Abstract
Introduction: Hypercalcaemia is a commonly encountered electrolyte imbalance.We report a case of severe hypercalcaemia which was resistant to conventional treatment approach. Case Report: A 52 year old lady presented to hospital with tiredness, constipation, confusion and reduced mobility for 3 weeks.She had complex past medical history including Papillary carcinoma of thyroid treated with total thyroidectomy and parathyroidectomy and Radioactive Iodine ablation 16 years ago and depression. She was taking Levothyroxine , oral calcium & 1-alfacalcidol. On physical examination, she was dehydrated and confused. Her biochemistry revealed Acute kidney Injury(AKI) with Urea: 15.6 (n:2.5-7.8mmol/l), Creatinine: 177 (n: 50-104 micromol/l), eGFR:32ml/min and corrected Calcium 5.71 (n:2.20-2.60mmol/l). PTH was suppressed at 0.1 (n:1.1-4.7pmol/l) and Vitamin D of 30 (n:50-250nmol/l). ECG showed shortened QTc. Initial management of her severe hypercalcaemia was by stopping her oral Calcium tablets and 1 alfacalcidol. She was treated with normal saline infusion.Pamidronate infusion was contraindicated because of AKI. She was therefore given Calcitonin infusion 400 International units resulting in improvement in her corr. Ca+ to 4.77 mmol/l within 24 hours. She continued to receive normal saline and her biochemistry improved. ECG changes were also resolved. Work up for non PTH dependent severe hypercalcaemia included a CT Thorax Abdomen Pelvis, which did not show any evidence of malignancy, bone lesions or nephrocalcinosis. Her Immunoglobulin electrophoresis was normal. Her severe hypercalcaemia was thought to be multifactorial - contributed by her oral calcium and 1 alphacalcidol supplements and exacerbated by immobility and acute kidney injury. After 5 days of hospital admission, her corr. Ca+ dropped to 2.11 mmol/l. Her calcium tablets and 1 alfacalcidol 1.5microgram OD were restarted.However, her bloods showed worsening hypocalcaemia with corr. Ca+ 1.50 mmol/l despite ongoing treatment with calcium gluconate infusion for 10 days. She was therefore started on Indapamide 2.5 mg once daily which was uptitrated to 5mg once daily. Her corr. Ca+ improved to 2.15mmol/l and she was discharged from hospital. Her bone profile has been followed up since discharge and calcium levels have been in normal range. Her Indapamide has now been discontinued. Conclusion: Although disorders of bone homeostasis are very commonly treated on medical wards, sometimes these electrolyte imbalances can be extremely severe and subsequent management could be quite challenging. Markedly high calcium levels due to primary hyperparathyroidism secondary to adenoma(parathyroid crisis) and malignancy have been reported in the past. However, our case report is the first to highlight such severe hypercalcaemia due to iatrogenic (oral supplements), AKI and immobility causes.