from UpToDate

www.uptodate.com 2015 UpToDate
Author
Steven A Abrams, MD
Section Editors
Joseph A Garcia-Prats, MD
Joseph I Wolfsdorf, MB,
BCh
Deputy Editor
Melanie S Kim, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2015. | This topic last updated: Apr 15, 2014.
INTRODUCTION Hypocalcemia is a common metabolic problem in newborns.
The diagnosis, clinical manifestations, and treatment of neonatal hypocalcemia are reviewed here. Calcium (Ca)
requirements and the etiology of hypocalcemia after the neonatal period are discussed elsewhere. (See
"Management of neonatal bone health" and "Etiology of hypocalcemia in infants and children".)
PERINATAL METABOLISM During pregnancy, calcium is transferred actively from the maternal circulation to
the fetus by a transplacental Ca pump regulated by parathyroid hormone-related peptide (PTHrP) [1]. The majority
of fetal Ca accretion occurs in the third trimester. This process results in higher plasma Ca concentrations in the
fetus than in the mother and leads to fetal hypercalcemia, with total and ionized Ca concentrations of 10 to 11
mg/dL (2.5 to 2.75 mmol/L) and 6 mg/dL (1.5 mmol/L), respectively, in umbilical cord blood at term [2].
After the abrupt cessation of placental transfer of Ca at birth, total serum Ca concentration falls to 8 to 9 mg/dL (2
to 2.25 mmol/L) and ionized Ca to as low as 4.4 to 5.4 mg/dL (1.1 to 1.35 mmol/L) at 24 hours [3,4]. Serum Ca
concentration subsequently rises, reaching levels seen in older children and adults by two weeks of age [5].
MEASUREMENT Within the plasma, calcium (Ca) circulates in different forms. Approximately 40 percent is
bound to serum proteins, principally albumin; 10 percent is complexed with citrate, bicarbonate, sulfate, or
phosphate; and 50 percent exists as the physiologically important ionized (or free) calcium [6]. The ionized Ca
concentration is tightly regulated by parathyroid hormone and vitamin D.
Measurement of the total plasma Ca concentration alone can be misleading because the relationship between total
and ionized Ca is not always linear (see "Relation between total and ionized serum calcium concentrations").
Correlation is poor when the serum albumin concentration is low or, to a lesser degree, with disturbances in acidbase status, both of which occur frequently in premature or ill infants. With hypoalbuminemia, the total Ca
concentration will be low while the ionized fraction will be normal unless some other factor is affecting Ca
metabolism. In general, the plasma calcium concentration falls by 0.8 mg/dL (0.2 mmol/L) for every 1 g/dL (10 g/L)
fall in the plasma albumin concentration.
Disturbances in acid-base status can change the ionized Ca concentration without affecting the total Ca level. An
elevation in extracellular pH, for example, increases the binding of calcium to albumin, thereby lowering the plasmaionized Ca concentration [7]. The fall in ionized calcium with acute respiratory alkalosis is approximately 0.16
mg/dL (0.04 mmol/L or 0.08 mEq/L) for each 0.1 unit increase in pH [7]. Thus, acute respiratory alkalosis can
induce signs of hypocalcemia, although the alkalosis is primarily responsible. Conversely, with metabolic acidosis,
binding of Ca to albumin is reduced, and the ionized Ca concentration will be increased.
For these reasons, we recommend the measurement of whole blood ionized Ca concentration in newborns who are
premature or ill, and are therefore at risk for hypocalcemia [8].
DEFINITION The definition of hypocalcemia depends upon gestational age and birth weight:
In term infants or premature infants greater than 1500 g birth weight, we define hypocalcemia as a total serum
Ca concentration less than 8 mg/dL (2 mmol/L) or an ionized fraction of less than 4.4 mg/dL (1.1 mmol/L).
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Premature infants with birth weight less than 1500 g are considered to have hypocalcemia if they have a total
serum Ca concentration less than 7 mg/dL (1.75 mmol/L). In general, symptoms are uncommon in infants
less than 1500 g whose ionized calcium is greater than 0.8 to 0.9 mmol/L.
EARLY HYPOCALCEMIA The causes of neonatal hypocalcemia are classified by the timing of onset.
Hypocalcemia is considered to be early when it occurs in the first two to three days after birth. Early hypocalcemia
is an exaggeration of the normal decline in calcium (Ca) concentration after birth. It occurs commonly in premature
infants and in infants of diabetic mothers (IDMs), and is seen also after perinatal asphyxia or intrauterine growth
restriction, and in infants with hypoparathyroidism.
