Medical Affairs

Department of Pediatrics
Clinical Practice Guideline

HYPOCALCEMIA IN CHILDREN

Document #

PEDS-ENDO # 002

Date CPG Formulated December 2007

Feb 2012
Date last CPG
Reviewed
Next Review Date

Jan 2014

IIntroduction:
In humans, 99 % of the total body calcium is stored in the bones in the form of
hydroxyapatite. The remaining 1% is distributed between the extra-cellular and intracellular compartments. Serum calcium exists in three forms; 50% ionized, 40% protein
bound, and 10% anion bound (phosphate, citrate, carbonate, etc.).
In addition to its important role in bone mineralization, calcium facilitates several other
functions such as:
Muscles contraction and relaxation
Nerves conduction
Cellular membranes integrity
Blood coagulation
IICalcium homeostasis:
Normocalcemia state is maintained by balancing calcium intake (adequate nutritional
calcium content and normal calcium absorption), and calcium excretion. This balance is
achieved through the interactive effects of the calcium sensing receptors (CaSR), PTH, and
vitamin D. CaSR detects the early changes in the level of serum ionized calcium and as a
result to that, it suppresses or stimulates PTH secretion when calcium level increases or
decreases, respectively. PTH increases calcium level by different mechanisms:

Stimulates 1-alpha hydroxylase in the kidney which activates 25-OH vitamin D

to 1,25 (OH)2 vitamin D. Active vitamin D stimulates intestinal calcium absorption.

Increases renal calcium re-absorption (and phosphorus excretion).

Increases bone resorption.

IIIClinical presentation:
Hypocalcemia, especially in the mild form, might be asymptomatic, but commonly, it
presents with one or more of the following symptoms:
Fatigue/irritability, poor feeding
Muscle cramping, spasm, or tetany
Peri-oral tingling,
Numbness of the fingers or toes
Positive Chvostek and/or Trousseau signs.
Apnea, Seizure.
IVCauses of hypocalcemia:
1- Decreased calcium absorption:
Nutritional calcium deficiency.
Vitamin D deficiency
Steroids
Hyperphosphatemia
Intestinal malabsorption
2- Increased calcium excretion:
Deficiency of or resistance to PTH.
Loop diuretics.
3- Increase calcium deposition in the bones (hungry bones syndrome).

VCauses of neonatal hypocalcemia:

Neonatal hypocalcemia is classified, per the timing of onset, into early (the first 72 hours after birth)
and late (after 3 days of birth):
I-

Early neonatal hypocalcemia:

The most common causes are prematurity, low birth weight and neonatal stress and asphyxia, but it can
also be secondary to maternal disorders such as diabetes mellitus and hyperpatahyroidism.
IILate neonatal hypocalcemia:
Hypocalcemia in this age group can be secondary to hypoparathyroidism, hypomagnesemia, vitamin D
deficiency, or increased phosphorus intake, such as that associated with formula feeding, which can be
exacerbated by the limited renal excretion of phosphate.
Due to the subtle clinical presentation, serum calcium should be checked in any infant with risk factor/s
or clinical symptoms suggestive of hypocalcemia:
1- Premature infants.
2- Infants of diabetic mother.
3- Maternal history of hyperparathyroidism or other calcium disorders, this should include
prolonged maternal treatment with MgSO4.
4- Severe perinatal asphyxia
5- Neonatal seizure/tetany
6- Congenital bone deformities.
VI.
Diagnosis of Hypocalcemia:
It is crucial when assessing patient with hypocalcemia to draw labs before the correcting
treatment, if possible, and to look at the relevant variables all together. The figure below
summarized the causes of hypocalcemia in relation to the PTH level:

Calcium-PTH Normogram. From Parathyroid.com

VII.

Diagnostic Algorhithm:

Hypocalcemia

Check (before correcting Ca level):

-Detailed H&P

-Urine Ca/Cr. -Phos.

- 25 (OH)D -Alk. P.
-PTH
-Mg

PTH

Phos

Phos
Urine Ca/Cr

2 Hyperparathyroidism

Vitamin D deficiency
Vitamin D Resistance

Meds
(Steroids, diuretics)

1: Primary
2: Secondary

Normal or PTH

1 Hypoparathyroidism

PHP?

Mg

GNAS 1 mutation

Phos (neonates)

PTH: Parathyroid hormone.

PHP: Pseudohypoparathyroidism

*Ionized calcium should be assessed in the light of acid-base status (calcium binding is suppressed
during acidosis and increases during alkalosis).
* Corrected calcium (mg/dL) = measured total calcium (mg/dL) + 0.8 (4-measured albumin g/dL)
* Consider doing renal US for nephrocalcinosis if urine Ca/Cr ratio is high.
* Karyotyping (for 22q11 mutations) and CXR to assess thymic shadow if DiGeorge is suspected.

VI. Treatment:
Patient should be NPO if presents with seizure.
Acute management:
o IV calcium gluconate 10% at 10-20 mg/kg elemental calcium (1-2ml/kg) over
10-20 minutes WITH CARDIAC MONITORING.
o IV calcium infusion at 50mg/kg/day of elemental calcium
o Calcitriol 0.5 mcg daily
o Check calcium level (ionized is preferred) every 6 hours
o Check IV site every 30 minutes for tissue necrosis
o NEVER USE the scalp veins for calcium infusion.
Maintenance treatment:
o Switch from IV to oral calcium when ionized calcium is 1.0 mmol/L, or
corrected calcium is 2.0 mmol/L.
o Oral calcium can be given as clacium globionate (elemental calcium is 6.5%,
oral syrup contains 23 mg of elemental calcium in each 1 ml) or carbonate (40%
elemental), starting between 50-100mg/kg/day elemental calcium.
o Patient on formula feeding should be switched to a low phosphate formula if
they have hyperphosphatemia on presentation.
o Calcium monitoring can be done 1-2/day once on oral supplementation.
o Calcitriol can be switched to ergocalciferol or cholecalciferol if no underlying
kidney or liver disease.
o Patient can be discharged home as soon as PO is well-tolerated, and corrected
calcium is maintained >2.0 mmol/L.

References:
1- Kovacs CS, Kronenberg HM : Maternal-fetal calcium and bone metabolism during pregnancy,
puerperium and lactation. Endoecr Rev 18:832, 1997
2- Barnes-Powell LL. Infants of diabetic mothers: the effects of hyperglycemia on the fetus and
neonate. Neonatal Netw. Sep-Oct 2007;26(5):283-90.
3- Williams Textbook of Endocrinology, 12th Edition

Calciu
m
reabso
Approval:
Signature

Name
Head of the Department: Dr. Aiman Rahmani

Other involved Dept

Head/Division Chief

Dr. Walid Kaplan

Dr. Suha Hadi

A/Chief Medical Officer
& division Chief

Dr.Walid Kaplan

Reviewed By Johns Hopkins Member:

Yes
No
Johns Hopkins Member

Date