Immobilization Hypercalcemia

Most cases of immobilization hypercalcemia are seen in adolescent boys following recent spinal cord injuries. 16 Risk factors include age less than 21 years, complete neurologic injuries, cervical injuries, prolonged immobilization, and dehydration. 16 Presenting symptoms include anorexia, nausea, headache, malaise, and depression in mild cases. In more severe cases, patients may have persistent nausea and vomiting, gastric dilatation, fecal impaction, and abdominal pain. Microscopic calcium deposition in the kidney may impair its ability to concentrate urine, leading to polyuria and polydipsia. Patients may also develop cardiac dysrhythmias and seizures.16

The pathophysiology of immobilization hypercalcemia is thought to be due to the combination of increased bone resorption and the inability of the kidneys to excrete the excess calcium. Compared to other age groups, an adolescent has a higher than normal bone turnover rate and more total bone mineral. 16 Immobilization causes a decrease in osteoblastic activity in the weight-bearing bones and an increased rate of bone resorption. Together, these factors lead to a higher-than-normal serum calcium level when subjected to a prolonged period of immobilization. In most cases, the kidneys can usually excrete the calcium, but in some patients this ability breaks down.

Treating immobilization hypercalcemia starts with hydration and diuresis with normal saline solution 2 to 3 L/day with the addition of furosemide. Calcitonin in doses of 1 to 4 IU/kg subcutaneously every 12 h can also effectively reduce the serum calcium level.16

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