Prematurity Approximately one-third of premature infants and the majority of very low birth weight infants have
low total serum Ca concentrations during the first two days after birth [9,10]. Multiple factors contribute to the fall in
total serum Ca and include hypoalbuminemia, which does not lower the ionized Ca, and factors that lower both total
and ionized Ca such as reduced intake of Ca because of low intake of milk, possible impaired response to
parathyroid hormone (PTH), increased calcitonin levels, and increased urinary losses accompanying high renal
sodium excretion [5]. Most premature infants are asymptomatic because the fall in total serum Ca typically is
greater than the fall in ionized Ca; this fall results from hypoalbuminemia and, in some cases, mild metabolic
acidosis, which tends to raise the ionized Ca. (See 'Measurement' above.)
Infants of diabetic mothers Hypocalcemia occurs in at least 10 to 20 percent of IDMs and in as many as 50
percent in some series [11,12] (see "Infant of a diabetic mother"). The lowest serum Ca concentration typically
occurs between 24 to 72 hours after birth and often is associated with hyperphosphatemia. The extent of
hypocalcemia is related to the severity and duration of maternal diabetes. Hypocalcemia is thought to be caused by
lower PTH concentrations after birth in IDMs compared with normal infants [13]. Why this lower concentration
occurs is not well understood. Higher serum ionized Ca concentrations in utero in IDMs may suppress the fetal
parathyroid glands [13]. The development of hypomagnesemia, prematurity, and birth asphyxia may be contributing
factors.
Birth asphyxia Infants with birth asphyxia frequently have hypocalcemia and may also have
hyperphosphatemia. Possible mechanisms include increased phosphate load caused by tissue catabolism,
decreased intake due to delayed initiation of feedings, renal insufficiency, acidosis, and increased serum calcitonin
concentration [14,15].
Intrauterine growth restriction Hypocalcemia occurs with increased frequency in infants with intrauterine
growth restriction. The risk increases with the severity of growth failure [16,17]. The mechanism is thought to involve
decreased transfer of calcium across the placenta.
Hypoparathyroidism Hypoparathyroidism associated with excess phosphorus intake is a common cause of
early neonatal hypocalcemia [18]. Hypoparathyroidism also can occur as part of a syndrome.
DiGeorge syndrome The most prevalent syndrome that includes hypoparathyroidism is the DiGeorge
syndrome (DGS, also called DiGeorge anomaly). This disorder arises from a failure of migration of neural crest cells
into the third and fourth pharyngeal pouches. Affected patients typically present in the first week after birth with
signs of hypocalcemia, such as tetany or seizures, secondary to hypoplastic or absent parathyroid glands. They
have characteristic facial features that include a small mouth, a submucous cleft palate, abnormal and low set ears,
upturned nose, and a widened distance between the inner canthi (telecanthus) with short palpebral fissures [19,20].
Cardiac defects, especially abnormalities of the outflow tract or aortic arch (eg, truncus arteriosus, tetralogy of
Fallot, or interrupted aortic arch), frequently are present. Thymic hypoplasia results in an immune defect that is
highly variable. (See "DiGeorge (22q11.2 deletion) syndrome: Epidemiology and pathogenesis" and "DiGeorge
(22q11.2 deletion) syndrome: Management and prognosis".)
Approximately 80 to 90 percent of patients with DGS have microdeletions involving chromosome 22q11-pter [21];
fluorescence in situ hybridization with DNA probes specific for this region establishes the diagnosis. DGS appears
to be the most severe phenotype of a group of related disorders known as CATCH 22 syndrome, an acronym for
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cardiac defects, abnormal facies, thymic hypoplasia, cleft palate, and hypocalcemia caused by chromosome 22q11
deletion [21]. Other rarer syndromes that include hypoparathyroidism are Kearns-Sayre and Kenny-Caffey
syndromes, which are mitochondrial cytopathies.
Maternal hyperparathyroidism Infants born to mothers with hyperparathyroidism frequently have
hypocalcemia. The mechanism is related to increased transplacental transport of Ca caused by high maternal Ca
concentrations, which results in fetal hypercalcemia that exceeds physiologic levels and leads to suppression of
fetal and neonatal parathyroid hormone (PTH) secretion. Affected infants typically develop increased neuromuscular
irritability in the first three weeks after birth, but they can present later [5]. Some infants also have
hypomagnesemia.
Hypomagnesemia Hypomagnesemia causes resistance to PTH and impairs PTH secretion, both of which
can result in hypocalcemia. The most common etiology in newborns is transient hypomagnesemia, although rare
disorders of intestinal and/or renal tubular magnesium transport can occur. In transient cases, the serum
magnesium concentration typically is 0.8 to 1.4 mg/dL (0.33 to 0.58 mmol/L) (normal values are 1.6 to 2.8 mg/dL
[0.66 to 1.16 mmol/L]); more severe reductions occur in the transport defects [5].
