Post-parathyroidectomy thyrotoxicosis and atrial flutter: a case for caution

Abstract

Despite transient hyperthyroidism reportedly occurring in ∼30% of post-parathyroidectomy (PTX) patients with primary hyperparathyroidism, it has rarely been described in the internal medicine literature. It occurs within days of surgery, is usually clinically mild or silent, and typically spontaneously resolves within weeks. Patients can, however, unusually present with symptoms and signs of thyrotoxicosis, including arrhythmias. We report a case of a hemodialysis patient who developed self-limited hyperthyroidism after intra-operative thyroid manipulation and excision during PTX surgery for secondary hyperparathyroidism that failed medical management. The patient was symptomatic with agitation, restlessness and new-onset atrial flutter, which required electrical cardioversion and temporary beta blockade. It is important that clinicians be aware of this potential surgical complication, so as to not attribute manifestations to post-PTX divalent cation disorders (i.e. hungry bone syndrome), thereby allowing prompt diagnosis and treatment. Post-operative monitoring of thyroid function is warranted for at least some subsets of patients: individuals who undergo thyroid exploration and palpation as part of their surgery to localize the parathyroid glands, as well as those with underlying cardiac disease or who are otherwise at high risk from even mild states of hyperthyroidism.

Forestalling Hungry Bone Syndrome after Parathyroidectomy in Patients with Primary and Renal Hyperparathyroidism

“…Additionally, another retrospective cohort (N = 19 patients with PHPT) showed that none of the 11 participants who received zolendronic acid (a dose of 4 mg within 1 or 2 days before PTx) developed HBS, while 3/8 individuals who did not receive the drug experienced HBS [45] Post-PTx acute bone pain in individuals with HBS might be differentiated from other post-operatory complications such as chrondrocalcinosis due to sudden drop of calcium and magnesium [7]. Older reports suggested that post-PTx-associated transitory thyrotoxicosis due to gland manipulation might mimic HBS [166].…”

“…One mechanism of serum calcium fall, especially if the patient experienced thyrotoxicosis-associated hypercalcemia, is increased osteoblastic activity, bone formation Post-PTx acute bone pain in individuals with HBS might be differentiated from other post-operatory complications such as chrondrocalcinosis due to sudden drop of calcium and magnesium [7]. Older reports suggested that post-PTx-associated transitory thyrotoxicosis due to gland manipulation might mimic HBS [166].…”