Hyperphosphatemia in rhabdomyolysis is explained by which mechanism?

Hyperphosphatemia in rhabdomyolysis is explained by which mechanism?

• A. Massive cellular lysis or crush injury releasing intracellular phosphate
• B. Inability to excrete phosphate
• C. Increased calcium citrate complexation
• D. Massive transfusion

Answer: (A)

Massive cellular lysis from muscle crush injury releases intracellular phosphate into the bloodstream. Muscle cells store a lot of phosphate as part of ATP and phosphocreatine, so when they rupture, this phosphate floods into circulation and raises serum phosphate levels. Kidney excretion can modulate how high it goes, and if there’s concurrent kidney injury from the rhabdomyolysis, hyperphosphatemia can be amplified, but the primary mechanism is the release of phosphate from damaged muscle cells. The other options don’t fit as the initiating cause: inability to excrete phosphate happens mainly with renal failure, calcium citrate complexation is a downstream interaction involving calcium, and massive transfusion isn’t the fundamental driver of phosphate rise in rhabdomyolysis.

Massive cellular lysis from muscle crush injury releases intracellular phosphate into the bloodstream. Muscle cells store a lot of phosphate as part of ATP and phosphocreatine, so when they rupture, this phosphate floods into circulation and raises serum phosphate levels. Kidney excretion can modulate how high it goes, and if there’s concurrent kidney injury from the rhabdomyolysis, hyperphosphatemia can be amplified, but the primary mechanism is the release of phosphate from damaged muscle cells. The other options don’t fit as the initiating cause: inability to excrete phosphate happens mainly with renal failure, calcium citrate complexation is a downstream interaction involving calcium, and massive transfusion isn’t the fundamental driver of phosphate rise in rhabdomyolysis.