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Neonatal Hypocalcemia & Hypomagnesemia. S – Ghami MD. Neonatal Hypocalcemia. Hypocalcemia is a common metabolic problem in newborns. Hypocalcemia in full-term infants or preterm infants >1500 gr: Ca 2+ <4.4 mg/dl Total Ca<8 mg/dl Hypocalcemia in preterm infants<1500 gr Ca 2+ <4mg/dl

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Neonatal Hypocalcemia

Hypocalcemia is a common metabolic problem in newborns.

Hypocalcemia in full-term infants or preterm infants >1500 gr:

Ca2+ <4.4 mg/dl

Total Ca<8 mg/dl

Hypocalcemia in preterm infants<1500 gr

Ca 2+ <4mg/dl

Total Ca <7 mg/dl

40%Ca is bound to albumin - 50% as ionized Ca (free)-

10% as ca complexed to serum anions .


Early onset → occurs during the first 4 days of life


Late onset → occurs after the first 4 days of life.

Early onset hypocalcemia

I-In preterm infants:

The frequency of hypocalcemia varies inversely with Birthweight & Gestational age.

Many LBW infants & nearly all ELBW infants exhibit<7mg/dl by day 2.

The majority of fetal ca accretion occurc in the third trimester.

Etiology of Hypocalcemia in preterm infants:

1) Abrupt interruption of the placantal supply .

2) Low intake of ca by nutrition.

3) Insufficient release of PTH.

4) Rise in calcitonin secretion.

5) In VLBW infants renal Na excretion ↑ → calciuric losses.

6) Hypoalbuminemia.

Hypocalcemia is temporary 1-3days normal
  • ↑Ca intake with feeding.
  • ↑Renal phosphorus excretion.
  • ↑ parathyroid function.
II-Maternal Diabetes:
  • In IDMS, hypocalcemia → related to hypomagnesemia .
  • In the diabetic mother → increased urinary Mg losses → fetal Mg↓ → fetal & neonatal hypoparathyroids.
  • Prematurity.
  • Asphyxia.
III-perinatal Asphyxia:
  • Decreased Ca intake .
  • Increased endogenous phosphorus load , resulting from reduction of GFR.
  • Increased calcitonin concentration.
  • Correction of acidosis → hypocalcemia.
IV- Maternal Anticonvulsants:

Phenobarbital & diphenylhydantoin → increased hepatic catabolism of vitamin D → vitamin D ↓

The infant of epileptic mothers → neonatal hypocalcemia

Terapy with vitamin D supplementation (1000 Iu/day ) during pregnancy.

Late onset Hypocalcemia:

Occurs after the first 4 days of life.

1)Phosphate loading


a) relative resistance of immature kidney to PTH →


b) Renal retention of phosphorus → hypocalcemia.

c) Low GFR → limiting to excrete the phosphorus load

d) P↑ → increased ca bone deposition → ca↓

Late hypocalcamia observed in infants fed cow`s milk and formula fed infants, → ca 2+ ↓and P↑ in first week of life than those of breast fed infants .

2- Hypomagnesemia :

Mg<0.8 mg/dl

Magnesium deficiency inhibits the secretion of PTH → hypocalcemia.

Mg ↓ a-primary → ca↓

b-Transient → ca ↓

a- primary hypomagnesemia:

It is a autosomal recessive disorder → hypocalcemia & sezures.

That cannot be controlled with anticonvulsants and/or calcium gluconate.


Mg< 0.8 mg/dl (1.6-2.8 mg/dl) & PTH↓

Treatment:with magnesium → PTH↑ → ca↑


b- Transient neonatal hypomagnesemia

  • Mg< 0.8-1.4 mg/dl


Renal magnesium wasting 2-Aminoglycosides

caused by administration of : 3-Amphotericin B

4-U.T obstruction

5-Diuretic phase of acute

renal failure

  • low serum Mg levels
  • high urinary Mg excretion
  • Hypokalemia

Treatment :

  • in many infants → incareased serum Mg level spontaneously (as the serum ca level return to normal) after the administration of ca supplements and normocalcemia.
3-Neonatal Hypoparathyroidism:

Hypoparathyroidism associated with excess phosphorus intake, is the most common cause of late neonatal hypocalcemia.

Characteristics of hypoparathyroidism:

ca ↓ & p ↑ & normal renal function , PTH↓.

a- Digeorge syndrome(DGS)

hypoplastic or absence of parathyroid gland and thymic gland.

