hypocalcemia & hypercalcemia

8/10/2019 Hypocalcemia & Hypercalcemia

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Hypocalcemia & Hypercalcemia

Emergency pediatric PICU divisionPediatric DepartmentMedical Faculty, University of Sumatera Utara H. Adam Malik Hospital

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HYPOCALCEMIA

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Because of potentially severe symptoms such as

laryngospasm and seizures, hypocalcemia needs to beidentified and treated expeditiously The ionized calcium concentration is low in true hypocalcemia The total calcium concentration does not accurately predict

the ionized calcium concentration in the patient withhypoalbuminemia the ionized calcium concentrationshould be determined in patients with suspectedhypocalcemia when the patient is hypoalbuminemic and/or iscritically ill

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SPECIFIC CAUSES IN THE NEONATEEarly neonatal hypocalcemiaLate neonatal hypocalcemiaMaternal hypercalcemia

HYPOPARATHYROIDISM

DiGeorge syndrome (MIM *

188400)X-linked hypoparathyroidism (MIM 307700)Parathyroid hormone (PTH) gene mutations (MIM 168450)Calcium-sensing receptor mutation (MIM 601199)Autosomal recessive hypoparathyroidism with dysmorphic features (MIM 241410)HDR (or Barakat) syndrome (MIM 146255)

Autoimmune polyglandular syndrome type I (MIM 240300)Kearns-Sayre syndrome (MIM 530000)HemochromatosisWilson disease (MIM 277900)Postsurgical hypoparathyroidismRadioactive iodine ablation of the thyroid gland

Hypomagnesemia

Causes of hypocalcemia

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LACK OF RESPONSE TO PTH

Pseudohypoparathyroidism type IA (MIM 103580)Pseudohypoparathyroidism type IB (MIM 603233)Pseudohypoparathyroidism type IIHypomagnesemia

VITAMIN D DEFICIENCY

Poor intakeLack of sunlightMalabsorptionIncreased metabolism (e.g., anticonvulsants)Failure to form 25-hydroxyvitamin D in the liverVitamin D dependent rickets type 1 (MIM 264700)Vitamin D dependent rickets type 2 (MIM 277420)Renal insufficiency

Causes...REDISTRIBUTION OF PLASMA CALCIUM

HyperphosphatemiaRhabdomyolysisTumor lysis syndromeBlood transfusionsHungry bone syndromeAcute pancreatitis

Osteopetrosis, infantile (MIM 259700)

INADEQUATE CALCIUM INTAKE

Calcium-poor diet or TPNDietary calcium chelatorsMalabsorption

UNKNOWN

Septic shockCritical illness

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Clinical Manifestation

Mild hypocalcemia is usually asymptomatic The clinical manifestations are mostly due to neuromuscular irritability Older children: paresthesias, typically perioral or of the hands and feet Tetany is the classic manifestation of hypocalcemia, and symptoms may

include carpopedal spasm, laryngospasm, and seizures Seizures may be the first manifestation of hypocalcemia, especially in

infants Symptoms of tetany may be provoked in patients with hypocalcemia by

hyperventilation, which by raising the pH causes calcium to bind toalbumin, thereby lowering the ionized calcium concentration

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Newborn infants with hypocalcemia usually do not have carpopedal

spasm. Along with seizures, manifestations in newborns may includeirritability, muscular twitching, jitteriness, and tremors. Alternatively,newborns with hypocalcemia may have symptoms suggestive of sepsis,such as poor feeding, vomiting, and lethargy

The consequences of long-standing hypocalcemia depend on the etiology.In children with inadequate vitamin D, there is concomitanthypophosphatemia and secondary hyperparathyroidism. These patientshave inadequate bone mineralization, and consequently develop rickets

Rickets may also occur with severe dietary calcium deficiency

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Chvostek and Trousseau signs

may be elicited in patients withhypocalcemia

A positive Chvostek sign occursif tapping the facial nerve anteriorto the external auditory meatuselicits a twitch of the upper lip orentire mouth. This is not a very

specific sign because it ispositive in about 10% of patientswithout hypocalcemia

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Trousseau sign is more specific, butquite uncomfortable to elicit andgenerally not an appropriate test ina child

A blood pressure cuff is inflatedslightly above the systolic bloodpressure for more than 3 min;carpopedal spasm occurs if

hypocalcemia is present as a resultof the ischemia of the motor nerves


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Diagnosis & Treatment

Diagnosis of the patient with hypocalcemia

should begin with a thorough history of dietary

intake.