Other causes
Gentamicin therapy In one case report, gentamicin therapy was associated with a decrease in serum Ca
[22]. Further studies are needed to confirm whether or not there is a causal relationship between this medication
and calcium to evaluate the effects of different gentamicin regimens on ionized Ca.
Maternal vitamin D deficiency Neonatal hypocalcemia due to severe maternal vitamin D deficiency has
been noted in a single case report from Australia and a case series from the Middle East [23,24]. In these patients,
neonatal hypocalcemia mostly occurred during the second week of life, which is later than is typical for other
causes of hypocalcemia [24]. Levels of 25-hydroxyvitamin D were extremely low in mothers and most infants;
however, it remains uncertain whether vitamin D deficiency was the primary etiology. Further confirmation is
required to establish causality. Nevertheless, these findings emphasize the importance of adequate maternal
vitamin D intake, such as the 600 int. units/day recommended in the Recommended Dietary Allowance by the
Institute of Medicine [25].
LATE HYPOCALCEMIA Late hypocalcemia develops after the second or third day after birth and typically
occurs at the end of the first week [18].
Vitamin D insufficiency Any disorder of vitamin D metabolism can lower serum Ca. In a case series of 78
neonates who presented with severe neonatal hypocalcemia, levels of 25-hydroxyvitamin D were deemed by the
authors to be insufficient (ie, <25 ng/mL [62.4 nmol/L]) in all of the 42 infants in whom they were determined [18].
However, this value of 25 ng/mL has not been established in infants or in any age group to be biologically the value
for any clinical disorders. Therefore, the true role of low vitamin D status has yet to be determined. Maternal levels
of low 25-hydroxyvitamin D levels were not measured, but the authors speculate based on other reports that
maternal vitamin D insufficiency was a contributing factor to neonatal vitamin D insufficiency. In addition, these
infants had severe hypomagnesemia and PTH levels that were inappropriately low. The combination of multiple
biochemical abnormalities may have led to severe late-onset hypocalcemia. (See "Etiology of hypocalcemia in
infants and children".)
High phosphate intake Intake of excess phosphate is an historically important cause of late hypocalcemia that
was seen in term infants fed bovine milk or a bovine milk-based formula with a high phosphorus concentration. The
mechanism is uncertain, but the high phosphorus level may antagonize PTH secretion or actions, or it may produce
increased Ca and phosphorus deposition in bones, leading to hypocalcemia [26]. Symptomatic infants typically
present with tetany or seizures at 5 to 10 days of age [26]. Severe hyperphosphatemia and hypocalcemia also can
be caused by phosphate enemas [27].
Other causes Critically ill or premature infants are exposed to many therapeutic interventions that may cause
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transient hypocalcemia.
Bicarbonate infusion, resulting in metabolic alkalosis, or transfusion with citrated blood, leading to formation of
Ca complexes, decreases ionized Ca concentration. Lipid infusions also may reduce ionized Ca levels by
formation of Ca complexes with free fatty acids.
Mild hypocalcemia has been associated with phototherapy for hyperbilirubinemia. The mechanism may be
related to decreased melatonin secretion, leading to increased Ca uptake by bone [28].
Other causes include:
Acute renal failure of any cause, usually associated with hyperphosphatemia. (See "Acute kidney injury
(acute renal failure) in the newborn".)
Hypocalcemia has been described with rotavirus infection [29]. (See "Clinical manifestations and diagnosis of
rotavirus infection".)
CLINICAL MANIFESTATIONS Most infants with hypocalcemia are asymptomatic. Among those who become
symptomatic, the characteristic sign is increased neuromuscular irritability. Such infants are jittery and often have
muscle jerking that is induced by environmental noise or other stimuli. Generalized or focal clonic seizures may
occur. Rare presentations include inspiratory stridor caused by laryngospasm, wheezing caused by bronchospasm,
or vomiting possibly resulting from pylorospasm [5].
In the previously mentioned case series of 78 full-term neonates admitted with late severe hypocalcemia (median
levels of total and ionized calcium of 1.5 and 0.81 mmol/L [6 and 3.24 mg/dL]), most presented with seizure-like
activity that was deemed consistent with tetany in the context of low calcium levels [18]. These patients also had
hyperphosphatemia (median level of 3.2 mmol/L [9.9 mg/dL]), hypomagnesemia (median level of 0.58 mmol/L [1.4
mg/dL]), and inappropriately low parathyroid hormone levels.
