Endocrine Abstracts (2017) 51 CME5 | DOI: 10.1530/endoabs.51.CME5

An approach to investigation and management of hypo and hypercalcemia

Raja Padidela


Manchester.


Hypocalcemia is defined as serum calcium (Ca) level below the lower limit of the normal range of 2.2–2.7 mmol/l. It may arise because of inadequate Ca supply (dietary deficiency, Vitamin D deficiency or resistance), impaired parathyroid hormone secretion or resistance (pseudohypoparathyroidism). Hypomagnesemia may lead to hypocalcemia due to impaired parathyroid hormone secretion and/or end organ resistance, and hence it is important to promptly recognize and treat it concomitantly. Neonates can present with jitteriness, irritability, apnoea, and generalized or focal convulsions. In older child mild hypocalcemia is associated with numbness and tingling sensation while severe hypocalcemia can cause muscle cramps, tetanic carpopedal spasm, laryngospasm with stridor, and convulsions. Hypercalcemia develops when the rate of Ca entry into the extracellular fluid exceeds the kidneys’ capacity for its excretion. Mechanisms include increased absorption of Ca from the gastrointestinal tract, increased release of Ca from the skeleton or decreased excretion of Ca from the kidneys. Symptoms of hypercalcemia in infants are often nonspecific and include feeding difficulties, vomiting, constipation, failure to thrive, irritability and hypotonia. Older children may present with anorexia, nonspecific abdominal pain, muscle weakness and neuropsychiatric symptoms. Polydipsia and polyuria may lead to dehydration and fever. Chronic hypercalcemia and accompanying hypercalciuria may predispose to nephrocalcinosis, nephrolithiasis and, if left untreated, to renal impairment. Measurement of bone profile, parathyroid hormone, magnesium, 25 OHD, 1,25 (OH)2 D (sample to be stored) and urine calcium creatinine ratio measurement helps in identifying a cause for hypo and hypercalcemia. In addition, renal ultrasound scan may be required for assessment of nephrocalcinosis. Depending on aetiology, hypocalcemia is managed by increasing Ca intake (IV for acute severe hypocalcaemia), Vitamin D or analogues of active Vitamin D (hypoparathyroidism and pseudohypoparathyroidism) and rarely parathyroid hormone injection/infusion. The principles of management of hypercalcemia include hydration and sodium diuresis, reduction of gastrointestinal Ca absorption, inhibition of bone resorption and dialysis.

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