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
S – Ghami MD
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 .
Late onset → occurs after the first 4 days of life.
I-In preterm infants:
The frequency of hypocalcemia varies inversely with Birthweight & Gestational age.
Many LBW infants & nearly all ELBW infants exhibit t.ca<7mg/dl by day 2.
The majority of fetal ca accretion occurc in the third trimester.
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.
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.
Occurs after the first 4 days of life.
a) relative resistance of immature kidney to PTH →
b) Renal retention of phosphorus → hypocalcemia.
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 .
Magnesium deficiency inhibits the secretion of PTH → hypocalcemia.
Mg ↓ a-primary → ca↓
b-Transient → ca ↓
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↑
Renal magnesium wasting 2-Aminoglycosides
caused by administration of : 3-Amphotericin B
5-Diuretic phase of acute
Hypoparathyroidism associated with excess phosphorus intake, is the most common cause of late neonatal hypocalcemia.
Characteristics of hypoparathyroidism:
ca ↓ & p ↑ & normal renal function , PTH↓.
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.
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.
Cessation of therapy → return to normal calcium levels.
Most infant in early onset are asymptomatic , in contrast , in late onset may presents hypocalcemic seizures.
Clinical signs of hypocalcemia :
Lethargic & eat poorly
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.
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.
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.
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
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.
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.
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.
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.
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.