DIAGNOSIS Because most infants with hypocalcemia are asymptomatic, we monitor serum calcium (Ca) in
infants with risk factors. Ionized Ca is optimal and should be the primary measurement used because only this
measurement accurately assesses the risk of symptoms in all age groups. Total serum Ca is measured if ionized
Ca is unavailable. However, one should recognize that relatively low total Ca values (5.5 to 7 mg/dL [1.4 to 1.75
mmol/L]) may not be pathologic in premature infants. Similarly, ionized Ca values of 0.8 to 1 mmol/L are
uncommonly associated with symptoms in very low birth weight infants.
In infants who are extremely low birth weight (less than 1000 g) or who are ill, we measure the Ca concentration at
12, 24, and 48 hours of age. In premature infants with birth weight 1000 to 1500 g, Ca is measured at 24 and 48
hours. We continue monitoring until Ca values are normal and Ca intake from milk or parenteral nutrition is
adequate, which usually occurs by 96 hours. The use of early parenteral nutrition is usually the optimal route for
providing calcium to this group.
Serum Ca also is measured in any infant with signs consistent with hypocalcemia and in infants with congenital
heart disease. We do not routinely monitor asymptomatic healthy premature infants with birth weight greater than
1500 g or healthy infants of diabetic mothers who are taking milk feedings on the first day. (See "Infant of a diabetic
mother".)
The effect of hypocalcemia on cardiac repolarization may be reflected in prolongation of the QTc interval (QT interval
corrected for heart rate) on the electrocardiogram (ECG) to greater than 0.4 seconds. However, the QTc interval
does not correlate reliably with blood ionized Ca levels [30]. We do not recommend use of the ECG to screen for
hypocalcemia.
Infants require further evaluation if they have persistent early hypocalcemia that does not respond to treatment,
develop late hypocalcemia, or have associated seizures. Genetic and cardiac studies are performed to detect
possible DiGeorge syndrome. Serum levels of magnesium and phosphorus should be measured; additional studies
may include serum parathyroid hormone (PTH) and 25-hydroxyvitamin D levels, urinary Ca concentration, and
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assessment of renal function.

MANAGEMENT Most early hypocalcemia is asymptomatic and resolves without treatment. Thus, management
is directed at providing adequate calcium (Ca) intake by initiating early feedings, if possible. For infants who require
parenteral nutrition, Ca is added to the solution as 10 percent Ca gluconate (500 mg/kg, 50 mg/kg of elemental
calcium) per day and given as a continuous infusion. If parenteral Ca infusion is continued for more than 48 hours,
additional phosphorus (P) also must be provided based on serum phosphorus measurements.
Treatment also should be directed against any underlying disease, if possible. Examples include hypomagnesemia,
hyperphosphatemia, and vitamin D deficiency (See 'Correction of hypomagnesemia' below and 'Hyperphosphatemia'
below and 'Vitamin D insufficiency' above.). For the last disorder, we give the vitamin D analogue calcitriol and
monitor serum Ca levels at least weekly.
Symptomatic infants Infants with signs of hypocalcemia, including severe neuromuscular irritability or seizures,
are treated with 10 percent calcium gluconate (100 mg/kg or 1 mL/kg IV) [18]. The solution is infused over 5 to 10
minutes while the heart rate and infusion site are monitored. The dose can be repeated in 10 minutes if no response
occurs. Alternatively, calcium chloride (20 mg/kg or 0.2 mL/kg) can be given; this preparation is metabolized more
rapidly and may be preferable if it is readily available.
After acute treatment, maintenance Ca gluconate should be added to the intravenous solution. If enteral feedings
are tolerated, we use Ca glubionate (oral administration of 30 to 50 mg/kg per day in four divided doses), although
its high osmolality and sugar content can cause gastrointestinal irritability or diarrhea. Alternatively, 10 percent Ca
gluconate (500 mg/kg per day of the gluconate) can be divided and given in four to six feedings. At present time, Ca
glubionate is not readily available in the United States. Caution should be used in providing calcium carbonate as
an alternative in the newborn period due to the possibility, not tested in clinical studies, that the higher pH of the
neonatal stomach may limit solubility and absorption of the calcium carbonate.
For late hypocalcemia, some recommend the use of calcitriol as an adjuvant therapy to gastrointestinal absorption
of calcium. We prefer to provide 400 int. units/day of vitamin D3 rather than calcitriol. If calcitriol is used, a dose of
0.08 to 0.1 mcg/kg is provided. This usually is discontinued after one to two weeks.
