Hypocalcemia in the newborn

Dr Theresa L Mendonca

Introduction

 During the 3rd trimister ,calcium is transferred from mother to the fetus by active transport
,as demonstrated high level of serum concentration in cord blood compared to maternal
serum.

 Once the baby is born calcium level depends on PTH secretion, dietary calcium ,renal
calcium reabsorption ,skeletal calcium stores and vitamin D

 Hence after delivery calcium level starts to decreasing and reaches 7.5-8.5 mg/dl. In
healthy term babies by day of 2.

 The drop in postnatal serum calcium is related to hyperparathyroidism, abnormality of vit

D metabolism hyper phosphatemia, hypomagnesimia and hypercalcitonemia which
occurs by 12-24 hrs of life.

 PTH levels increase gradually in the first 48 hrs of life and normal level of serum calcium
level is regained by 3rd day of life.

 The efficacy of the intestinal absorption of calcium and the renal handling matures at 2to
4 weeks. This transition phase is responsible for the increased risk of early onset of
hypocalcaemia in high-risk neonates.

Calcium haemostasis in newborn

 Calcium exists in two major forms

A) skeleton(99%) b) extracellular fluid (1%)

Calcium in the extracellular fluid is present in three forms

 A) bound to albumin

 B)Bound to anions like phosporous, citrate, sulfate and lactate

 C)free ionised form

With hypoalbuminemia total calcium concentration will be low

In general plasma calcium level falls by 0.8mg/dl for every 1.0g/dl fall in the plasma
albumin concentration.

Definition

 Hypocalcemia is defined as total serum calcium <7mg/dl or ionised calcium <4mg /dl.

Calcium Haemostasis
 Etiology

 Neonatal hypocalcemia:

Early neonatal hypocalcemia (48-72 hours)

Prematurity

Poor intake, hypoalbuminemia, reduced responsiveness to vitamin D

Birth asphyxia

Delay feeding, increased calcitonin, endogenous phosphate load high, alkali therapy

Infant to diabetic mother

Magnesium depletion → functional hypoparathyroidism → hypocalcemia

IUGR

Premature babies are at increased risk of early neonatal hypocalcemia in the first three days of
life This is due to premature termination of trans placental supply ,exaggeration of the post natal
drop to hypocalcemic level and diminished target organ responsiveness to parathyroid harmone.

Infant of diabetic mother (gestational and insulin dependent) Related to increased calcium
demand of a macrosomic baby

Maternal hypoparathyroidism

Intrauterine hypercalcemia suppressing the parathyroid activity in the fetus resulting in impaired
parathyroid responsiveness to hypocalcemia after birth. Hypocalcemia may be severe and
prolonged.

Perinatal asphyxia

Hypocalcemia related to renal insufficiency ,metabolic acidosis and diminished parathyroid

hormone secretion
 Etiology

Late neonatal hypocalcemia

Exogenous phosphate load

Phosphate-rich formulas / cow’s milk

Magnesium deficiency

Transient hypoparathyroidism of newborn

Hypoparathyroidism

Gentamycin (24 hourly dosing schedule)

Clinical Presentation

 Asymptomatic –early onset of hypocalcemia is usually asymptomatic

 Symptomatic-neuromuscular irritability :myoclonic jerks.jitteriness,exaggertaed

startle,seizures

 They may involve cardiac involvement like tachycardia,heart failure,prolonged QT

interval ,decreased contractibility

Diagnosis

Laboratory –

 otal or ionised serum calcium (total<7mg /dl or ionised <4.0 mg /dl.

ECG –

QoTc>0.2 sec or QTc >0.45sec

(QoTc = QoTcinterval in sec/sqaure root R-Rinterval in sec

QTc= QT interval in seconds /square root R-R interval in secs

 (QT interval is measured from origin of Q wave to end of T wave on ECG .QoT interval
is measured from origin q wave to origin of T wave. )

Treatment of Hypocalcemia

Symptomatic hypocalcaemia

 IV Calcium should only be given with close monitoring

 Should be on cardiac monitor

 Mix with NaCl or 5 % D/W (not bicarbonate/lactate containing solutions)

Risks

 Tissue necrosis/calcification if extravasates

 Calcium can inhibit sinus node ® bradycardia + arrest

 Stop infusion if bradycardia develops

 Avoid complete correction of hypocalcaemia

 With acidosis and ¯ S-Ca – give Ca before correcting acidosis

 If ¯ Mg is cause of ¯ S-Ca – treat and correct hypomagnesaemia

Symtomatic Hypocalcemia

Early neonatal hypocalcaemia

– Neonates: Ca gluconate:10 mg/kg (1 ml/kg of 10% solution) Slowly IV +

monitoring ECG

– Occasionally associated transient hypomagnesaemia

 Treat prior to Ca administration

– Start oral Calcium as soon as possible

 – Early neonatal hypocalcaemia normalizes in 2-3 days

– Oral Ca usually necessary for 1 week

Late neonatal hypocalcaemia

– Associated with S-phosphate

– Decrease phosphate intake

– Give calcium containing phosphate binder

– Oral calcium (gluconate) supplementation100 mg/kg/dose 4 hourly

– Bolus of 2ml/kg/dose diluted 1:1 with 5% dextrose over 10 minuts. ,under cardiac
monitoring

– This should be followed by continuous infusion of 8o mg/kg/day elemental calcium for

48 hrs.

– Calcium infusion should be dropped to 50 % of the original dose for the next 24 hrs. and
then discontinued.

– The infusion may be replaced with oral calcium therapy on the last day . Normal calcium
values should be documented at 48 hrs before weaning the infusion.

– All categories of hypoglycemia should be treated for atleast 72 hrs

Asymptomatic Hypocalcemia

 80 mg /kg/day elemental calcium (8ml /kg/day of 10% calcium gluconate )for 48 hrs. this
may be tapered to 50 % dose for another 24 hrs and then discontinued.

 Neonates tolerating oral feeds are treated with oral calcium.

Patient with increased risk of hypocalcemia

 Pre term Infants (<_32 weeks ), sick neonates of diabetic mothers and those with severe
perinatal asphyxia should receive 40mg/kg/day of 10% calcium gluconate. ) infants
tolerating oral feeds may receive this calcium orally q 6 hrly. For 3 days.

Precaution and side effects of calcium gluconate

 Bradycardia and arrhythmia are known side effects of bolus IV calcium administration
and bolus doses of calcium should be diluted 1:1 with 5% dextrose and given under
cardiac monitoring .

 Hepatic necrosis may occur if the tip of the umbalical venous catheter lies in the branch
of poratal vein (it should be in the inferior vena cava )

 . Umbalical artery catheter should never be used. Accidentaly administration may cause
arterial spasm and intestinal necrosis.

 Skin and subcutaneous tissue necrosis may occur due to extravasation

 Hence IV sites where calcium is being administerd should be checked every 2 hrs to
monitor for extravasation and avoid subcutaneous tissue necrosis