Phosphorus Dynamics During Rhabdomyolysis
During rhabdomyolysis, phosphorus levels typically rise initially due to massive release from damaged muscle cells, followed by potential hypophosphatemia during the recovery phase, which can lead to significant morbidity and mortality if not properly managed.
Initial Hyperphosphatemia Phase
- When muscle breakdown occurs, large amounts of intracellular phosphorus are released into the bloodstream 1
- This release causes acute hyperphosphatemia, which can contribute to:
Mechanisms and Complications
Hyperphosphatemia during rhabdomyolysis can lead to:
Calcium phosphate deposits in the kidney:
Recovery Phase Hypophosphatemia
As recovery begins, phosphorus levels may paradoxically drop due to:
- Renal losses during polyuric phase
- Cellular uptake during muscle repair
- Decreased intake during illness
Severe hypophosphatemia (<2.0 mg/dL) during recovery can cause:
Management Considerations
Monitor serum phosphorus levels frequently during both acute and recovery phases 7
During hyperphosphatemic phase:
During recovery/hypophosphatemic phase:
Clinical Pearls and Pitfalls
- Pitfall: Failing to recognize that ongoing rhabdomyolysis may mask severe underlying hypophosphatemia 4
- Pearl: Six laboratory predictors of rhabdomyolysis in hypophosphatemic patients: sodium, chloride, glucose, BUN, uric acid, and serum osmolality 4
- Pitfall: Assuming stable phosphorus levels throughout the course of rhabdomyolysis
- Pearl: In patients requiring dialysis, longer and more frequent sessions may be needed for phosphorus control 2
Special Considerations
In patients with pre-existing CKD, phosphorus management is even more critical:
Intensive dialysis may be required for severe hyperphosphatemia: