Why does a patient with lactic acidosis and rhabdomyolysis (muscle breakdown) secondary to status epilepticus (prolonged seizure) present with hypocalcemia (low calcium levels)?

From the Guidelines

Hypocalcemia in a patient with lactic acidosis and rhabdomyolysis secondary to status epilepticus occurs primarily due to calcium sequestration in damaged muscle tissue and calcium-phosphate deposition. This condition is further complicated by the release of large amounts of phosphate into the bloodstream from damaged muscle cells, which binds with calcium to form calcium-phosphate complexes that deposit in tissues 1. The acidosis initially present can mask hypocalcemia by increasing the ionized calcium fraction, but as acidosis is corrected, total calcium levels may drop further, as noted in the context of trauma patients where ionised calcium levels are crucial for coagulation and cardiac function 1. Key factors contributing to hypocalcemia in this scenario include:

• Calcium sequestration in damaged muscle tissue
• Calcium-phosphate deposition due to high phosphate levels from muscle breakdown
• Acidosis masking initial hypocalcemia, with potential worsening as acidosis is corrected
• Release of intracellular components that can chelate calcium from damaged muscle cells Management should focus on:
• Careful calcium replacement, potentially with calcium chloride as the preferred agent due to its higher elemental calcium content compared to calcium gluconate 1
• Correction of the underlying acidosis
• Aggressive hydration to prevent acute kidney injury
• Monitoring of phosphate levels to avoid worsening calcium-phosphate deposition It's crucial to approach calcium replacement cautiously to avoid overly aggressive correction, which can worsen tissue deposition of calcium-phosphate complexes once the acute phase resolves 1.

From the Research

Pathophysiology of Lactic Acidosis and Rhabdomyolysis

• Lactic acidosis and rhabdomyolysis can occur secondary to status epilepticus, as seen in the cases presented in 2 and 3.
• The pathogenesis of lactic acidosis involves the accumulation of lactate, a crucial intermediate in carbohydrate and nonessential amino acid metabolism, as discussed in 4.
• Rhabdomyolysis, on the other hand, is a complex medical condition involving the rapid dissolution of damaged or injured skeletal muscle, as described in 5.

Hypocalcemia in the Context of Rhabdomyolysis

• Hypocalcemia can occur in patients with rhabdomyolysis, although the exact mechanism is not fully understood.
• It is possible that the release of intracellular contents, including calcium, from damaged muscle cells may contribute to hypocalcemia.
• However, there is limited direct evidence in the provided studies to support this claim, and further research is needed to fully understand the relationship between rhabdomyolysis and hypocalcemia.

Clinical Implications

• The presence of lactic acidosis and rhabdomyolysis in patients with status epilepticus can have important implications for morbidity and mortality, as discussed in 4 and 2.
• Clinicians should be aware of the potential for these complications and monitor patients closely for signs of muscle damage and metabolic disturbances.
• The use of propofol infusion should also be carefully considered, as it has been associated with metabolic acidosis, rhabdomyolysis, and death in adults, as reported in 6.