Immobilization-induced hypercalcemia and heterotopic ossification in a burn patient. A 29-year-old male with no significant past medical history sustained an 85% total body surface area burn from a house fire. He had a prolonged ICU course with significant immobilization. He spent nearly two months undergoing continuous renal replacement therapy, and during that time required ventilator support for one month. Hypercalcemia developed two months after admission. After extensive evaluation, the etiology was determined to be immobilization-induced hypercalcemia. Despite treatment with low calcium dialysate, calcium levels remained elevated. After six weeks with hypercalcemia, concerns for restricted elbow extension were brought to the attention of the treatment team by therapists. Initial radiographs were negative for ossification, and nuclear medicine bone scan was not pursued. However, the clinical picture was most consistent with heterotopic ossification. The patient was admitted to inpatient rehabilitation, where calcium levels remained elevated and range of motion in elbows continued to worsen despite daily therapy. The decision was made to administer IV pomidronate for management of hypercalcemia and in an effort to prevent advancement of heterotopic ossification. Forty-eight hours after treatment with pomidronate, the patient's serum calcium level normalized and remained within normal limits for the duration of his hospitalization. Clinical progression of his heterotopic ossification in bilateral elbows halted after treatment. Range of motion in elbows then improved progressively with intensive physical and occupational therapy interventions. Some limitation of range of motion persisted, and radiographs were able to demonstrate heterotopic ossification of bilateral onal-humeral joints. Additionally, the patient had severe nausea for several weeks through his hospital stay concurrent with his hypercalcemia. Following bisphosphonate administration and normalization of serum calcium, his nausea improved dramatically after other interventions had not been successful. While the mechanism of heterotopic ossification is poorly understood, this presentation and course suggest that elevated levels of extracellular calcium may contribute to the heterotopic ossification process and that normalization of serum calcium with bisphosphonate administration may slow or stop mineralization. In this patient, we were able to appreciate significant changes in range of motion, which had significant functional implications for this patient. To our knowledge, these two syndromes of immobilization-induced hypercalcemia and heterotopic ossification have not been described concurrently, but they may be co-occurring in many rehabilitation patients that are severely immobilized. Recognition of such concurrence may prompt a similar management strategy for heterotopic ossification to the one described above. Heterotopic ossification has limited evidence-based interventions, so efficacious strategies should be welcomed. And bisphosphonate administration proved to be a very beneficial strategy for this patient. In conclusion, calcium is a known promoter of osteogenesis and prompt recognition and treatment of immobilization-induced hypercalcemia may help to arrest or even prevent heterotopic ossification.

burn patient

immobilization-induced hypercalcemia

heterotopic ossification

bisphosphonate administration

hypercalcemia treatment