Pediatric Hypercalcemia Follow-up

  • Author: Ilene A Claudius, MD; Chief Editor: Stephen Kemp, MD, PhD   more...
 
Updated: Apr 3, 2012
 

Further Inpatient Care

  • Admit any patient requiring treatment for hypercalcemia.
    • Continue the previously mentioned medications as needed.
    • Continue an appropriate workup for the etiology of hypercalcemia.
  • For neonates, specifically, Oski recommends 5% dextrose (D5) in one-half isotonic sodium chloride solution with 30 mEq/L potassium chloride at 2 times the maintenance dose along with 2-3 mg/kg/d furosemide and adequate phosphate supplementation to maintain normal levels.[10] Strongly consider surgical correction of primary hyperparathyroidism.
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Further Outpatient Care

  • Daily calcium intake should be limited, and restriction of vitamin D (sunlight, dairy) may be warranted in certain disorders.
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Inpatient & Outpatient Medications

  • Long-term therapy can begin while the patient is in the hospital and continue following discharge.
  • Corticosteroids are helpful in certain disorders, particularly malignancy-associated hypercalcemia, granulomatous disease, or vitamin D ingestion; and they can be given either IV or orally as prednisone in doses of 40-60 mg/m2/d or 1.5-2 mg/kg/d to inhibit osteoclast action and decrease intestinal calcium absorption.
  • Aminohydroxypropylidene (APD) can induce remissions of malignancy-associated hypercalcemia.
  • If serum phosphate is low, intravenous (IV) phosphorus is no longer recommended because of the risk of intravascular precipitation with calcium; however, oral phosphate supplementation is recommended because this binds calcium in the intestine and diminishes calcium absorption. The dose is 1-3 g/d for an adult-sized person. Phosphate is contraindicated in renal failure and requires 2-3 days before it becomes effective.
  • Bisphosphonates may also be continued as outpatient medications. One should consider alendronate as an oral preparation. However, note that no pediatric experience is noted.
  • Indocin may be of some use in certain disorders that lead to hypercalcemia.
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Transfer

  • As in any patient, transfer is acceptable when patient is stable or when a higher level of care is required. However, consider the possibility of coma or cardiovascular collapse in a patient with an excessively high calcium level. Begin close observation/therapy before transfer.
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Deterrence/Prevention

  • Carefully monitor patients with risk factors for hypercalcemia, such as known malignancy, thiazide diuretic use, total parenteral nutrition, retinoid use for acne, or lithium use.
  • Counsel patients to consume adequate phosphate and to avoid excessive calcium-containing antacids, vitamin D, and herbal preparations with vitamin A.
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Complications

  • Primarily ectopic calcifications may occur (see Physical).
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Prognosis

  • Hypercalcemia is frequently noted during laboratory testing while the patient is asymptomatic or mildly symptomatic. Prognosis depends on the underlying disorder.
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Contributor Information and Disclosures
Author

Ilene A Claudius, MD  Assistant Professor of Pediatrics, Division of Emergency Medicine, Children's Hospital, Los Angeles

Ilene A Claudius, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Coauthor(s)

Oved Fattal, MD  Staff Physician, Department of Pediatrics, Kaiser Permanente Medical Group

Oved Fattal, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Jon Nakamoto, MD  Consulting Staff, Department of Pediatric Endocrinology, Quest Diagnostics

Jon Nakamoto, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Pisit (Duke) Pitukcheewanont, MD  Associate Professor of Clinical Pediatrics, University of Southern California, Keck School of Medicine, Childrens Hospital Los Angeles

Pisit (Duke) Pitukcheewanont, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, American Society for Bone and Mineral Research, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Thomas A Wilson, MD  Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London)  Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Merrily P M Poth, MD  Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences

Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD  Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

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Investigations flowchart.
Table 1
Laboratory Test Reference Range Normal Response to Increased Calcium
Serum calcium8.5-10.2 mg/dLNA
Ionized calcium1-1.3 mmol/LNA
PTH (intact)10-55 pg/mL*Decrease
Serum phosphateAge-dependentIncrease
1,25-dihydroxyvitamin D36-108 pmol/LDecrease
Alkaline phosphatase68-217 U/LNormal
Urine calcium4 mg/kg/dIncrease
Urine Ca/Cr ratioSee note†Increase
Urine cAMP‡< 5 molDecrease
*Note that 1 mmol/L equals 4 mg/dL. †In infants younger than 7 months, the reference range is less than 0.86; in infants aged 7-18 months, the reference range is less than 0.6. By age 6-7 years, the adult reference range of less than 0.21 is reached.‡The urine cAMP level generally parallels the PTH level.
Table 2
Condition Serum Phosphorus Serum Alkaline Phosphatase Urine Calcium Urine Phosphate PTH
HyperparathyroidismLowNormal-highHigh*HighHigh
Vitamin D excessNormal-highLowHighHigh
MalignancyOften lowHigh † VariableHigh
Granulomatous diseaseNormal-highNormal-highHighNormal
Milk alkali syndromeNormal-highNormalNormalNormal
FHHNormal or lowNormalLow (< 200mg/d)NormalLow
*67% of the time



† Except hematologic malignancies, in which alkaline phosphatase is normal



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