In a single case report, recombinant parathyroid hormone (PTH) therapy in a 17-day-old infant successfully
corrected hypocalcemia with hypoparathyroidism that was refractory to calcium and calcitriol therapy [31].
However, the long-term effects of PTH therapy are unknown and further studies are needed to determine whether
recombinant PTH is efficacious and safe in neonates before this intervention can be recommended.
Risks of calcium infusion Intravenous infusion of Ca gluconate is associated with risks that must be
weighed against the benefits of treatment [32]. Risks include bradyarrhythmias that can result from rapid elevations
in serum Ca concentration, and extravasation into subcutaneous tissues, resulting in necrosis and subcutaneous
calcifications. Hepatic necrosis can be caused by infusion through an umbilical venous catheter if the tip is in a
branch of the portal vein.
Ca should not be infused into an umbilical artery catheter because arterial spasm may result, potentially
compromising intestinal blood flow.
Correction of hypomagnesemia When hypocalcemia is associated with hypomagnesemia, correction of the
hypocalcemia requires correction of the hypomagnesemia. We treat with 50 percent magnesium sulfate solution
(500 mg or 4 mEq/mL). Magnesium sulfate (25 to 50 mg/kg or 0.2 to 0.4 mEq/kg per dose Q12h, IV over at least
two hours or IM) is given until the serum magnesium concentration is greater than 1.5 mg/dL (0.62 mmol/L). The
magnesium concentration is measured before each dose. One or two doses usually is adequate to achieve normal
levels. We avoid rapid intravenous infusions that may cause arrhythmias.
Hyperphosphatemia Infants with hyperphosphatemia are fed a diet high in calcium and low in phosphorus.
Human milk is preferable; if it is not available, we use a formula with low phosphorus content such as Similac PM
60/40 or Good Start. We also provide oral calcium supplements
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Serum concentrations of Ca and P improve within three to five days after starting therapy. We discontinue Ca
supplements gradually after one week, and switch the infant to routine formula after two to four weeks.
SUMMARY Hypocalcemia is a common metabolic problem in newborns.
In the neonate, hypocalcemia is defined by birth weight (BW). In infants with BW greater than 1500 g,
hypocalcemia is defined as a total serum calcium (Ca) concentration less than 8 mg/dL (2 mmol/L) or an
ionized fraction of less than 4.4 mg/dL (1.1 mmol/L). In very low birth weight premature infants (BW <1500),
hypocalcemia is defined as a total serum Ca concentration less than 7 mg/dL (1.75 mmol/L) or an ionized
fraction of less than 4 mg/dL (1 mmol/L). (See 'Definition' above.)
Causes of hypocalcemia are classified based upon their time of onset. Etiologies of early hypocalcemia
(occurs in the first two to three days after birth) include prematurity, maternal diabetes, birth asphyxia, and
intrauterine growth restriction. (See 'Early hypocalcemia' above.)
Late hypocalcemia usually occurs at the end of the first week of life, but may occur earlier after the second or
third day after birth. Causes of late hypocalcemia include hypoparathyroidism and high phosphate intake.
(See 'Late hypocalcemia' above.)
Most infants with hypocalcemia are asymptomatic. If symptomatic, neuromuscular irritability is the most
common sign with jitteriness and muscle jerking. Less common findings include seizures, and rarely
laryngospasm, wheezing, or vomiting. (See 'Clinical manifestations' above.)
The diagnosis is most commonly made because of the detection of an abnormally low serum Ca value during
routine monitoring. (See 'Diagnosis' above.)
Early hypocalcemia generally resolves without treatment. In asymptomatic infants, management is directed at
providing adequate Ca intake by initiating early feedings, if possible, or parenteral nutrition and correcting any
underlying disorder resulting in a low calcium value. (See 'Management' above.)
In symptomatic patients, parenteral calcium therapy is provided as a 10 percent calcium gluconate solution at
a dose of 100 mg/kg or 1 mL/kg. Further supplementation is provided either parenterally or orally, if enteral
feeds are tolerated. (See 'Management' above.)
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Topic 5060 Version 11.0
Disclosures
Disclosures: Steven A Abram s, MD Grant/Research/Clinical Trial Support: Mead-Johnson, Nutrition
[Pediatric Nutrition (Infant formulas)]. Consultant/Advisory Boards: MilkPrep [dairy products (fluid milk)].
Joseph A Garcia-Prats, MD Nothing to disclose. Joseph I Wolfsdorf, MB, BCh Nothing to disclose.
Melanie S Kim , MD Nothing to disclose.
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for references
to be provided to support the content. Appropriately referenced content is required of all authors and
must conform to UpToDate standards of evidence.
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