Review Article
Introduction
Total thyroidectomy is a common surgical procedure and is often the treatment of choice for a number of benign and malignant conditions. However, despite being a relatively safe procedure in experienced hands, hypoparathyroidism remains one of the most common complications [1,2]. Patients suffering from postoperative hypoparathyroidism generally present with a low postoperative serum calcium [Ca], a high phosphate and a low parathyroid hormone [PTH] level. Symptomatic hypocalcemia [such as numbness, muscle spasms, confusion] may occur, although it is getting less common because of the improved postoperative Ca management [3]. Regarding the etiology of postoperative hypoparathyroidism, it is generally thought that it is due to a transient reduction in blood supply of in situ parathyroid glands [PGs], which results in a transient reduction of parathyroid function [or hormone secretion]. Although inadvertent removal of PGs [i.e., incidental parathyroidectomy] may contribute to hypoparathyroidism, it does not happen often. As a result, provided the PG is not entirely stripped of its blood supply, normalization of parathyroid function is expected for the majority of patients. Nevertheless, this recovery phase may take several weeks to months [i.e., protracted hypoparathyroidism] [2]. After normalization, patients are usually able to stop their oral Ca ± calcitriol supplements. However, a small proportion [