Immobilization Hypercalcemia (IH) in an Adult After Spinal Cord Injury

Background: Immobilization hypercalcemia (IH) is an uncommon diagnosis and little has been published about management of this condition. We present a case of IH and discuss clinical aspects of this unique bone metabolism state. Case: 32-year-old female with history significant for IV drug use, presented to the hospital with features of septic shock, Work up showed MRSA bacteremia associated with tricuspid endocarditis and septic pulmonary emboli. MRI of the spine done for progressive weakness of extremities revealed a cervical epidural abscess leading to spinal cord compression and myelomalacia. She underwent spinal abscess drainage and corpectomy, remained quadriplegic. 8 weeks later we were consulted to see her at inpatient rehabilitation facility for hypercalcemia. Labs showed Creat(0.6 mg/dl), hypercalcemia with corrected Calcium of 12.9 mg/dl f. Further workup showed suppressed PTH (< 6), V D-25 at (< 10 mg/dl). Phosphate (normal). ACE levels, PTHrp, Vit. D 1,25, SPEP, UPEP,and TSH were all normal. 24 hours urine calcium showed hypercalciuria, 400 mg/ml. Fasting Bone markers were elevated with serum N-telopeptide > 40 nM BCE, ref range (6.2–19.0) and C-Telopeptide is 2060 pg/ml ref range (60–650), which indicates increase bone turnover. IH was diagnosed and hydration attempted for few weeks. Serum calcium remained at 13 mg/dl, so she received a single slow infusion of pamidronate 30 mg. 4 days after infusion, calcium levels decreased to normal value of 10.2 mg/dl without any side effects. She remained normocalcemic 5 weeks post infusion. Discussion: IH is an uncommon condition but early recognition and intervention will minimize secondary long-term complications such as kidney stones, Osteoporosis or low bone mass, renal failure and acute pancreatitis. Albert, Fuller described IH in 1941(1). Most cases of IH had been reported in children and adolescents with high bone turn over following recent spinal cord injury(2–3). Very few reports have been published in young adults such as our patient,IH is attributed to prolonged immobilization from paralysis due to spinal cord injury,and other etiology (2–4), Proposed mechanism includes decreased mechanical stress on the bone which leads to increase bone resorption and remodeling and demineralization. To establish the diagnoses of IH, an exhaustive evaluation is warranted to rule out other causes of PTH dependent and independent hypercalcemia(5). Multiple treatment approaches have been used over the past few decades including early mobilization, hydration., saline diuresis, subcutaneous Calcitonin, glucocorticoids (6), IV sodium sulphate and phosphate (7). Bisphosphonates are the preferred pharmacological treatment of IH. Nonnitrogen containing bisphosphonates including clodronate and etidronate (8–9),. are not preferred due to concern for bone demineralization and osteomalacia. (10). Pamidronate has been used to treat IH due to its efficacy, safely and cost (11). Caution to be exercised in those patients with kidney disease.