Biphasic Calcium Response to Rhabdomyolysis.

Nina Wietek, Demelza Vinnicombe, Gemma Hopkins, Alex Sumption, Roaa Al-Bedaery, Rabia Topan, Sagen Zac-Varghese, Stephen Robinson, Jeremy Cox


A 27 year old female was brought in by ambulance with collapse. Prior to admission she had felt unwell and the previous day developed nausea, vomiting and rigors. Immediately following arrival in A&E, she had a PEA arrest and CPR was started. Her blood gas at the time of arrest revealed low ionised calcium (0.78 mmol/L) and she was given 30 mmol calcium chloride. Following return of spontaneous circulation she was intubated and transferred to ITU. She developed acute kidney injury secondary to rhabdomyolysis and was anuric requiring haemofiltration. She remained on ITU for three weeks and was stepped down to the wards with a tracheostomy.

She was referred to the endocrine team at this time for investigation of hypercalcaemia. It was noted that following the hypocalcaemia on admission, the calcium levels had steadily risen over the three week period to a peak of 3.4. Her phosphate level fluctuated, however, was always on the high normal side. Further investigations revealed a normal serum ACE, a non-reactive Elispot test for TB, low vitamin D levels and, a low PTH. Her calcium remained high for 10 days and was unresponsive to aggressive fluid administration.

It was suspected that the biphasic changes in calcium were caused by rhabdomyolysis induced AKI. During the oliguric phase, hypocalcaemia and hyperphosphataemia were seen. This occurs due to calcium influx into damaged muscle. The initial muscle injury acts as a nidus for calcium deposition and this process is accelerated by hyperphosphataemia. Following this, during the diuretic phase, there was marked hypercalcaemia. This develops as a result of secondary hyperparathyroidism and the extrusion of calcium from recovering muscle cells.

Learning points:

1. Fluctuations in calcium levels following trauma are often missed and should be actively sought

2. Treatment of hypocalcaemia during the oliguric phase can be problematic and may lead to an exaggerated second phase.

3. Hypercalcaemia is usually treated with rehydration only. However, in this case of rhabdomyolysis induced hypercalcaemia, fluid diuresis was insufficient and IV bisphosphonates had been used. It is recommended that an endocrine opinion is sought early in the course of such patients.