Case Presentation: The patient is a 63-year-old female who presented with 3 days of new-onset facial flushing, dysphagia, and diffuse left upper extremity and perioral paresthesias. She underwent a total thyroidectomy 4 days before admission for multinodular goiter with an NRAS mutation positive nodule, which carries a 75% risk of malignancy and a RYGB >10 years ago. Vitals on admission were normal. Physical exam was notable for a positive Chvostek’s sign and bilateral hand tetany. Labs revealed a serum calcium of 6.5 mg/dL, an ionized calcium of 0.76 mmol/L, a magnesium of 1.5 mg/dL, a PTH level of 4 pg/mL, and a normal vitamin D level of 54 ng/mL. Pathology confirmed intact PTH glands without parathyroid tissue in the surgical specimen. The patient received 30G of IV calcium gluconate with only partial symptomatic improvement. She received magnesium supplementation, calcium carbonate 1000 mg three times daily, calcitriol 0.5 mcg twice daily, and IV calcium gluconate as needed for a serum calcium of < 7 mg/dL. With this regimen, the patient noted resolution of her symptoms, yet her serum calcium remained < 7.5 mg/dL. Endocrinology recommended switching oral calcium carbonate to liquid suspension with meals to improve gut absorption. Her serum calcium improved to 7.9 mg/dL at discharge and 8.3 mg/dL at outpatient follow-up.
Discussion: Despite recurrent administration of IV calcium gluconate and escalating doses of oral calcium carbonate and calcitriol, this patient’s serum calcium remained low, suggesting other etiologies of her hypocalcemia. One possibility was her hypomagnesemia, which can suppress PTH secretion and contribute to hypocalcemia. Additionally, hungry bone syndrome (HBS), which presents as a serum calcium level < 8.4 mg/dL for at least 4 days in 12% of all patients after thyroid or parathyroid surgery, was considered. However, HBS is linked with pre-existing hyperthyroidism or prolonged PTH exposure. This was not the case here, as her TSH and free T4 were normal before surgery. Hypocalcemia secondary to the absence of PTH glands was also less likely given intact PTH glands, but any trauma or devascularization during surgery may have contributed. Most importantly, this patient’s RYGB increased her risk for severe hypocalcemia. In 2011, Sakhaee and Pak demonstrated that liquid calcium led to more superior bioavailability compared to tablet formulation in patients after a RYGB due to limited GI absorption. Routine outpatient monitoring is encouraged to prevent hypercalcemia in those on long-term repletion.
Conclusions: This case highlights the multifactorial nature of hypocalcemia management and illustrates the importance of individualizing treatment plans, particularly in cases of malabsorption, to prevent prolonged hospitalizations.