Abstract
Postoperative hungry bone syndrome remains a clinically significant complication following parathyroidectomy for primary hyperparathyroidism, characterized by profound and prolonged hypocalcemia, hypophosphatemia, and hypomagnesemia resulting from rapid skeletal remineralization after abrupt normalization of parathyroid hormone levels. This updated review synthesizes contemporary evidence on the pathophysiology, risk stratification, and management of hungry bone syndrome, emphasizing its increasing recognition in an era of earlier surgical intervention and advanced metabolic profiling. Key predisposing factors include severe preoperative bone disease, elevated bone turnover markers, large parathyroid adenomas, concurrent vitamin D deficiency, advanced age, and impaired renal function. Modern diagnostic approaches integrate dynamic calcium monitoring, predictive scoring models, and preoperative assessment of bone mineral density to enable proactive intervention. Recent therapeutic advances highlight the efficacy of risk-adapted supplementation protocols, combining high-dose oral calcium, active vitamin D analogs, and targeted magnesium repletion, while minimizing reliance on prolonged intravenous infusions through standardized discharge algorithms. Emerging data also underscore the role of preoperative vitamin D optimization and novel biomarkers in predicting syndrome onset and severity. Despite evolving management strategies, hungry bone syndrome continues to contribute to extended hospitalizations, increased healthcare utilization, and patient morbidity when unrecognized. This review advocates for routine preoperative risk assessment, institutionalized postoperative monitoring pathways, and personalized supplementation regimens to mitigate complications. Therefore, combining collaboration and structured patient education are equally vital for ensuring safe recovery. Additionally, future prospective studies and consensus-driven guidelines remain indispensable to find preventive strategies, optimize calcium homeostasis, and improving long-term skeletal and metabolic outcomes in patients undergoing curative parathyroid surgery.