X linked or autosom recessive


ca ↓ (tetany or seizures) + facial

Malformation (small mouth, submucous cleft palate, low set ears,…..) + cardiac defects.

b-Matenal hyperparathyroidism (benign adenoma)

increased maternal ca concentration → fetal hypercalcemia→ suppression of fetal & neonatal PTH secretion hypocalcemia.

This condition spontaneously in days to week,

therapy with ca & 1.25(OH)2 D3 or both.



4) Other causes:
  • Bicarbonate infusion → metabolic alkalosis → decreased ca 2+
  • Transfusion with citrated blood → decreased ca 2+
  • Lipid infusions → decreased ca 2+.
  • Phototherapy →decreased melatonin secretion → increased ca uptake by bone.
  • Acute renal failure →hyperphosphatemia .
  • Any disorder of vitamin D metabolis →hypocalcaemia .
  • Furosemide & xanthine therapy → calciuresis + nephrolithiasis.
  • Rotavirus infection → hypocalcaemia.

Cessation of therapy → return to normal calcium levels.

Clinical Manifestation:

Most infant in early onset are asymptomatic , in contrast , in late onset may presents hypocalcemic seizures.

Clinical signs of hypocalcemia :



Lethargic & eat poorly


Abdominal distention

a-schedule for monitoring ca levels:
  • 1- in infants <1000gr or who are ill, ca is measured at:12,24,48 h of age
  • in infants 1000-1500 gr ,ca is measured at:

24 and 48 h of age .

continue monitoring until 96 h .

3- in healthy asymptomatic premature infants, birth weight >1500 g and healthy IDMs who begin milk feeding on the first day, do not routinely monitor.

4-sick or stressed infants, ca is measured at: 12-24 and 48 hour of age

5-if the infants does no respond to treatment:

Mg, P, PTH, 25-hydroxy-VD levels, urinary ca, renal function, cxray, should be measured.

b-In ECG Qt interval>0.4"

Do not recommend use to screen for hypocalcemia.


I-treatment of early onset hypocalcemia:

1-Hypocalcemic preterm infants who have no symptoms and are well newborns donot require specific treatment, only initiating early feeling ,if possible, because hypocalcemia resolve spontaneously by day 3.

2- If the serum ca level<6.5 mg/dl (in VL Bw newborns) → continuous ca infusion is recommended.

a- does:500 mg/kg ,45 mg/kg /day of elemental ca (5cc/kg/day of ca gluconate 10%,1cc= 9 mg elemental ca ),until sustaining serum ca level (7-8 mg/dl)

b- bolus infusions are ineffective and hazardous.

c- If parenteral ca infusion is continued for more than 48h , additional P also must be provided.

3-prevent the onsot of hypocalcemia for newborns who are ill (eg.severe RDS , asphyxia, septice shock, PPHN,….) to maintain a total ca>7.0 mg/dl

II-treatmnt of symptomatichypocalcemicinfants, seizures, apnea, severe jitteriness,(serum ca level< 5.0 mg/dl):

1- treatment with 10% ca gluconate (100 mg/kg or 1cc/kg Iv or 9-18 mg of elemental ca/kg) by interavenous infusion over 5-10 minutes.

a. monitor heart rate and the infusion site.

b. repeat the dose in 10 minutes if there is no clinical response.

c. after acute treatment, maintenance ca gluconate. Should be added to the intravenous solution.

d. If enteral feeding are tolerated , ca gluconate 10% (500 /kg/duy) can be given in four – six feedings.

e. For late hypocalcemia as a consequence of the hyperparathyroidism (Digeorge syndrome) may require both ca and vitamin D (calcitriol) to maintain normocalcemia.

Risks of calcium infusion:

1-Bradyarrhythmias rapid elevations in serum ca concentration.

2-extravasation into subcutaneous tissues → necrosis and subcutaneous calcification.

3-Hepatic necrosis infusion through an umbilical

venous catheter , if the tip is in a branch of portal vein.

4-Intestinal necrosis rapid infusion by umbilical

artery and arterial spasms.

result from

Caused by

result from

2-symptomatic hypocalcemia unresponsive to ca therapy


therapy with 50% magnesium sulfate solution(500 mg or 4meg/ml)

Dose:25-50mg/kg or 0.2-0.4 meq/kg/dose Iv or IM.


Infant should be fed a diet high in calcium and low in phosphorus.

Such as human milk or formula with low phosphorus, or oral ca supplements.

3- vitamin D deficiency

Secondary to maternal vitamin D deficiency (anticonvulsant therapy).

Treatment with 1000-2000 Iu /day of oral vitamin D +40 mg/kg/day of elemantal ca for 4 weeks.