Immobilization Hypercalcemia

Abstract

A 15-year-old boy had hypercalcemia and renal insufficiency secondary to immobilization for multiple fractures. After being immobilized for 12 weeks he was noted to have hypercalcemia, a metabolic alkalosis, and renal insufficiency. Renal function studies demonstrated reduction in iothalamate sodium I 125 clearance, increase in fractional excretion of sodium and phosphorus, and increased urinary excretion of calcium and magnesium. Except for increase in urinary magnesium excretion, results of repeat renal function studies were normal nine months later.Immobilization hypercalcemia with renal insufficiency in adolescence appears to be related to the high rate of bone turnover. Reduction in renal function may be related to direct effect of excess calcium on the kidney.Other metabolic abnormalities may be related to decreased renal function or to effects of bone dissolution.Possible therapeutic regimens include furosemide, corticosteroids, phosphate salts, and mithramycin.Si nce the original description by Albright et al' in 1941 of "acute bone atrophy" complicating immobilization in a 14-year-old boy, it has become accepted that long-stand¬ ing immobilization may lead to bone demineralization, hypercalcemia, and occasionally decreased renal func¬ tion.2" However, renal function studies have been done only in a few patients with immobilization hyper¬ calcemia.21 This communication de¬ scribes an additional patient with immobilization hypercalcemia, meta¬ bolic alkalosis, osteoporosis, and de¬ creased renal function who was stud¬ ied with special regard to glomerular filtration rate, phosphate, calcium, and sodium excretion, and urine con¬ centrating ability. The original patient of Albright et al was a previously active adolescent boy who developed bone atrophy, hy¬ percalcemia, and decreased renal function during immobilization for a fractured femur. Two surgical explo¬ rations of the neck revealed no abnor¬ malities of the parathyroid glands. The patient's symptoms disappeared following mobilization.1 In 1952 Dodd et al2 described a 12-year-old boy who developed osteoporosis, hyper¬ calcemia, renal insufficiency, hyper¬ tension, and encephalopathy compli¬ cating immobilization for multiple fractures. During the height of his hypercalcemia (14.9 mg/100 ml), the patient's urea clearance decreased to 43.5% of normal. He became normotensive, and his urea clearance re¬ turned to normal after mobilization.2

Retracted: Effect of immobilization on vitamin D status and bone mass in chronically hospitalized disabled stroke patients

“…The mean serum 25-OHD concentration in our population was similar to that previously reported for elderly people in nursing homes [17][18][19][20]. Generally, immobilization-induced hypercalcaemia is associated with conditions in which bone turnover is high, as in children or adolescents with acute neurologic diseases (such as poliomyelitis or spinal cord injury [21][22][23][24][25]). The serum ionized calcium level is chronically low in isolated 25-OHD deficiency, resulting in feedback stimulation of the parathyroid glands, which causes secondary hyperparathyroidism.…”

Hypercalcaemia in adolescent tetraplegic patients: case report and review

“…The onset may occur early after immobilisation or there may be a delay of 1 to 3 months. Impairment of renal function has been reported by most observers and has been extensively studied by Hyman (1972). His patient, a 15-year-old boy, was found to have a decreased glomerular filtration rate, creatinine clearance and urine concentrating ability.…”

Immobilization-induced hypercalcemia in a patient with renal failure

“…Elevated calcium levels have widespread clinical implications including decreased QT-interval, bradycardia, neuropsychiatric disturbances, such as depression and cognitive dysfunction, as well as both acute and chronic renal insufficiency (3). Previous literature has demonstrated cases of immobilization induced hypercalcemia among patients with spinal cord injury (4,5,6), traumatic fractures (7,8), and Guillan Barre syndrome (9). The development of this disease tends to occur on average after a few months (10) after the onset of immobilization though in some cases it can develop sooner (8).…”