Etiology and Diagnosis of Permanent Hypoparathyroidism after Total Thyroidectomy

Abstract

Postoperative parathyroid failure is the commonest adverse effect of total thyroidectomy, which is a widely used surgical procedure to treat both benign and malignant thyroid disorders. The present review focuses on the scientific gap and lack of data regarding the time period elapsed between the immediate postoperative period, when hypocalcemia is usually detected by the surgeon, and permanent hypoparathyroidism often seen by an endocrinologist months or years later. Parathyroid failure after thyroidectomy results from a combination of trauma, devascularization, inadvertent resection, and/or autotransplantation, all resulting in an early drop of iPTH (intact parathyroid hormone) requiring replacement therapy with calcium and calcitriol. There is very little or no role for other factors such as vitamin D deficiency, calcitonin, or magnesium. Recovery of the parathyroid function is a dynamic process evolving over months and cannot be predicted on the basis of early serum calcium and iPTH measurements; it depends on the number of parathyroid glands remaining in situ (PGRIS)-not autotransplanted nor inadvertently excised-and on early administration of full-dose replacement therapy to avoid hypocalcemia during the first days/weeks after thyroidectomy.

Keywords: PGRIS; hypoparathyroidism; parathyroid failure; recovery; splinting; thyroidectomy.

Figure 1

Nomogram to calculate the probability of recovering from protracted hypoparathyroidism based on s-Ca and iPTH (intact parathyroid hormone) measurements one month after total thyroidectomy (Readapted with permission from ref. [15]).

Figure 2

Hypothetical flow diagram showing the different stages of postoperative hypoparathyroidism (red pathway) or recovery of the parathyroid function (green pathway) after 100 total thyroidectomies performed in a high volume and experienced surgical unit (based on refs. [3,4,14,17]).