Hypocalcemia

Hypocalcemia
Introduction
Pathophysiology
Etiology
Diagnostic approach
Management principles
Introduction
Calcium is the most abundant mineral in the

body.
In pediatric ICU, hypocalcemia has higher

mortality then normocalcemia.
We are interested in ionized calcium levels
Calcium homeostasis
Regulation of parathyroid function by calcimimetic compounds

E. Nemeth, http://www.ndt-educational.org/nemethslide.asp
Introduction to Anatomy andPhysiology,

http://ncwcbio101.wordpress.com/2008/11/23/14-introduction-to-anatomy-and-
Pathophysiology
Ionized calcium is affected by:
Albumin
Blood pH
Serum phosphate
Serum magnesium
Serum bicarbonate
Exogenous factors
Citrate / free fatty acids (TPN)
Why do we need it?
Calcium messenger system regulates cell

function
Activates cellular enzyme cascades
Smooth muscle and myocardial contraction
Nerve impulse conduction
Secretory activity of exocrine glands
Symptoms and signs of hypocalcemia
Neuromuscular irritability
Paresthesias
Laryngospasm / Bronchospasm
Tetany
Seizures
Chvostek sign
Trousseau sign
Prolonged QTc time on ECG
Tetany is not caused by increased excitability

of the muscles.
Muscle excitability is depressed
hypocalcemia impedes ACh release at NM

junctions
However, the increase in neuronal excitability

overrides the inhibition of muscle contraction.
Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright 2007 Lippincott
Williams & Wilkins, www.wrongdiagnosis.com/bookimages/14/4721.1.png
Trousseau sign:
(very uncomfortable and
painful)
A blood pressure cuff is

inflated to a pressure
above the patients systolic
level.
Pressure is continued for
several minutes.
Carpopedal spasm:
* flexion at the wrist
* flexion at the MP joints
* extension of the IP joints
* adduction
thumbs/fingers
Long QT interval with

normal T waves
Prolongation of the ST
segment with little
shift from the baseline
History that suggests hypocalcemia
Newborns (can be unspecific)
Asymptomatic
Lethargy
Poor feeding
Vomiting
Abdominal distention
Children
Seizures
Twitching
Cramping
Laryngospasm
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
Etiology
Late neonatal hypocalcemia
Exogenous phosphate load

Phosphate-rich
formulas / cows milk
Magnesium deficiency
Transient hypoparathyroidism of newborn
Hypoparathyroidism
Gentamycin (24 hourly dosing schedule)
Etiology
Infants
and children
Hypoparathyroidism
Impaired synthesis / secretion

Loss/ lack of PTH tissue or defective synthesis
Primary or acquired conditions
Defective calcium sensing receptor
End organ resistance to PTH
(pseudohypoparathyroidism)
Hypovitaminosis D (MUCH MORE COMMON)
Hypomagnesemia
Other
Synthesis / secretion of PTH

Genetic
Autosomal dominant
Autosomal recessive
X-Linked
HDR (hypoparathyroidism associated with
sensorineural deafness and renal dysplasia)
DiGeorge's syndrome
Mitochondrial disorders:
MELAS
(mitochondrial encephalopathy, lactic

acidosis and stroke-like episode),
Synthesis / secretion
Autoimmune
APECED (autoimmune
polyendocrinopathy-candidiasisectodermal dystrophy syndrome)
Hypoparathyroidism
Primary adrenal insufficiency
Chronic mucocutaneous candidiasis
Synthesis / secretion
Acquired
Thyroid surgery
Parathyroidectomy
Iron deposition with chronic transfusions
Wilsons disease
Gram negative sepsis, toxic shock, AIDS
? Macrophage-generated cytokines
Pseudohypoparathyroidism
Target
organ insensitivity to PTH

(bone / kidney)
Hypocalcemia
Hyperphosphatemia
Elevated PTH
Pseudohypoparathyroidism (PHP)
GNAS1
gene mutations intracellular
signals
Expression in tissues either paternally /
maternally determined
Example: renal expression is maternal
Type
1a PHP
AD (maternal transmission)
Albrights hereditary osteodystrophy
Albrights
Short stature &

