From the Guidelines
The patient in status epilepticus has hypocalcemia primarily due to calcium sequestration in damaged muscle tissue from rhabdomyolysis, as evidenced by elevated CPK levels which are a sign of muscle breakdown 1. During rhabdomyolysis, extensive muscle breakdown occurs, releasing large amounts of phosphate into the bloodstream. This hyperphosphatemia causes reciprocal hypocalcemia as calcium and phosphate form complexes and precipitate in tissues. Additionally, the lactic acidosis exacerbates hypocalcemia by altering protein binding of calcium, reducing the ionized (active) calcium fraction. The damaged muscle cells also directly sequester calcium, further depleting serum levels. This hypocalcemia can worsen seizure activity, creating a dangerous cycle. Some key points to consider in the management of this condition include:
- Addressing the underlying status epilepticus with appropriate anticonvulsants, as outlined in clinical policies for the evaluation and management of adult patients presenting to the emergency department with seizures 1
- Aggressive fluid resuscitation to prevent acute kidney injury from myoglobinuria, which is a significant concern in patients with rhabdomyolysis and elevated CPK levels 1
- Careful calcium replacement if symptomatic hypocalcemia is present, while avoiding rapid correction to prevent calcium-phosphate precipitation in tissues when hyperphosphatemia is present
- Monitoring of calcium, phosphate, and renal function is essential during management of this condition.
From the Research
Rhabdomyolysis and Lactic Acidemia
- Rhabdomyolysis is a serious complication of status epilepticus, which can lead to acute kidney injury (AKI) and other severe consequences 2.
- Lactic acidemia can also occur in patients with status epilepticus, and it may be associated with rhabdomyolysis 3.
- The combination of rhabdomyolysis and lactic acidemia can lead to a range of electrolyte imbalances, including hypocalcemia.
Hypocalcemia in Rhabdomyolysis
- Hypocalcemia is a common complication of rhabdomyolysis, and it is thought to be caused by the release of calcium from damaged muscle cells into the bloodstream, where it is then deposited in tissues such as the kidneys and liver 4.
- Additionally, the acute kidney injury that often accompanies rhabdomyolysis can also contribute to hypocalcemia by reducing the kidney's ability to activate vitamin D, which is necessary for calcium absorption.
Relationship between Status Epilepticus and Hypocalcemia
- Status epilepticus can lead to rhabdomyolysis, which in turn can cause hypocalcemia 2, 3.
- The exact mechanisms by which status epilepticus leads to rhabdomyolysis and hypocalcemia are not fully understood, but it is thought to involve a combination of factors, including muscle damage, metabolic disturbances, and electrolyte imbalances.
- In some cases, hypocalcemia may be exacerbated by the use of certain antiepileptic drugs, which can interfere with calcium metabolism 4.