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ABSTRACT: This entity is an infrequently reported phenomena, because its manifestations are nonspecific and protean. Three young patients are described who developed hypercalcemia during immobilization following multiple injuries including femoral fractures. This syndrome presented itself with symptoms of continuous anorexia and nausea. Gastrointestinal symptoms occurred within two weeks of immobilization, but the diagnosis was not made for a month. They were treated for hypercalcemia by a decrease in calcium intake, saline infusion, phosphates and mobilization when possible. As the serum calcium levels reached normal limits, the symptoms of anorexia and nausea were alleviated. Mobilization was the definitive treatment for their immobilization hypercalcemia. The protean manifestations of hypercalcemia must be emphasized. When they occur in patients with multiple trauma, hypercalcemia must be evaluated and treated.
Immobilization hypercalcemia is an infrequently reported phenomenon,1 because its manifestations are nonspecific and protean. These include nausea, anorexia, vomiting, irritability and a minimally elevated blood calcium level. Unrecognized and untreated, they can progress to seizures, cardiac arrhythmias, respiratory and cardiac arrest2
It occurs in both sexes, usually in youth and without pre-existing metabolic or bone disease3'4. It has no relationship to hyperparathyroidism, Paget's disease, renal dysfunction or malignancy.
This paper presents three cases of immobilization hypercalcemia occurring among 25 patients with multiple fractures of the lower extremities. Clinical observations are presented, therapy is discussed and the literature is reviewed.
Case Report
Patient No. 1
F.F., a 22-year-old white female, was admitted shortly after sustaining multiple injuries to her right lower extremity in a motorcycle accident (Fig. 1). These included an open comminuted, midshaft fracture of the right femur, an open segmental fracture of the right tibia and fibula and a laceration of the posterior right hindfoot. Neurovascular status was normal. Serum values for alkaline phosphatase, blood urea nitrogen, calcium and phosphate were normal (Table 1).
Under general anesthesia her wounds were irrigated, debrided and loosely closed, and her fractures were stabilized with Steinmann 's pins. On the second postoperative day, symptoms and signs consistent with fat embolism appeared, including a decreased arterial p02, petechiae and anemia. She was treated successfully with 40% oxygen by mask, IPPB, with normal saline IV SoluMedrol and transfusion of 2 units of whole blood,
Recovery was uneventful for the next 12 days, when continuous...