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

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

1 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, anatomy-and-physiology/

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 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 PHP Ia PHP Ib PHP II PPHP Albright’s phenotype Serum calcium   NL Response to PTH cAMP   NL Response to Phosphorus   (  )NL 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 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 Hypomagnesemia  Primary  Autosomal recessive  Present at 1 month age with seizures  Secondary  Intestinal absorption vs renal excretion

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

31 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 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 Workup - other  ECG  Malabsorption workup  Karyotyping and family screening

35 Management 1. Dependent on the underlying cause and severity 2. Administration of calcium alone is only transiently effective 3. Mild asymptomatic cases: Often adequate to increase dietary calcium by 1000 mg/day 4. 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  Zalman et al. Treatment of hypocalcemia. May  Zalman et al. Diagnostic approach to hypocalcemia. May  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  Jeha GS et al. Etiology of hypocalcemia in infants and children. May A cknowledgement: Dr. Ida van Biljon Consultant Paediatric Nephrology Department Paediatrics and Child Health Steve Biko Academic Hospital


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