Cause of hypocalcemia

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Cause of hypocalcemia

Author: Pediatric Oncall

Question
A two months old child born of non-consanguineous marriage presented with not gaining weight and lumps over the cheek. The child was a full-term delivery but did not cry immediately after birth and required NICU stay for birth asphyxia for 7 days and also required ventilatory support for hypoxic-ischemic encephalopathy (HIE) Stage 3. There were no convulsions, fever, jaundice, or urinary complaints. He had received IV antibiotics and Calcium Gluconate injections during his NICU stay. On examination, weight was 2 kg and there was subcutaneous fat necrosis over the cheeks. The rest of the examination was normal. Investigations showed normal hemogram, serum calcium = 13.6 mg/dl, phosphorus = 3.9 mg/dl, alkaline phosphatase = 236 IU/L (Normal), normal renal and liver function tests.

What is the cause of hypercalcemia?

Answer Discussion :

L

lusungu muchelenganga

0

Although the child was preterm.A history of hypoxia predisposed them from having subcutaneous fat necrosis which can cause hypercalcemia. Because it's not known when exactly the child was discharged from the NICU we cannot ignore the possibility of iatrogenic causes with calcium gluconate. which I presume might have been given due to hypocalcemia from an induced alkalosis(both respiratory from ventilator use and metabolic from alkali solutions in treating the HIE).There's clearly nothing wrong with the parathyroid as the phosphate is normal. And it's less likely from bone resorption as the ALP is normal

1 year ago

S

Shaima Hassan

1

Hpocalciuric hypercalcemia

1 year ago

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Answer 1

This child has subcutaneous fat necrosis of the cheeks. Subcutaneous fat necrosis leads to endogenous production of 1,25 dihydroxy Vitamin D which may lead to increased calcium absorption from the intestine and hypercalcemia. Hypercalcemia can lead to failure to thrive, vomiting, polyuria, and polydipsia. Subcutaneous fat necrosis can occur commonly following birth asphyxia. The increased 1,25 (OH) Vitamin D3 levels lead to secondary hypoparathyroidism (hypercalcemia suppresses the parathyroid hormone). The treatment, in this case, would be to increase calcium excretion in the urine by hydration and furosemide; decrease calcium absorption from intestines by giving steroids (steroids are useful in only hypercalcemia due to Vitamin D overdose or excess production) and bisphosphonate therapy (IV Pamidronate). Calcitonin may be tried in severe acute hypercalcemia to decrease the level of active calcium in the blood. In this child 25 hydroxy Vitamin D levels were normal, parathyroid hormone levels were low and 1, 25 dihydroxy Vitamin D3 levels were elevated suggestive of endogenous Vitamin D production.

Cause of hypocalcemia

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