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newborns
Dr. Bhushan
Introduction
Calcium is most abundant mineral in the body and
together with phosphorus form a major inorganic
constituent of bone.
In circulation the amount of calcium and magnesium is
less 1% of their respective total body content.
Total body content of calcium and magnesium in skeleton
are about 99% and 60%respectively.
Hormonal regulation:
Parathyroid- renal hormonal axis:
Parathyroid hormone mobilizes calcium and phosphorus from
bone.
It stimulates calcium reabsorption and inhibits phosphorus
reabsorption by kidney.
Stimulates VIT D3 synthesis which help in intestinal
absorption of ca and phosphorus.
serum Ca rise and phosphorus level normal or decline.
Hypocalcemia
Clinical presentation:
Sign usually non specific.
Apnea
Seizure, Jitteriness
Hyperreflexia.
Stridor
Early onset hypocalcemia: often asymptomatic but may show
apnea or may show abnormalities of cardiac function.
Late onset hypocalcemia: may present as hypocalcemia seizures.
Diagnosis
Early onset hypocalcemia:
Laboratory: total or ionized serum calcium low.
ECG:prolonged QT interval but clinically not useful in
newborn period.
Late onset hypocalcemia:
first line
Serum phosphate
Serum alkaline phosphate
Second line
Serum magnesium
Serum parathormone level
Urine calcium creatinine ratio
Maternal calcium,phosphate,alkaline phosphatase
Asymptomatic
80mg/kg/day for 48 hours
(8ml/kg/day of 10%calcium gluconate)
Symptomatic
Bolus of 2ml/kg calcium gluconate 1:1 diluted with 5% dextrose
over 10 min under cardiac monitoring
Management
If the ionized ca level drop to 0.8mmol/l therapy with
calcium alone is usually adequate but in some cases
Magnesium is also indicated(should receive 2 doses of
0.2ml/kg).
10 %calcium gluconate solution is preferred for IV use.
Dose of elemental ca is 50mg/kg/day
Precaution:
rapid infusion of ca lead to brady arrythmias.
Calcium should only be pushed for treatment of
hypocalcemia crisis and done with careful cardiac
monitoring.
Calcium should not be infuse through umbilical line.
Management :
Management (Ctd..):
Hypocalcemia associated with hyperphosphatemia:
Mostly presenting after day of life 3
Goal of therapy is to reduce renal phosphate load by feeding
human milk or low phosphorus formulas.
Avoid the use of preterm formula, lactose free or other special
formulas.
Increase the oral calcium supplement (20 to 40 mg/kg/day of
elemental calcium).
Gradually wean calcium supplements over 2 to 4 weeks.
Monitor serum calcium and phosphorus level two times
weekly.
Use of vit D in this circumstance not usually necessary and
1000IU daily is used only if serum 25(OH)D level less than
10ng/ml.
Osteopenia of prematurity
Osteopenia is defined as postnatal bone mineralization that is
inadequate to fully mineralize bone.
Occurs most commonly in VLBWs.
CAUSE:
Deficiency of calcium and phosphorus(principal cause).
Vitamin D DEFICINCY.
VLBW
Long term steroids
prolonged parental nutrition
Hypercalcemia
Serum total calcium level more than 11mg/dl and serum ionized
calcium level more than 1.45mmol/l
Severe hypercalcemia: Serum total calcium level more than
16mg/dl and serum ionized calcium level more than 1.8mmol/l
Causes of Hypercalcemia
Extreme prematurity
Hyperparathyroidism
Vit D intoxication
Excessive exogenous calcium administration
Hypophosphatemia
Increase intestinal absorption of calcium
Decease renal calcium clearance.
Williams syndrome
Hyperthyroidism
Thiazide diuretics
Milk alkali syndrome.
Clinical features:
Weakness
Irritability
Lethargy
Seizures
Coma
Vomiting
Polyuria
Polydipsia
renal calculi
Investigations
Blood:
Serum Total and ionized ca
Serum phosphate
Alkaline phosphatase
Total protein ,albumin
BUN
Serum creatinine
25OH VIT D
ECG: SHORT QT interval
X-ray KUB : look for renal calculi
Management
Treat the underlying cause.
Emergency medical treatment: Increase urine output and ca
excretion by giving Furosemide 1mg/kg IV. Volume expansion with
isotonic saline solution( @10-20 ml/kg ).
Low calcium, low vitamin D intake.
Calcitonin
Parathyroidectomy in severe cases.
Magnesium
Hypomagnesaemia
Etiology
Increased urinary loss
1.Diuretics
2.Renal tubular acidosis
Increase GIT loss
1.Malabsorption syndrome.
2.Sever malnutrition
3.Diarrhea
4.Vomiting
Hypercalcemia
Chemotherapy
Endocrine etiologies:
1.Diabetes mellitus
2.Parathyroid hormone disorders
3.Hyperaldosterone states
Decrease intake:
Prolonged parental fluid therapy with magnesium free solution.
Clinical manifestation
Hyperreflexia
Carpopedal spasm
Clonus
Tetany
Investigations
Blood:
Serum magnesium.
Serum total ca and ionized ca.
management
hypermagnesemia
Clinical features:
Depressed deep tendon reflexes
Lethargy
Management:
Stop supplemental magnesium
Diuresis
Calcium supplements