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Dr. Nicolette du Plessis Department Paediatrics University of Pretoria

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Presentation on theme: "Dr. Nicolette du Plessis Department Paediatrics University of Pretoria"— Presentation transcript:

1 Dr. Nicolette du Plessis Department Paediatrics University of Pretoria
Hypocalcemia Dr. Nicolette du Plessis Department Paediatrics University of Pretoria

2 Introduction Pathophysiology Etiology Diagnostic approach Management principles

3 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

4 Calcium homeostasis Regulation of parathyroid function by calcimimetic compounds E. Nemeth,

5 Introduction to Anatomy and Physiology, http://ncwcbio101. wordpress

6 Pathophysiology Ionized calcium is affected by: Albumin Blood pH
Serum phosphate Serum magnesium Serum bicarbonate Exogenous factors Citrate / free fatty acids (TPN)

7 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

8 Symptoms and signs of hypocalcemia
Neuromuscular irritability Paresthesias Laryngospasm / Bronchospasm Tetany Seizures Chvostek sign Trousseau sign Prolonged QTc time on ECG

9 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.

10 Signs & Symptoms: A 2-in-1 Reference for Nurses, Copyright © 2007 Lippincott Williams & Wilkins,

11 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

12 Long QT interval with normal T waves
Prolongation of the ST segment with little shift from the baseline

13 History that suggests hypocalcemia
Newborns (can be unspecific) Asymptomatic Lethargy Poor feeding Vomiting Abdominal distention Children Seizures Twitching Cramping Laryngospasm

14 Neonatal hypocalcemia:
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

15 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)

16 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

17 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),

18 Synthesis / secretion Autoimmune
APECED (autoimmune polyendocrinopathy- candidiasis-ectodermal dystrophy syndrome) Hypoparathyroidism Primary adrenal insufficiency Chronic mucocutaneous candidiasis

19 Synthesis / secretion Acquired Thyroid surgery Parathyroidectomy
Iron deposition with chronic transfusions Wilson’s disease Gram negative sepsis, toxic shock, AIDS ? Macrophage-generated cytokines

20 Pseudohypoparathyroidism
Target organ insensitivity to PTH (bone / kidney) Hypocalcemia Hyperphosphatemia Elevated PTH

21 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) Albright’s hereditary osteodystrophy

22 Albright’s Short stature & limbs Obesity Round, flat face
Short 4e/5e metacarpals Archibald sign Brachydactyly Potter's thumb Eye problems IQ problems Basal ganglia calcifications

23 Pseudopseudohypoparathyroidism
Phenotype of Albright’s NORMAL serum calcium NO PTH resistance Paternal GNAS1 gene mutation

24 Pseudohypoparathyroidism
Type 1b Hypocalcemia, no phenotypic abnormality AD, maternal transmission Type 1c Looks like type 1a Type 2 No features of Albright’s

25 PTH target tissues only
PHP Ia  PHP Ib  PHP II  PPHP Albright’s phenotype  - + Serum calcium  NL Response to PTH cAMP NL  Response to Phosphorus ()NL Hormone Resistance  All hormones  PTH target tissues only  None Molecular defect  Gsa  ?PTH R  Unknown  Gsa

26 Hypovitaminosis D Decrease intake or production Increased catabolism
Decrease 25-hydroxylation by liver Decrease 1-hydroxylation by kidney

27 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

28 Magnesium is required for PTH release
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

29 Primary Secondary Hypomagnesemia Autosomal recessive
Present at 1 month age with seizures Secondary Intestinal absorption vs renal excretion

30 Pancreatitis Citrated products Hungry bone syndrome Hyperphosphatemia
Other Pancreatitis Citrated products Hungry bone syndrome Hyperphosphatemia Fluoride poisoning

31 Following parathyroidectomy
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

32 Total and ionized calcium Magnesium Phosphate UKE and s-glucose PTH
Workup - blood Total and ionized calcium Magnesium Phosphate UKE and s-glucose PTH Vitamin D metabolite Urine-CMP and –creatinine S-ALP

33 Workup - imaging CXR Ankle and wrist XR

34 Karyotyping and family screening
Workup - other ECG Malabsorption workup Karyotyping and family screening

35 Management 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

36 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

37 Treatment of hypocalcaemia
Symptomatic hypocalcaemia 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

38 Treatment of hypocalcaemia
Symptomatic hypocalcaemia 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

39 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

40 References Acknowledgement: Dr. Ida van Biljon
Zalman et al. Treatment of hypocalcemia. May 2008. Zalman et al. Diagnostic approach to hypocalcemia. May 2008. Gernter JM. Disorders of calcium and phosphorus homeostasis. Pediatr Clin North Am. Dec 1990; 37(6): Lorraine a et al. Hypocalcemia: Diagnosis and Treatment. Metabolic diseases. Sept 2002. Jeha GS et al. Etiology of hypocalcemia in infants and children. May 2008. Acknowledgement: Dr. Ida van Biljon Consultant Paediatric Nephrology Department Paediatrics and Child Health Steve Biko Academic Hospital

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