limbs
Obesity
Round, flat face
Short 4e/5e
metacarpals
Archibald sign
Brachydactyly
Potter's thumb
Eye problems
IQ problems
Basal ganglia
calcifications
Pseudopseudohypoparathyroidism
Phenotype of
Albrights
NORMAL serum
calcium
NO PTH resistance
Paternal GNAS1
gene mutation
Pseudohypoparathyroidism
Type
1b
Hypocalcemia, no phenotypic
abnormality
AD, maternal transmission
Type
Looks like type 1a
Type
1c
2
No features of Albrights
Albrights
phenotyp
e
Serum
calcium
Response
to PTH
cAMP
Response
to
Phosphor
us
PHP Ia
PHP Ib
PHP II
PPHP
NL
NL
()NL
NL
Hormone
All
PTH target PTH target
Resistanc hormones
tissues
tissues
None
Hypovitaminosis D
Decrease
intake or production
Increased
catabolism
Decrease
25-hydroxylation by liver
Decrease
1-hydroxylation by kidney
Delayed closure of
fontanels
Bossing
Craniotabes
Delayed eruption of teeth
Rickety rosary
Pectus carinatum
Harrison sulcii
Splaying of distal ends of
long bones bones
Hypotonia
Weakness
Growth retarded
Recurrent chest infections
Hypomagnesemia
Magnesium
is required for PTH
release
May also be required for effects on
target organs
Mechanisms:
End-organ unresponsiveness to PTH

Impaired release of PTH
Impaired formation of 1,25-vitamin D3
Hypomagnesemia
Primary
Autosomal recessive
Present at 1 month age with seizures
Secondary
Intestinal absorption vs renal excretion
Other
Pancreatitis
Citrated
Hungry
products
bone syndrome
Hyperphosphatemia
Fluoride
poisoning
Other
Hungry
bone syndrome
After
prolonged period of calcium

absorption
Rebound phase
Avid uptake of calcium by bone
Parallel uptake of magnesium by
bone
Following
parathyroidectomy
Workup - blood
Total
and ionized calcium

Magnesium
Phosphate
UKE and s-glucose
PTH
Vitamin D metabolite
Urine-CMP and creatinine
S-ALP
Workup - imaging
CXR
Ankle
and wrist XR
Workup - other
ECG
Malabsorption
workup
Karyotyping and family screening
Management
1.
2.
3.
4.
Dependent on the underlying cause

and severity
Administration of calcium alone is only
transiently effective
Mild asymptomatic cases: Often
adequate to increase dietary calcium
by 1000 mg/day
Symptomatic: Treat immediately
Treatment of hypocalcaemia
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
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) supplementation
100 mg/kg/dose 4 hourly per os
Hypocalcaemia in older children
Same dose IV as for neonates

More often require continuous infusion
Oral supplementation 50 mg/kg/24 hr elemental Ca
Ca binds with phosphate in gut Ca absorption

Advantage in conditions with s-phosphate
Renal failure
Hypoparathyroidism
Tumor lysis
Most need Vit D supplementation

Hypocalcemia

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Hypocalcemia

Calcium is the most abundant mineral in the

In pediatric ICU, hypocalcemia has higher

We are interested in ionized calcium levels

Regulation of parathyroid function by calcimimetic compounds

Introduction to Anatomy andPhysiology,

Ionized calcium is affected by:

Citrate / free fatty acids (TPN)

Why do we need it?

Calcium messenger system regulates cell

Activates cellular enzyme cascades

Smooth muscle and myocardial contraction

Nerve impulse conduction

Secretory activity of exocrine glands

Symptoms and signs of hypocalcemia

Prolonged QTc time on ECG

Tetany is not caused by increased excitability

Muscle excitability is depressed

hypocalcemia impedes ACh release at NM

However, the increase in neuronal excitability

A blood pressure cuff is

Long QT interval with

History that suggests hypocalcemia

Newborns (can be unspecific)

Early neonatal hypocalcemia (48-72

Late neonatal hypocalcemia

Exogenous phosphate load

formulas / cows milk

Transient hypoparathyroidism of newborn

Gentamycin (24 hourly dosing schedule)

Impaired synthesis / secretion

Synthesis / secretion of PTH

(mitochondrial encephalopathy, lactic

organ insensitivity to PTH

gene mutations intracellular

Short stature &

Looks like type 1a

is required for PTH

End-organ unresponsiveness to PTH

Intestinal absorption vs renal excretion

prolonged period of calcium

and ionized calcium

Dependent on the underlying cause

IV Calcium should only be given with close monitoring

Tissue necrosis/calcification if extravasates

Stop infusion if bradycardia develops

Avoid complete correction of hypocalcaemia

Early neonatal hypocalcaemia

Neonates: Ca gluconate:10 mg/kg (1 ml/kg of 10%

Treat prior to Ca administration

Start oral Calcium as soon as possible

Late neonatal hypocalcaemia

Associated with S-phosphate

Hypocalcaemia in older children

Same dose IV as for neonates

Ca binds with phosphate in gut Ca absorption

Most need Vit D supplementation

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