SFEBES2022 Poster Presentations Bone and Calcium (40 abstracts)
Norfolk and Norwich University Hospital, Norwich, United Kingdom
We present an interesting case of immobilisation hypercalcaemia. Case: A 22-year-old female with no significant past medical history was admitted following a road traffic accident (RTA). She suffered severe abdominal injury, skull and multiple limb fractures and underwent left below-knee amputation, bowel resection and nephrostomy. The admission to ITU was prolonged, and seven weeks into the admission, she developed hypercalcaemia (adjusted calcium: 3.8, N: 2.2 2.6 mmol/l) with a suppressed PTH (1.1, N:1.6 6.9 pmol/l). She required prompt treatment with intravenous hydration, calcitonin and bisphosphonate as her ECG showed shortened QTc interval. After an initial improvement, calcium climbed again. She was then stepped down to the ward for rehabilitation. Further investigations: alkaline phosphatase 124 (38-126U/l), vitamin D 29(> 50 nmol/l), TSH <0.01miu/l, FT4 57 pmol/l, cortisol 487 nmol/l. Carbimazole and Colecalciferol were started with subsequent biochemical improvement. However, her calcium remained elevated (3.22 mmol/l). She had also developed depression and was reluctant to mobilise due to low mood and pain. Psychological support was sought, and antidepressants were started. Her bone markers were consistent with increased bone resorption with elevated C-terminal telopeptide of type 1 collagen (CTX) (2.25, N: 0.10 - 0.50ug/l). Furthermore, there was no evidence of metabolic bone disease on the isotope bone scan. Hence the diagnosis of immobilisation hypercalcemia (IH) was considered. She was treated with hydration and pamidronate infusions. Serum calcium stabilised once she started rehabilitation.
Conclusion: IH is an uncommon diagnosis and may go unrecognised in hospitals or rehabilitation settings. In the young patients with reduced mobility, it usually occurs after four to six weeks of immobilisation but may present months after. Increased bone resorption causes hypercalcaemia. The diagnosis requires intensive investigations and exclusion of other causes of PTH independent hypercalcaemia. Although treatment with hydration and bisphosphonate infusion help prevent acute manifestations of hypercalcaemia, early mobilisation remains the mainstay of management.