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Pediatric Hypocalcemia Workup

  • Author: Yogangi Malhotra, MD; Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Nov 18, 2014
 

Approach Considerations

The following should be assessed in patients with hypocalcemia:

  • Total and ionized serum calcium levels
  • Serum magnesium levels
  • Serum electrolyte and glucose levels
  • Phosphorus levels
  • Parathormone levels
  • Vitamin D metabolite (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) levels
  • Urine calcium, magnesium, phosphorus, and creatinine levels
  • Serum alkaline phosphatase levels

Total and ionized serum calcium levels

Measuring ionized calcium level is essential to differentiate true hypocalcemia from a mere decrease in total calcium concentration. A decrease in total calcium can be associated with low serum albumin concentration and abnormal pH.

Serum magnesium levels

Serum magnesium levels may be low in patients with hypocalcemia, which may not respond to calcium therapy if hypomagnesemia is not corrected. Severe hypomagnesemia (0.46 mmol/L) causes hypocalcemia by impairing the secretion and action of parathormone (PTH).

Serum electrolyte and glucose levels

Seizures and irritability in newborns and children can be associated with hypoglycemia and sodium abnormalities. Low bicarbonate levels and acidosis may be associated with Fanconi syndrome and renal tubular acidosis.

Phosphorus levels

Estimating the phosphate level is essential to establish the etiology of hypocalcemia. Phosphate levels are increased in cases of exogenous and endogenous phosphate loading and renal failure and are usually high in patients with hypoparathyroidism. Phosphate levels are low in cases of vitamin D abnormalities and rickets.

Parathormone levels

Hormone studies are indicated if hypocalcemia persists in the presence of normal magnesium and normal or elevated phosphate levels.

Low PTH levels suggest hypoparathyroidism; serum calcium rises in response to PTH challenge. Oppositely, PTH levels are elevated in patients with vitamin D abnormalities and pseudohypoparathyroidism, and calcium levels do not rise in response to PTH challenge.

The N -terminal fragment of PTH is the only biologically active fragment of PTH. It is difficult to measure because of its short half-life of 2-5 minutes. Circulating PTH levels are determined by assaying for intact PTH peptide.

Vitamin D metabolite (25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) levels

These may be assessed, along with hormone concentrations, to eliminate uncommon causes of hypocalcemia (e.g., malabsorption, disorders of vitamin D metabolism).

Urine calcium, magnesium, phosphorus, and creatinine levels

These values should be assessed in patients with suspected renal tubular defects and renal failure. Urine should also be evaluated for pH, glucose, and protein.

In patients with renal defects, calcium excretion is high in presence of hypocalcemia. A urine calcium-to-creatinine ratio of more than 0.3 on a spot sample in presence of hypocalcemia suggests inappropriate excretion.

Serum alkaline phosphatase levels

Values are generally elevated in patients with rickets.

Additional tests

Additional tests in the diagnosis of hypocalcemia include the following:

  • Malabsorption workup
  • Total lymphocyte and T-cell subset analyses - Findings are decreased in patients with DiGeorge syndrome
  • Chest radiography - Evaluate for thymic shadow, which may be absent in patients with DiGeorge syndrome
  • Ankle and wrist radiography - Evaluate for evidence of rickets; changes appear at an early stage in the radius and ulna (the distal ends are widened, concave, and frayed)
  • Electrocardiography - A prolonged QTc (>0.4 s), a prolonged ST segment, and T-wave abnormalities may be observed; measurements of specific intervals are of little value in predicting hypocalcemia (see the image below)
    Electrocardiogram (ECG) findings in severe hypocal Electrocardiogram (ECG) findings in severe hypocalcemia.
  • Karyotyping - To assess for 22q11 and 10p13 deletion
  • Maternal and family screening - This is helpful in familial forms of hypocalcemia, such as those caused by activating mutations of the calcium-sensing receptor
 
 
Contributor Information and Disclosures
Author

Yogangi Malhotra, MD Assistant Professor, Department of Pediatrics, Division of Neonatology, Albert Einstein College of Medicine; Attending Neonatologist, Montefiore New Rochelle Hospital

Yogangi Malhotra, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, New York State Perinatal Association

Disclosure: Nothing to disclose.

Coauthor(s)

Deborah E Campbell, MD, FAAP Professor of Clinical Pediatrics, Albert Einstein College of Medicine; Director, Department of Pediatrics, Division of Neonatology, Children's Hospital at Montefiore

Deborah E Campbell, MD, FAAP is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Pediatric Society, American Medical Association, National Perinatal Association, New York Academy of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former 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, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

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.

Robert J Ferry Jr, MD Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Eli Lilly & Co Grant/research funds Investigator; MacroGenics, Inc Grant/research funds Investigator; Ipsen, SA (formerly Tercica, Inc) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Grant/research funds Investigator; Bristol-Myers-Squibb Grant/research funds Other; Amylin Other; Pfizer Grant/research funds Other; Takeda Grant/research funds Other

Abhay Singhal, MD Assistant Professor of Clinical Pediatrics, Department of Pediatrics, Division of Neonatology, Indiana University School of Medicine

Abhay Singhal, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Sunil Sinha, MD Assistant Professor, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Sunil Sinha, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, Endocrine Society, and Pediatric Endocrine Society

Disclosure: Nothing to disclose.

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.

References
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Electrocardiogram (ECG) findings in severe hypocalcemia.
 
 
 
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