It should also include an investigation of familyhistory of rickets, hypocalcemia and endocrine

disorders. Physical examination should include

a close evaluation of the bones and joints

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A primary tenet in the treatment of hypocalcemia is to tailor the therapy to

the cause of hypocalcemia Calcium may be given IV or orally Acute symptomatic hypocalcemia: a bolus dose of Ca gluconate (100-

200mg/kg or 9-18 mg/kg elemental Ca to a maximum of 1-3 g in adults)

should be administered over 10-20 mins. A continuous infusion of Cagluconate inf may be administered at starting dose of 10-30 mg/kg/hr, therate can then be titrated based on serial Ca measurement

All patients receiving IV Ca require close monitoring of total or ionized C

levels and cardiac ECG

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Rogers textbook of pediatric intensive care, 4th ed, 2008


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For symptomatic hypocalcemia in neonates, calcium gluconate is givenat a dose of 100 200 mg/kg (1 2 mL/kg of a 10% solution; 9 18 mg ofelemental Ca/kg)

This dose may be repeated every 6 8 hr until the calcium levelstabilizes

Alternatively, calcium gluconate may be given as a constantintravenous infusion, with neonates typically requiring 500 750 mg/kg/24 hr of calcium gluconate

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Nelson Textbook of pediatrics, 17 th ed, 2004


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HYPERCALCEMIA

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Hypercalcemia is frequently discovered incidentally on a routinechemistry profile

This is because hypercalcemia is an uncommon electrolyte disorder, and

its clinical manifestations are fairly nonspecific There are, however, some clinical situations in which hypercalcemia

should be suspected

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EXCESS PARATHYROID HORMONEPrimary hyperparathyroidism

Sporadic adenomaFamilial isolated hyperparathyroidism (MIM * 145000)Multiple endocrine neoplasia type I (MIM 131100)Multiple endocrine neoplasia type II (MIM 171400)Hyperparathyroidism jaw tumor syndrome (MIM 145001)Calcium-sensing receptor mutation (MIM 239200)

Transient secondary neonatal hyperparathyroidismTertiary hyperparathyroidism

EXCESS VITAMIN DHypervitaminosis DSubcutaneous fat necrosisSarcoidosisGranulomatous diseasesLymphomas

EXCESS CALCIUM INTAKECalcium supplementsIatrogenic (e.g., total parenteral nutrition)

EXCESS RENAL REABSORPTION OF CALCIUM

Familial benign hypocalciuric hypercalcemia (MIM 145980)Thiazide diuretics

RELEASE FROM BONEThyrotoxicosisHypervitaminosis AMalignancy associated

Ectopic parathyroid hormone (PTH)PTH-related peptideBone metastasisOther factors

ImmobilizationRenal osteodystrophy

Low turnover diseaseAluminum deposition

MISCELLANEOUSWilliams syndrome (MIM 194050)HypophosphatemiaPheochromocytoma

Adrenal insufficiencyRecovery phase of rhabdomyolysisJansen metaphyseal chondrodysplasia

(MIM 156400)Hypophosphatasia (MIM 241500)

Causes of hypercalcemia


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Clinical Manifestation

The signs and symptoms of hypercalcemia are related to the magnitude ofthe problem

Hypercalcemia is conventionally classified as mild (15 mg/dL)

Many patients with mild or moderate hypercalcemia are asymptomatic,with the diagnosis resulting from an incidental laboratory test

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GASTROINTESTINAL

Nausea and vomitingPoor feedingFailure to thriveConstipationAbdominal painPancreatitis

Peptic ulcer

CARDIACHypertensionDecreased QT intervalArrhythmias

CENTRAL NERVOUS SYSTEMLethargyHypotoniaPsychiatric disturbancesComa

KIDNEY

Polyuria and dehydrationHypernatremiaRenal failureNephrolithiasis

Clinical manifestations of hypercalcemia


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Treatment Dependent on its severity

The initial basic tenets of therapy are to restore intravascular volume and toenhance renal excretion, which can be accomplished by administration ofnormal saline at 2 or 3 times maintenance fluid rate

If the patient is adequately rehydrated and Ca levels do not decrease, loop

diuretics may be administered, but should be done judiciously Calcitonin and biphosponate are useful adjuncts in hypercalcemia In severe cases in which hydration and medications fail to reduce serum Ca

levels, hemodialysis using a low Ca dialysate can be performed

Glucocorticoids have been useful in treating hypercalcemia secondary tosarcoidosis and vit D deficiency

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Rogers textbook of pediatric intensive care, 4th ed, 2008


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TH NK YOU

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hypocalcemia & hypercalcemia

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