Approach to

hypocalcemia in

childrenDr.Yassin M. Al-saleh

Case scenario 1

8 years old girl presented with history of

vomiting.

Case scenario

History of organophosphorus poisoning (spray

) to hair .

There is history of frequent twitching of the

hand over last one month.

Perinatal, past medical and surgical ,blood

transfusion :unremarkable

Medication: unremarkable

Development: good in school.

Family history: unremarkable for autoimmune

or inherited disease.

On exam:

Not dysmorphic.

no hypo or hyperpigmentation

Wt:75th HT:75th

Vital sign normal

No goitre

Chevostic +ve.

Initial impression :Hypocalcemia

Differential diagnosis Hypoparathyrodism (isolated).

Hypoparathyrodism (APS).

Pseudohypoparathyrodism.

CKD.

Vit d deficiency.(nutritional).

Hypomagnesemia.

kyperventilation

Investigation Biochem: na ,k ,cl WNL

Renal :BUN and creatinine WNL

Ca:1.6 , albumin 38

phosphrus 3, Mg:0.7 WNL

ALK 120 N

PTH: 330 high

Urine for ca: low

Vit d level: 15 ng/dl (20-30)

LFT:WNL. VBG: WNL

Renal US: WNL

impression

Pseudohypoparathyrodism 2B

Treatment:

One alpha or calctriol

Calcium

Hypocalcemia

Normal level of calcium : 2.3-2.7 mmol/l

Hypocalcemia

Decrease inflow of calcium to circulatory

compartment from intestine, bone or

kidney.

Increase excretion from intestine or kidney.

causes of hypocalcemia in children other

Pseudohypoparathyroidis

m classified as type 1

A,B,C , type II

Vitamin D disorders

( nutritional or inherited)

Hungry bone syndrome

Medication ( high mg,

bisphosphonate, Lasix

High phosphate

Pancreatitis

Mal absorption

Hypoparathyroidism

isolated (autoimmune)

part of syndrome (APS1)

complex congenital anomalies like Disgorge,

SSS, barakate syndrome

sporadic or familial

AR or AD

defect in parathyroid gland development

defects in parathyroid hormone synthesis or

secretion

familial hypercalcuric hypocalcemia

Acquired (surgical removal or vascular injury,

storage accumulation like iron, copper

granulomatous diseases or irradiation

History

Symptoms of hypocalcemia

Hx of recurrent infection ( Digeorge), deafness ( barakat), any other endocrine disorders ( APS1 )

Hx of recurrent blood Tx ( iron deposition ).

Hx of previous irradiation or surgery

Hx for Vit D ( diet, sun exposure and prophylaxis vitD

Hx of medication

Family Hx of poly endocrinopathy, nephrocalcinosis, hypoparathyroidism

Physical examination

Well or ill, jaundice, dysmorphology,

hyperpigmentation

Growth parameter

Vital sign

Hand and nail dystrophy (APS1), wide wrist (

Ricket), goiter, oral candidiasis,

CVS murmur

Skin : vitiligo and alopecia

investigation

Bone and renal profile

PTH if low or realtively low

(hypoparathyroidism either congenital or

acquired )

If high PTH either vit D disorders, renal failure

or pseudo hypoparathyroidism

management

In acute hypocalcemia give elemental ca 10-

20 mg/kg ( 1-2 ml/kg ca gluconate) over 10

min, then continuous infusion under cardiac

monitor

After stabilization treat according to the

cause.

Case scenario 2

One month with abnormal movement.

Case scenario 2

Abnormal movement for one day

Active ,feeding well, Perinatal, past medical

and surgical ,blood transfusion :unremarkable

Medication: unremarkable

Development: smile

Family history: unremarkable for autoimmune

or inherited disease.

On exam:

soft dysmorphic. Depressed nasal bridge.

no hypo or hyperpigmentation

Wt:10th HT:10th

Vital sign normal

CVS:murmur

Initial impression :abnormal

movement

Differential diagnosis Hypocalcemia

Hypoparathyrodism,

Pseudohypoparathyrodism.

Vit d deficiency.(nutritional or inherited).

Hypomagnesemia or hypermagnesemia

Hypoglycemia, hyponatremia,

Sepsis, seizure disorder, metabolic disease.

investigation Biochem: na ,k ,cl WNL

Renal :BUN and creatinine WNL

Ca:1.6 , albumin 38

phosphrus 3, Mg:0.7 WNL

ALK 120 N

PTH: normal

Urine for ca: low

Vit d level: 22 ng/dl (20-30)

LFT:WNL. VBG: WNL

ECHO: VSD

FISH: digorge

impression

Hypoparathyrodism

Digorge

The causes of early neonatal

hypocalcemiaPrematurity

Low birth weight

Asphyxia

Infant of diabetic mother

Hypoparathyroidism

Maternal hyperparathyroidism

Maternal intake of calcium

Neonatal jaundice requiring phototherapy

or exchange transfusion

Metabolic or respiratory

alkalosis

Medication: NaHco3,

chelating agent ( like citrate

in blood transfusion,

phosphate, soy milk),

aminoglycosides

Osteopetrosis

The causes of late neonatal

hypocalcemiaHigh phosphate

Low or high mg

Vitamin D disorder

Hypoparathyroidism either transient or permanent

PTH receptor anbnormality

Mitochondrial disorders ( Kearen Sayer syndrome, MELAS

History - Symptoms of hypocalcemia ( seizure, feeding

intolerance etc)

- Prenatal Hx: parity ( multipara), maternal illnesses ( like DM, GDM, hyperparathyroidism, toxemia) , medication ( ca carbonate , mg)

- Perinatal Hx: mode of delivery, term or preterm, birth weight and apgar score

- Postnatal Hx: jaundice, medication (aminoglycoside, NaHco3 etc), blood transfusion, high Po4 formula, sepsis

- Family and social Hx: family member with hypocalcemia, dysmorphic, renal calculi, reckit, seizure disorder, maternal Hx of sun exposure and her diet

Physical examination:

- Well or ill, term or preterm, jaundice,

dysmorphic features

- Growth parameter

- Vital signs ( fever, hypotensive ? sepsis)

- Signs of ricket

- CVS : murmur

Lab Chemistry: BUN & creatinine ( renal failure),

PH alkalosis)

Ca, po4, mg, ALK

Urine for calcium: creatinine ratio

PTH level

Low calcidiol level indicate (maternal low Vit D or

rarely 25 hydroxylase mutation)

Low calcitriol indicate ( hypoparathyroidism, defect

in one alfa hydroxylase or severly compromised

renal failure)

High calcitriol indicate Vit D resistant

Imaging

- Skeletal survey : rickets sign, dysplasia or

osteopetrosis

- Chest X- ray thymic shadow ( disgorge)

management

In acute hypocalcemia give elemental ca 10-

20 mg/kg ( 1-2 ml/kg ca gluconate) over 10

min, then continuous infusion under cardiac

monitor

After stabilization treat according to the

cause.