SFEBES2008 Poster Presentations Clinical practice/governance and case reports (86 abstracts)
Salisbury District Hospital, Salisbury, Wiltshire, UK.
A 71-year-old man with carcinoma of prostate and bony metastasis, presented with acute bradyarrhythmia, severe hypocalcaemia and acute renal failure 72 h after intravenous infusion of zoledronate. Before therapy, serum calcium was 2.14 mmol/l (normal, 2.102.55 mmol/l), serum phosphate 1.4 mmol/l (normal, 0.81.5 mmol/l), serum creatinine 95 umol/l and eGFR 74 ml/min. 25OH vitamin D was not measured. Three days later he presented with a syncopal episode. Initial blood pressure was 100/60 and cardiac monitoring showed nodal escape rhythm (35/min) with prolonged episodes of sinus arrest necessitating urgent cardiac pacing. His albumin-corrected serum calcium was 1.3 mmol/l, phosphate 1.29 mmol/l, 25-hydroxyvitamin D 9.5 ng/ml (normal, 2060 ng/ml), magnesium 0.9 mmol/l (normal, 0.700.90 mmol/l), potassium 5.8 mmol/l, parathyroid hormone 23 pmol/l (normal, 1.56.0 pmol/l) and creatinine 214 μmol/l.
He required 2 weeks of continuous intravenous calcium gluconate. For the first 10 days he required 120 ml of 10% solution per day with 1 μg of 1αcalcidol to maintain a serum calcium above 1.70 mmol/l. Within 3 days of commencing calcium and vitamin D replacement, normal sinus rhythm and renal function were restored.
Zoledronate is a long-acting bisphosphonate that inhibits osteoclast-mediated bone resorption and thereby reduces serum calcium concentration. Severe acute hypocalcaemia is rarely reported and acute bradyarrhythmia necessitating urgent cardiac pacing complicating severe hypocalcaemia has not been reported.
Vitamin D deficiency has been well documented in elderly and inpatient populations and may have an incidence as high as 60%. Undiagnosed deficiency would increase the risk of acute hypocalcaemia subsequent to zoledronate and we suggest that serum calcium and vitamin D concentrations should be measured before initiating treatment. After treatment, serum calcium concentration should be monitored so that replacement therapy can be initiated as early as possible and symptomatic hypocalcaemia prevented.