Abstract
Postoperative hypoparathyroidism is the most common complication following total thyroidectomy and is usually transient. Calcium supplementation is guided by serial biochemical monitoring, targeting low-normal serum calcium to avoid hypocalcaemia while facilitating parathyroid recovery. Respiratory alkalosis reduces ionized calcium, though its impact postoperatively is under-recognized. We report a 30-year-old male who developed hypoparathyroidism after total thyroidectomy and neck dissection for medullary thyroid carcinoma. Anxiety-driven hyperventilation caused recurrent respiratory alkalosis, producing symptomatic reductions in ionized calcium despite escalating intravenous replacement. This culminated in a code blue activation, ICU admission, and subsequent hypercalcaemia. We propose that respiratory alkalosis contributed to apparent refractory hypocalcaemia, and that aggressive calcium replacement may have delayed parathyroid recovery through iatrogenic suppression. This case highlights the importance of recognizing respiratory alkalosis as a reversible contributor to hypocalcaemia and exercising caution with calcium supplementation in postoperative hypoparathyroidism.