Endocrine Complications of Surgical Treatment of Thyroid Cancer: An Update

Abstract

Postoperative hypoparathyroidism (HypoPT) and hypothyroidism (HypoT) are the main endocrine complications after the surgical treatment for thyroid cancer. Postsurgical HypoPT can be transient, protracted or permanent. Its frequency varies according to the underlying cervical pathology, surgical technique, and mainly the experience of the surgeon. Risk factors for HypoPT include aggressiveness of the tumor, extent of surgery, the presence of parathyroid gland in the pathologic specimen, and surgeon experience. Clinical manifestations of postsurgical HypoPT can be acute or chronic. An adequate surgical technique that minimizes trauma and preserve the vascularization of the parathyroid glands is the better procedure to reduce the risk of postoperative HypoPT. Acute hypocalcemia may be managed with intravenous or oral calcium supplements, according to the level of serum calcium and the presence of signs and symptoms. Patients with permanent HypoPT require lifelong calcium and vitamin D supplementation. Calcitriol is the vitamin D metabolite of preference because of its high activity and short half-life. Both PTH (1-34) and intact PTH (1-84) have demonstrated to be attractive options in hypoparathyroid patients who cannot maintain stable serum and urinary calcium levels with calcium and vitamin D supplementation. However, the long-term safety of these preparations has not been established. Postsurgical HypoT is an unavoidable consequence of total or near-total thyroidectomy for thyroid cancer. Replacement and suppressive therapy are necessary in these patients. Thyroid hormone suppression therapy has shown to be accompanied by a decreased risk of disease progression and recurrence; however, it may also be associated with increased risk of dysrhythmia and loss of bone mass. Therefore, the intensity of TSH suppression must be established in a personalized way after balancing risk and benefits, according to the severity of the thyroid cancer, the response to therapy, and the individual risk factors for adverse events.

Randomized Controlled Trial Comparing White Light with Near-Infrared Autofluorescence for Parathyroid Gland Identification During Total Thyroidectomy

“…Postoperative hypocalcemia is a frequent complication of total thyroidectomy. 1 The incidence of this complication reported in the literature is between 18% and 59%. [2][3][4][5][6] The most common reason for hypocalcemia is inadvertent damage to parathyroid gland circulation, which, in turn, is secondary to the glands' small size, soft texture, and variable location and number.…”

Late Recovery of Parathyroid Function After Total Thyroidectomy: A Case-Control Study

“…Total thyroidectomy is one of the most performed endocrine operations. Definitive or permanent postoperative hypoparathyroidism is the most common chronic complication of this procedure [1,2]. However, the time points used to determine when postoperative hypoparathyroidism should be classified as permanent have been a matter of debate among researchers in the last years [3,4].…”

Postoperative Hypoparathyroidism: Prognosis, Prevention, and Treatment (Review)

“…Most often, hypocalcemia develops after operations performed for diffuse toxic goiter (Graves–Basedow disease) and thyroid cancer [ 5 , 14 ]. This is probably associated with metabolic disorders against the background of accelerated bone tissue remodeling in diffuse toxic goiter [ 15 , 16 ], the technical aspects of surgical intervention and the need for lymphadenectomy in patients with thyroid tumors [ 17 , 18 ]. As a rule, a decrease in calcium levels is recorded 24–48 h after surgery [ 9 , 16 , 19 ].…”

“…The sign of permanent PSHP is hypocalcemia in combination with low levels of PTH during 6 months or more after surgery [ 16 , 19 , 22 , 23 ]. This type of PSHP is observed in 1–7% of patients who underwent thyroidectomy in combination with paratracheal lymphadenectomy or repeated interventions on the thyroid gland [ 17 , 18 , 22 – 24 ]. Inadequate width of surgical margins and surgical injury can lead not only to PTG devascularization, but also to their accidental removal [ 22 , 23 , 25 ].…”