SAT-339 Calcium Level in a Patient with Rhabdomyolysis. A Tale of Two Phases

Background: Calcium kinetics can be challenging during the different phases of rhabdomyolysis(1). We herein report a case of sever hypercalcemia refractory to hemodialysis following a period of hypocalcaemia that developed in a patient with rhabdomyolysis. Case: A 27-year-old male patient was diagnosed with meningoencephalitis complicated with septic shock, continuous seizures, rhabdomyolysis, acute kidney injury and oliguria. His creatinine was 219 μmol/L (53–115), urea was 8 mmol/L (2.5–6.4). Creatine kinase (CK) was significantly high above assay range. Corrected serum calcium was 1.82 mmol/L (2.12- 2.52), phosphate was 0.48 mmol/L (0.81–1.58). He required intermittent sessions of hemodialysis and antibiotics therapy which both have been initiated since the first day of admission. Initially he had hypocalcaemia but as rhabdomyolysis improved, his calcium levels started to rise to reach normal levels by day 13 post admission. By day 16, he started to gradually develop hypercalcemia. Initially, it was 2.73 mmol/L and in another 10 days it was 3.39 mmol/L and reached maximum of 3.90 mmo/L despite the intermittent dialysis sessions. PTH was supressed at 0.62 Pmol/L. Over that time, his renal functions and urine output were gradually improving. The clinical impression was PTH independent hypercalcemia and the work up for that was initiated. CT chest, abdomen and pelvis did not reveal any suspicious masses, lytic bone lesions, or lymphadenopathies. His acid fast bacilli stain and culture were both negative. His chest imaging did not show any findings to suggest sarcoidosis. TSH was normal and random cortisol was 339.2 nmol/l with albumin 20g/L. HIV serology came back negative. He received Calcitonin 500 IU BID for three days and Denosumab 120 mg SC in order to control the hypercalcemia along with, cautious intravenous hydration. Within one week after Denosumab therapy, serum corrected calcium decreased to 3.07 mmol/L. After another week, corrected calcium reached 2.53 mmol/L. When his urine output improved further and his calcium levels dropped, hemodialysis was discontinued. His calcium level later normalised to 2.49 mmol/L. After ruling out the common differential of PTH independent hypercalcemia, and from the diuretic phase the patient went through with concomitant hypercalcemia following hypocalcaemia, it was concluded that the cause of hypercalcemia was rebound hypercalcemia following rhabdomyolysis recovery. Conclusion: hypercalcemia can complicate the recovery phase of rhabdomyolysis. Careful monitoring of calcium levels and management are warranted. References: [1] Mohsin N, Budruddin M, Pakkyara A. Calcium Kinetic in a Patient with Acute Renal Failure due to Rhabdomyolysis: A Case Report and Review of Literature. Oman Medical Journal. 2010;25:324–326.