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Abstract: TH-PO177

Resolution of Intramuscular Calcifications on CT Scan Correlating with Severe Hypercalcemia in the Recovery of Rhabdomyolysis

Session Information

Category: Trainee Case Report

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Maike, Andrew S., Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Maddatu, Judith, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Vickery, Matthew R., Medical College of Wisconsin, Milwaukee, Wisconsin, United States
  • Sturgill, Daniel Allen, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
Introduction

Calcium homeostasis in rhabdomyolysis often follows a biphasic pattern of hypocalcemia during the oliguric phase followed by potentially life-threatening hypercalcemia during the non-oliguric phase. We present a case of sudden onset severe hypercalcemia corresponding with improved urine output and dissolution of intramuscular calcium deposits as identified on commuted tomography (CT).

Case Description

A 23-year-old male was admitted after drowning and subsequent cardiac arrest resulting in anuric AKI due to rhabdomyolysis. Initial lab work demonstrated a creatinine kinase > 50,000 µ/L, hyperkalemia, hypocalcemia, and hyperphosphatemia. On the day the patient became non-oliguric his calcium began gradually rising to a peak ionized calcium of 1.91 mmol/L requiring multiple sessions of hemodialysis. Workup demonstrated depressed intact parathyroid hormone, Vitamin D 25-OH and 1-25(OH)2 Vitamin D as well as ongoing hyperphosphatemia and a marginally elevated 24-hour urine calcium. Comparison of two CT scans obtained during the oligoanuric/hypocalcemic and non-oliguric/hypercalcemic phases of AKI demonstrated a clear reduction in intramuscular calcification. Calcium levels improved spontaneously after 11 days along with complete renal recovery.

Discussion

Sudden onset of severe hypercalcemia during the non-oliguric phase of AKI in the setting of rhabdomyolysis is due to mobilization of intramuscular calcium as evidenced by decreased intramuscular calcification observed on CT scan, a novel finding. Previous cases have described secondary hyperparathyroidism as the driving cause of hypercalcemia, although PTH was appropriately suppressed in this case, which is a unique finding. The temporal relationship between renal recovery and hypercalcemia could be explained by contemporaneous recovery of renal and skeletal tissue. Nephrologists must remain vigilant during the recovery phase of rhabdomyolysis and monitor for potentially life-threatening hypercalcemia.

CT abdomen on days 14 (L) and 29 (R) during the oliguric and non-oliguric phases of rhabdomyolysis induced AKI with improving intramucular calcification