%0 Journal Article
%T The Use of Hemodialysis in Refractory Hypercalcemia Secondary to Parathyroid Carcinoma
%A Huai Heng Loh
%A Nurain Mohd Noor
%J Case Reports in Critical Care
%D 2014
%I Hindawi Publishing Corporation
%R 10.1155/2014/140906
%X Parathyroid carcinoma is a rare cause of hypercalcemia. Hypercalcemic crisis is a medical emergency. Hemodialysis is rarely needed to treat hypercalcaemia. We report a case of refractory hypercalcaemia secondary to parathyroid carcinoma requiring haemodialysis. 1. Introduction Parathyroid carcinoma is a rare cause of hypercalcaemia. Hypercalcaemic crisis is a medical emergency, which can lead to severe consequences involving neurological, cardiovascular, and renal systems [1]. Standard treatment for hypercalcaemia includes saline hydration, bisphosphonates, steroids, calcitonin [2], and the now commonly reported cinacalcet [3]. The use of haemodialysis to effectively lower serum calcium level in the emergency setting is documented as one of the modalities; however, its use is not commonly reported. We hereby report a patient with recurrent parathyroid carcinoma who had to undergo haemodialysis to effectively lower the calcium level before undergoing a repeat operation. 2. Case Report A 27-year-old lady, with recurrent parathyroid carcinoma, presented to a private hospital with generalized body ache. Her calcium level was 5.3£¿mmol/L. She was adequately resuscitated with saline hydration and intravenous. Zoledronic acid 4£¿mg was given. Upon transfer to our center two days later, her calcium level had fallen to 3.02£¿mmol/L. Despite five liters of hydration daily, three days of subcutaneous calcitonin 200£¿IU b.d. (total daily dose of 8£¿u/kg), and intravenous Pamidronate 90£¿mg, her calcium continued to rise to 4.0£¿mmol/L. Her intact parathyroid hormone (iPTH) level was 156£¿pmol/L. She subsequently developed supraventricular tachycardia, which did not respond to standard medical therapy. The arrhythmia was believed to be related to her hypercalcaemia as echocardiography was normal, potassium was 3.8£¿mmol/L and phosphate level was 0.9£¿mmol/L. As cinacalcet was not readily available, a decision was made for her to undergo urgent dialysis. Normal-heparin haemodialysis was initiated via a femoral catheter using low-calcium dialysate of 1£¿mmol/L, with blood flow rate (Qb) 200£¿mL/min and dialysate flow rate (Qd) 500£¿mL/min. Her potassium level reduced to 2.6£¿mmol/L and phosphate to 0.22£¿mmol/L after dialysis. Hypophosphatemia was not corrected; however it increased to 0.55£¿mmol/L the next day. Hypokalemia was aggressively corrected via intravenous route throughout and after her four-hour haemodialysis, which was otherwise uneventful. Post dialysis, her corrected calcium was lowered to 2.6£¿mmol/L. She required another session of haemodialysis five days later with
%U http://www.hindawi.com/journals/cricc/2014/140906/