Can rhabdomyolysis cause hypocalcemia in patients?

Rhabdomyolysis and Hypocalcemia

Yes, rhabdomyolysis commonly causes hypocalcemia during the acute phase, occurring in approximately 43% of patients, with the mechanism primarily involving calcium deposition into damaged muscle tissue and exacerbation by hyperphosphatemia. 1

Pathophysiology of Hypocalcemia in Rhabdomyolysis

The hypocalcemia in rhabdomyolysis results from two primary mechanisms:

• Calcium deposition into injured muscle tissue occurs in all patients with rhabdomyolysis independent of whether acute kidney injury (AKI) develops, as documented by technetium-99 scans showing soft tissue calcium deposition 2

• Hyperphosphatemia from muscle breakdown creates calcium-phosphate complexes that precipitate in damaged tissues, with peak inorganic phosphate levels significantly higher in hypocalcemic patients (1.77 ± 1.10 vs. 1.10 ± 0.35 mmol/L) 1

• Acute kidney injury exacerbates hypocalcemia by worsening the hyperphosphatemic effect of muscle damage, with 82% of hypocalcemic rhabdomyolysis patients having concurrent AKI compared to 55% of normocalcemic patients 1

• Impaired phosphate utilization by damaged muscle contributes to elevated serum phosphate levels, which further drives calcium precipitation 1

Clinical Significance and Severity

Hypocalcemia is more pronounced in patients with both rhabdomyolysis and AKI compared to those with rhabdomyolysis alone, making the combination particularly high-risk 2

• Patients with severe rhabdomyolysis (creatine kinase >10^6 U/L) demonstrate the most dramatic calcium disturbances 3

• Peak creatine kinase levels are significantly higher in hypocalcemic patients (39,100 ± 50,600 vs. 9,800 ± 11,900 IU/L) 1

Biphasic Calcium Pattern: Critical Safety Consideration

A dangerous biphasic calcium pattern occurs in approximately one-third of rhabdomyolysis patients with AKI, where initial hypocalcemia transitions to severe, potentially life-threatening hypercalcemia during the recovery/diuretic phase. 2, 4

• Hypercalcemia during recovery can reach dangerous levels (up to 17.1 mg/dL) and may cause severe neurological disturbances, short QT interval, Brugada-like syndrome, and risk of malignant arrhythmias 5, 4

• This hypercalcemia results from mobilization of calcium from calcium-phosphate deposits in injured muscles as renal function recovers, not from disruption of the parathyroid hormone-vitamin D axis 5, 3

• Parathyroid hormone levels are appropriately suppressed during the hypercalcemic phase, confirming the mechanism is calcium release from tissues rather than hormonal dysregulation 2, 4

• The recovery phase poses unexpected mortality risk when clinicians may wrongly assume major dangers have passed 4

Management Implications

Aggressive intravenous fluid resuscitation is critical not only for preventing AKI but also for potentially reducing hypocalcemia incidence by increasing oxygen supply to muscle and improving phosphate utilization 1, 6

• Target urine output of 300 mL/hour to facilitate myoglobin clearance 6

• Monitor electrolytes including calcium and phosphate every 6-12 hours in severe cases 6

• Correct hyperphosphatemia promptly as it directly contributes to hypocalcemia through calcium-phosphate precipitation 6, 1

• Avoid routine calcium supplementation during the oliguric phase unless symptomatic, as calcium may deposit further into damaged tissues 7

• Maintain vigilant monitoring during the recovery/diuretic phase for development of hypercalcemia, which may require hemodialysis with calcium-free dialysate and pamidronate administration 5, 4

Common Pitfalls

• Failing to anticipate the biphasic calcium pattern and discontinuing calcium monitoring after initial hypocalcemia resolves can miss life-threatening hypercalcemia 4

• Aggressive calcium supplementation during acute hypocalcemia may worsen tissue calcium deposition and predispose to more severe rebound hypercalcemia 5, 2

• Not recognizing that hypercalcemia can persist for 3 weeks during recovery, requiring prolonged monitoring 5