Refractory Hypercalcemia Following Recovery From Rhabdomyolysis – UROP Spring Symposium 2025

Refractory Hypercalcemia Following Recovery From Rhabdomyolysis

Syeda Rizvi

Research Mentor(s): Syed Raza
Mentor Department: Sinai Grace Hospital, Department of Internal Medicine
Authors: Syeda Rizvi, BBA, Syed Raza, MD
Session: Session 7 (4:00pm – 4: 50pm)
Presentation Type: Poster 61

Abstract

This case report describes a 33-year-old male who developed severe heat stroke, leading to rhabdomyolysis, acute kidney injury (AKI), and refractory hypercalcemia following recovery. The patient initially presented with hyperthermia (41.9°C), tachycardia, and multi-organ dysfunction, requiring intubation, aggressive cooling measures, fluid resuscitation, and subsequent hemodialysis for worsening renal function.
Severe rhabdomyolysis resulted in creatine phosphokinase (CPK) levels peaking at 505,000 U/L, leading to hyperkalemia, hyperphosphatemia, and initial hypocalcemia. The hypocalcemia was attributed to calcium deposition in damaged muscle tissue, a common phenomenon in the early phase of rhabdomyolysis. However, as rhabdomyolysis resolved and renal dysfunction persisted, the patient transitioned to refractory hypercalcemia, peaking at 14.1 mg/dL. This metabolic shift was likely driven by secondary hyperparathyroidism, ongoing calcium and phosphate imbalances, and prolonged calcium supplementation during dialysis. Despite medical management, including phosphate binders and dialysis, the patient remained hypercalcemic.
Complicating his clinical course, the patient also developed ventilator-associated pneumonia (VAP) and sepsis, necessitating broad-spectrum antibiotics and prolonged mechanical ventilation. A tracheostomy was performed due to respiratory failure. Persistent azotemia and hypercatabolism required continued dialysis, highlighting the prolonged renal impairment that often accompanies severe rhabdomyolysis.
This case underscores the complex interplay between rhabdomyolysis, AKI, and calcium dysregulation, particularly the transition from early hypocalcemia to refractory hypercalcemia. It highlights the importance of close metabolic monitoring and individualized management strategies in critically ill patients recovering from severe muscle breakdown. A multidisciplinary approach, involving nephrology, endocrinology, and critical care, is essential to optimizing patient outcomes and preventing long-term complications associated with dysregulated calcium homeostasis.

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