How can thyroidectomy lead to hypocalcemia due to hypoparathyroidism?

Updated: May 08, 2018
  • Author: Neerav Goyal, MD, MPH; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Reported rates of transient hypocalcemia vary in the literature from between 5-50%, but the rate of permanent hypocalcemia secondary to hypoparathyroidism (ie, lasting more than 6 months) is between 0.5-2%. The pathophysiology behind transient hypoparathyroidism and hypocalcemia is not well understood but is thought to be related to a transient ischemia to the parathyroid glands or perhaps an increased release of the acute phase reactant endothelin 1. [42] A systematic review of predictors of post-thyroidectomy hypocalcaemia found perioperative parathyroid hormone (PTH), preoperative vitamin D and postoperative changes in calcium to be biochemical predictors. [43] Patients who are at increased risk for this complication are those with Graves disease or malignancy or those undergoing total thyroidectomy, or total thyroidectomy with central compartment neck dissection.

Patients may initially be asymptomatic while hypocalcemic. Classic presenting symptoms include numbness and tingling of the digits or perioral area, carpopedal spasm, or the presence of a Chvostek sign or a Trousseau sign. In severe cases, patients may also experience tetany, EKG changes (QT prolongation), seizures, mental status changes, or cardiac arrest secondary to hypocalcemia. The Chvostek sign can be reproduced by tapping on the face just anterior to the ear, causing contraction of the ipsilateral facial muscles. A patient with a positive Trousseau sign will have spasm of the wrist, fingers, or thumb with inflation of a sphygmomanometer above the systolic blood pressure. Either sign is indicative of neuromuscular excitability associated with hypocalcemia.

Patients who are noted to have postoperative hypocalcemia should be managed with calcium supplementation. By following the trend of serum calcium levels, oral calcium supplementation can be titrated accordingly. If patients are receiving 2 grams of elemental calcium and continue to have decreasing or low serum calcium, calcitriol supplementation between 0.25-1 mcg per day can be considered. Additionally, intravenous calcium replacement may be necessary for patients refractory to oral management or those with severe symptomatic hypocalcemia. Endocrinology consultation should be considered in these patients. Of note, serum calcium levels should be corrected for concurrent hypoalbuminemia and any hypomagnesemia should be medically corrected.

Patients who develop hypocalcemia should be discharged with calcium and vitamin D supplementation and if necessary calcitriol supplementation. After a few months, weaning from the calcium supplementation can be considered.

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