The Silent Surge: A Case of Rhabdomyolysis-Induced Hypercalcemia

BACKGROUND Calcium is an essential extracellular cation that the body tightly regulates for numerous physiological functions. Rhabdomyolysis typically causes hypocalcemia due to calcium sequestration within damaged muscle tissue. However, in rare cases, it can progress to hypercalcemia, particularly during the recovery phase, often in patients with concurrent acute kidney injury. CASE REPORT A 48-year-old man with no prior medical or surgical history was admitted to the hospital after he had been found unresponsive at home. His initial toxicology screen revealed the presence of cocaine, fentanyl, and benzodiazepines. He was diagnosed with rhabdomyolysis complicated by acute kidney injury and left upper arm compartment syndrome, requiring emergent fasciotomy and renal replacement therapy. During hospitalization, he developed peritonitis secondary to bowel perforation, which warranted laparotomy. Six weeks later, he presented with nausea, vomiting, and constipation, leading to diagnosis of severe hypercalcemia (serum calcium level, 15.3 mg/dL [reference, 8.9-10.2 mg/dL]; albumin-corrected calcium level, 16.7 mg/dL). The patient received intravenous fluids and diuretics, followed by denosumab, which resulted in normalization of calcium levels and resolution of symptoms. CONCLUSIONS Rhabdomyolysis may initially present with severe hypocalcemia, followed by delayed hypercalcemia due to calcium sequestration and subsequent release from necrotic muscle tissue. In the present case, delayed hypercalcemia was successfully managed with intravenous fluids, diuretics, and denosumab. Recognition of this delayed pattern is critical for accurate diagnosis and appropriate management. Our patient exhibited a particularly delayed presentation of hypercalcemia and displayed an exceptionally high calcium level.