SAT-749 - Prolonged Hungry Bone Syndrome Following Parathyroidectomy Requiring 47 Days of Intravenous Calcium Therapy: A Case Report

Hungry Bone Syndrome (HBS) is a severe complication of Parathyroidectomy characterized by prolonged, symptomatic hypocalcemia due to rapid skeletal calcium uptake into chronically demineralized bone. Patients with tertiary hyperparathyroidism (THPT), markedly elevated parathyroid hormone (PTH) and alkaline phosphatase (ALP), and extensive skeletal involvement are at the highest risk. While most cases resolve within days to weeks, exceptionally prolonged courses requiring extended intravenous calcium therapy are rare.  
A 46-year-old man with end-stage renal disease on maintenance hemodialysis presented after a ground-level fall with pathological fractures of the left femoral neck, clavicle, and scapula secondary to extensive changes of renal osteodystrophy. Laboratory evaluation revealed severe THPT with intact PTH 4,300 pg/ml (normal 15-65), total calcium 10.6 mg/dl (normal 8.5-10.5 mg/dl), phosphorus 7.9 mg/dl (normal 2.5-4.5 mg/dl), and markedly elevated ALP 1,500 U/L. Whole-body bone scan demonstrated diffuse tracer uptake through the skeleton.
The patient underwent cemented hip hemiarthroplasty followed by subtotal parathyroidectomy with the removal of four parathyroid glands and one supernumerary gland (weights 800-2,000 mg) (normal 30-60 mg/gland), with reimplantation of the left inferior gland. Histopathology confirmed parathyroid gland hyperplasia.  
Postoperatively, the patient developed severe HBS with ionized calcium nadirs of 0.87 mmol/L (normal 1.15-1.35). He required continuous intravenous calcium gluconate infusion for 47 days despite aggressive oral calcium supplementation (maximum 3750 mg Calcium Carbonate four times daily) and escalation of calcitriol to 8 mcg daily. Multiple weaning attempts resulted in recurrent symptomatic hypocalcemia.
On Postoperative day 33, during attempted weaning, the patient developed a new displaced right femoral neck fracture, which was managed conservatively. Intravenous calcium was finally discontinued on postoperative day 47. Total hospitalization was 70 days, complicated by catheter-associated deep vein thrombosis, bacteremia, and pleural effusion. At discharge, the patient remained on calcium carbonate 2,500 mg three times daily, cholecalciferol 10,000 IU daily, and intravenous calcitriol 1 mcg three times weekly during hemodialysis.  
This case represents exceptionally severe and prolonged presentation of HBS requiring 47 days of continuous intravenous calcium therapy and 70-day hospitalization. Extreme PTH and ALP elevations, extensive brown tumors, large parathyroid gland burden, and multiple pathologic fractures were predictive of severe, protracted HBS. Clinicians managing high-risk THPT patients should anticipate prolonged hypocalcemia and prepare for extended hospitalization with aggressive supplementation, close monitoring, and multidisciplinary care coordination.

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